Category Archives: Human Genetics

Scientists have found evidence for mutations in some strains of the coronavirus that suggest the pathogen may be adapting to humans after spilling over from bats.

The analysis of more than 5,300 coronavirus genomes from 62 countries shows that while the virus is fairly stable, some have gained mutations, including two genetic changes that alter the critical spike protein the virus uses to infect human cells.

Researchers at the London School of Hygiene and Tropical Medicine stress that it is unclear how the mutations affects the virus, but since the changes arose independently in different countries they may help the virus spread more easily.

The spike mutations are rare at the moment but Martin Hibberd, professor of emerging infectious diseases and a senior author on the study, said their emergence highlights the need for global surveillance of the virus so that more worrying changes are picked up fast.

This is exactly what we need to look out for, Hibberd said. People are making vaccines and other therapies against this spike protein because it seems a very good target. We need to keep an eye on it and make sure that any mutations dont invalidate any of these approaches.

Studies of the virus revealed early on that the shape of its spike protein allowed it to bind to human cells more efficiently than Sars, a related virus that sparked an outbreak in 2002. The difference may have helped the latest coronavirus infect more people and spread rapidly around the world.

Scientists will be concerned if more extensive mutations in the spike protein arise, not only because they may alter how the virus behaves. The spike protein is the main target of leading vaccines around the world, and if it changes too much those vaccines may no longer work. Other potential therapies, such as synthetic antibodies that home in on the spike protein, could be less effective, too.

This is an early warning, Hibberd said. Even if these mutations are not important for vaccines, other mutations might be and we need to maintain our surveillance so we are not caught out by deploying a vaccine that only works against some strains.

The scientists analysed 5,349 coronavirus genomes that have been uploaded to two major genetics databases since the outbreak began. By studying the genetic makeup of the viruses, the scientists worked out how it has diversified into different strains and looked for signs that it was adapting to its human host.

In an unpublished study that has yet to be peer reviewed, the researchers identified two broad groups of coronavirus that have now spread globally. Of the two spike mutations, one was found in 788 viruses around the world, with the other present in only 32.

The study shows that, until January, one group of coronaviruses in China escaped detection because they had a mutation in the genetic region that early tests relied on. More recent tests detect all of the known types of the virus.

Last month, an international team of scientists used genetic analyses to show that the coronavirus likely originated in bats and was not made in a lab as some conspiracy theorists have claimed.

Continued here:
Scientists concerned that coronavirus is adapting to humans - The Guardian

As the virus that causes COVID-19 traveled out of China and proliferated across the globe, it developed small mutations that accumulated into distinct versions of the virus. Scientists can now tell these versions apart by peering into the viral genome.

For example, here in the United States, there is the "West Coast" version of the virus that came directly from Asia, and a slightly different "East Coast" version which traveled through Europe.

But is one version of coronavirus more dangerous than the other? And should we be afraid of these new mutations?

The short answer according to virologists, is no.

Viruses are constantly copying themselves, so it's rather frequent that some of those copies will have mistakes, or mutations. These mutations are neither inherently good nor bad and are random.

So far, the novel coronavirus responsible for the global pandemic is mutating normally as virologists expected to see based on their experience with other similar viruses.

"Viruses mutate," said Dr. Nels Elde, Ph.D., associate professor of human genetics at the University of Utah. "That's one of the things that makes them such a successful entity."

"The word 'mutation' to people means something bad because it's got that connotation to it," said Dr. Vincent Racaniello, Ph.D., Higgins professor of microbiology and immunology at Mt. Sinai School of Medicine of CUNY.

This handout illustration image taken with a scanning electron microscope shows SARS-CoV-2 (yellow)also known as 2019-nCoV, the virus that causes COVID-19 isolated emerging from the surface of cells (blue/pink) cultured in the lab.

"It simply means a change in the genome sequence. It doesn't mean that it's necessarily bad for you at all," Racaniello said. "Plants grow in the spring. Viruses mutate. It's no big deal."

Tune into ABC at 1 p.m. ET and ABC News Live at 4 p.m. ET every weekday for special coverage of the novel coronavirus with the full ABC News team, including the latest news, context and analysis.

But as scientists across the globe learn more about these mutations, many have been eager to use these discoveries to decipher whether the virus is becoming more or less dangerous.

For example, in early March a group of scientists in China identified two different types of the virus, the L-type and the S-type. The L-type was found to be more widespread, leading to early speculation that the virus had evolved into a more infectious version of itself.

More recently, similar research out of Los Alamos National Laboratory in the United States which has not been peer reviewed identified a common mutation in the virus that began spreading in Europe in early February. The scientists suggested this mutation may have helped the virus spread faster and farther because it is inherently more infectious, generating breathless news coverage about a dangerous "mutant" virus.

But another group of scientists from Arizona State University arrived at a nearly opposite interpretation of the mutations they discovered. Their research led them to believe the virus might become weaker and die off, just like the 2003 SARS outbreak.

So far, the speculation about the virus' infectiousness are guesses, said Racaniello. He said there is no iron-clad evidence that these mutations have made any one version of the virus more contagious, deadlier or more resistant to potential therapies.

That's probably good news for humankind, because it means the vaccines and therapies being tested right now are likely to work against all known versions of the virus.

Scientists are actively monitoring the virus to see if it develops potentially dangerous mutations -- or even if it dramatically transforms into a new "strain" -- a word that has a very specific meaning to virologists but has also been used colloquially to describe the different versions of the virus that exist so far.

A new strain would signal a dramatic event, meaning the virus has mutated so much that it is "functionally different" than its predecessor, Elde said. According to Elde, virologists generally agree there is only one "strain" of novel coronavirus, although there are several versions of the virus in different parts of the world.

In fact, what scientists are observing, in terms of the differences between these viruses, is a phenomenon called viral "isolates," said Racaniello. That's when the genetic material develops slight variations that are not significant enough to make the virus behave in a totally different way.

These small changes happen frequently -- sometimes developing within the same person as the virus spreads throughout the human body.

"You can have different isolates from a single patient, by taking different samples from the respiratory tract and in the lung, for example," said Racaniello. "It does not mean the differences have any significance whatsoever."

"I think the bottom line is we don't really know right now whether mutation signals good news or bad news. It is somewhere in between," said Dr. Jay Bhatt, former medical chief at the American Hospital Association and an ABC News contributor.

"I think we will understand this better in the coming months."

Angela N. Baldwin, M.D., M.P.H., is a pathology resident at Montefiore Health System in the Bronx and is a contributor to the ABC News Medical Unit. Sony Salzman is the unit's coordinating producer.

View post:
Yes, COVID-19 is mutating, here's what you need to know - ABC News

Stone artifacts from the Initial Upper Paleolithic at Bacho Kiro Cave: 1-3, 5-7 Pointed blades and fragments from Layer I; 4 Sandstone bead with morphology similar to bone beads; 8 The longest complete blade. Credit: Tsenka Tsanova, License: CC-BY-SA 2.0

Two studies report newHomo sapiensfossils from the site of Bacho Kiro Cave in Bulgaria. The Bacho Kiro Cave site provides evidence for the first dispersal ofH. sapiens across the mid-latitudes of Eurasia. Pioneer groups brought new behaviors into Europe and interacted with local Neanderthals. This early wave largely predates that which led to their final extinction in western Europe 8,000 years later, says Jean-Jacques Hublin, director at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany.

An international research team, led by Jean-Jacques Hublin, Tsenka Tsanova and Shannon McPherron of the Max Planck Institute for Evolutionary Anthropology, and Nikolay Sirakov and Svoboda Sirakova of the National Institute of Archaeology with Museum at the Bulgarian Academy of Sciences in Sofia, Bulgaria, renewed excavations at Bacho Kiro Cave in 2015. The most spectacular finds come from a rich, dark layer near the base of the deposits. Here the team uncovered thousands of animal bones, stone and bone tools, beads and pendants, and the remains of five human fossils.

Except for one human tooth, the human fossils were too fragmented to be recognized by their appearance. Instead, they were identified by analyzing their protein sequences. Most Pleistocene bones are so fragmented that by eye, one cannot tell which species of animal they represent. However, the proteins differ slightly in their amino acid sequence from species to species. By using protein mass spectrometry, we can therefore quickly identify those bone specimens that represent otherwise unrecognizable human bones, says Frido Welker, Postdoctoral Research Fellow at the University of Copenhagen and research associate at the Max Planck Institute for Evolutionary Anthropology.

To know the age of these fossils and the deposits at Bacho Kiro Cave, the team worked closely with Lukas Wacker at ETH Zurich, Switzerland, using an accelerator mass spectrometer to produce ages with higher precision than normal and to directly date the human bones.

The majority of animal bones we dated from this distinctive, dark layer have signs of human impacts on the bone surfaces, such as butchery marks, which, along with the direct dates of human bones, provides us with a really clear chronological picture of whenHomo sapiens first occupied this cave, in the interval from 45,820 to 43,650 years ago, and potentially as early as 46,940 years ago, says Helen Fewlass of the Max Planck Institute for Evolutionary Anthropology. The radiocarbon dates at Bacho Kiro Cave are not only the largest dataset of a single Palaeolithic site ever made by a research team, but also are the most precise in terms of error ranges, say researchers Sahra Talamo from the University of Bologna and Bernd Kromer from the Max Planck Institute in Leipzig.

Though some researchers have suggested thatHomo sapiensmay have already occasionally entered Europe by this time, finds of this age are typically attributed to Neanderthals. To know which group of humans were present at Bacho Kiro Cave, Mateja Hajdinjak and Matthias Meyer of the genetics team led by Svante Pbo at the Department of Evolutionary Genetics at the Max Planck Institute for Evolutionary Anthropology sequenced the DNA from the fragmented fossils bones.

Given the exceptionally good DNA preservation in the molar and the hominin fragments identified by protein mass spectrometry, we were able to reconstruct full mitochondrial genomes from six out of seven specimens and attribute the recovered mitochondrial DNA sequences from all seven specimens to modern humans. Interestingly, when relating these mtDNAs to those of other ancient and modern humans, the mtDNA sequences from Layer I fall close to the base of three main macrohaplogroups of present-day people living outside of Sub-Saharan Africa. Furthermore, their genetic dates align almost perfectly with those obtained by radiocarbon, says Mateja Hajdinjak, Postdoctoral Fellow at the Francis Crick Institute in London and research associate at the Max Planck Institute for Evolutionary Anthropology.

The results demonstrate thatHomo sapiensentered Europe and began impacting Neanderthals by around 45,000 years ago and likely even earlier. They brought into Bacho Kiro Cave high quality flint from sources up to 180 km from the site which they worked into tools like pointed blades perhaps to hunt and very likely to butcher the remains of the animals found at the site.

The animal remains from the site illustrate a mix of cold and warm adapted species, with bison and red deer most frequent, says paleontologist Rosen Spasov from the New Bulgarian University. These were butchered extensively but were also used as a raw material source. The most remarkable aspect of the faunal assemblage is the extensive collection of bone tools and personal ornaments, says zooarchaeologist Geoff Smith from the Max Planck Institute for Evolutionary Anthropology. Cave bear teeth were made into pendants, some of which are strikingly similar to ornaments later made by Neanderthals in western Europe.

Taken together, the Bacho Kiro Cave sediments document the period of time in Europe when Middle Paleolithic Neanderthals were replaced by Upper PaleolithicHomo sapiens(the so-called transition period), and the firstHomo sapiensassemblages are what archaeologists call the Initial Upper Paleolithic. Up to now, the Aurignacian was thought of as the start of the Upper Paleolithic in Europe, but the Initial Upper Paleolithic of Bacho Kiro Cave adds to other sites in western Eurasia where there is an even older presence ofHomo sapiens, notes Nikolay Sirakov of the National Institute of Archaeology with Museum at the Bulgarian Academy of Sciences.

The Initial Upper Paleolithic in Bacho Kiro Cave is the earliest known Upper Palaeolithic in Europe. It represents a new way of making stone tools and new sets of behavior including manufacturing personal ornaments that are a departure from what we know of Neanderthals up to this time, says Tsenka Tsanova of the Department of Human Evolution at the Max Planck Institute for Evolutionary Anthropology. The Initial Upper Paleolithic probably has its origin in southwest Asia and soon after can be found from Bacho Kiro Cave in Bulgaria to sites in Mongolia as Homo sapiensrapidly dispersed across Eurasia and encountered, influenced, and eventually replaced existing archaic populations of Neanderthals and Denisovans.

References:

Initial Upper Palaeolithic Homo sapiens from Bacho Kiro Cave, Bulgaria by Jean-Jacques Hublin et al., 11 May 2020, Nature.DOI: 10.1038/s41586-020-2259-z

A 14C chronology for the Middle to Upper Palaeolithic transition at Bacho Kiro Cave, Bulgaria by Helen Fewlass et al., 11 May 2020, Nature Ecology and Evolution.DOI: 10.1038/s41559-020-1136-3

See the original post:
DNA of Bones Found in Cave Reveals Major Cultural Transition in Europe Took Place Earlier Than Thought - SciTechDaily

this and countless other scientific findings led the President of the American Sociologicalin his 2005 presidential addressto call upon members to, Prepare to defend against the genomic data juggernaut heading their way down the pike.'

Introduction

The 2020 presidential campaign, particularly on the Democratic side, has thus far placed the concept of facts and the science at center stage. When former president Barack Obama endorsed his former Vice President, Joe Biden, for President of the United States on April 14th, former President Obama asserted that Vice President Biden wouldunlike conservativesadhere to the facts and the science in running his administration. Then, on April 28th, former Secretary of State Hillary Clinton added her endorsement of Vice President Biden. Secretary Clinton indicated her view that it was necessary to have a president, who listened to the science, put facts over fiction. As such, she suggested that Vice President Bidenunlike President Donald Trumpwould be that person.

Secretary Clintons endorsement of the former Vice President was followed almost immediately by The New York Times podcast When Science Is Partisan in which Frank Bruni stated: From the very start of his administration President Trump has shrugged off expertise, he has outright mocked experts, and he has shown special disregard for science. Even more dangerous he has frequently presented fiction as fact. So, again and again, Democrats have asserted that their Republican counterparts flagrantly ignore the research findings of experts, thereby regularly running afoul of reality. As I will argue, this Democratic line of argument is simply not correct, and I will trace each groups actual willingness to follow the facts and the science, wherever they might lead.

Failings When It Comes to Science

Conservatives, admittedly, either ignore or reject the well-demonstrated theory of evolution. Simply stated our planet (and all of its many species) were not created in six days. Our Universe is at least 14 billion years old, and the sphere on which we live congealed about 4.5 billion years in the past. But, in 2013, roughly 48% of conservative voters believed that creation according to The Book of Genesis is factual. This is as compared to the 67% of Democrats and 65% of Independents who believe humans evolved over time. As such, rather than alienate this large segment of the Republican electoral base, if a reporter asks a conservative candidate if he or she believes in evolution, the candidate will frequently duck the question. This position is a violation of both the facts and the science, and these Republican politicians should be ashamed of themselves for not endorsing the truth. This is a well-known example of conservatives choosing to ignore the evidence.

Turning to progressivesand the subject of abortionwe find that those on the Left either ignore or reject the scientific facts. In an October, 2019 Quillette article I Asked Thousands of Biologists When Life Begins. The Answer Was Not Popular, Steve Jacobs reported that he had polled 5,337 biologists asking each of them when life begins and 96% answered, at conception. Only 240 (4%) disagreed. Interestingly, 89% of these biologists self-identified as liberal; 85% said they were pro-choice; 63% were secular, and 92% were Democrats. The bottom line is that the scientific consensus does not materially influence their position on the question of life.

Many on the Left also deny the facts and the data regarding the allegation that rising inequality is occurring in the United States. The statistics that rebut this claim can be found in my article published in Merion West entitled In Reply to McManus: Harping on Income Inequality Ignores the Data.

Now we move on to the hard part. Ever since the polymath Francis Galton coined the term Nature Versus Nurture in the second half of the 19th century, the nature-nurture debate has raged on. As Nstor de Buen wrote in Merion West (When We Debate Biological Differences) this past July, All of these cases have one common thread: the Right will argue that differences between human groups (i.e. men and women, or Caucasians and African-Americans) are explained by biology, while the Left will argue that they are largely the result of socialization and historic circumstances. de Buens essay approaches the genes versus environment question from the Left, while my following arguments all spring from the biological side of this basic disagreement.

The first rejection of the idea of genes and human development (often called scientific racism) came from anthropologist Franz Boas. In his 1938 article entitled An Anthropologists Credo, he wrote,It is my conviction that the fundamental ethical point of view is that of the in-group, which must be expanded to include all humanity. This egalitarian bent was formalized in 1942 by one of Boass students, Ashley Montagu, in his book Mans Most Dangerous Myth: The Fallacy of Race. About this book, Aldous Huxley wrote that where most assume that facts speak for themselves, [Montagu] makes it clear that the facts are mere ventriloquists dummies, and can be made to justify a course of action that appeals to the socially conditioned passions of the individuals concerned.

Both men and much of the world were shocked and horrified by the countless travesties of Nazi Germany; as such, this social scientific idea spread far and wide. In his famous and extremely influential 1970 book, The Struggle of the Scientific Revolution, Thomas Kuhn reported:

Spending a year in a community composed predominantly of social scientists confronted me with unanticipated problems about the differences between such communities and those of the natural scientists among whom I had been trained. Particularly, I was struck by the number and extent of the overt disagreements between social scientists about the nature of legitimate scientific problems and methods [] Somehow, the practice of astronomy, physics, chemistry, or biology normally fails to evoke the controversies over fundamentals that today often seem endemic among say, psychologists or sociologists.

In short, the social sciences were rejecting on ethical grounds the findings of the hard sciences.

Then, in 1972, the Left altered course by asserting that the genetic findings of the hard sciences were simply wrong. Richard Lewontins paper The Apportionment of Human Diversity concluded that 80-85% of the variation within human populations is found within local geographic groups and the differences attributable to traditional race groups are a minor part of human genetic variability and thus race had to be a social construct. This idea that there exists no scientific basis for human races spread quickly through the academy and through much of the media.

Next, in their 1984 book Not in Our Genes, Richard Lewontin, Steven Rose, and Leon Kamin added a purely political goal: equal economic outcomes. In their own words, We share a commitment to the project of the creation of a more socially justsocialistsociety. And we recognize that a critical science is an integral part of the struggle to create that society. Their egalitarian goal was now obvious. Diminishing their stature was the recollection of Robert Trivers, a top-notch evolutionary biologist in his own right, who remembered in Vignettes of Famous Evolutionary Biologists Large and Small that Lewontin would lie openly and admit doing so. Lewontin would sometimes admit [] that some of his assertions were indeed fabrications, but he says the fight was ideological and politicalthey lied and so would he. Further deflating Lewontins image was his 1985 book, The Dialectical Biologist, which he co-authored with Richard Levins. In The Dialectical Biologist,they asserted that there was nothing in Marxist or Leninism that could be contradicted by objective reality.

In 1994, Richard Herrnstein & Charles Murray published The Bell Curve, and the battle was truly joined. A number of books written by social scientists were rushed into print all criticizing The Bell Curve, and a rebuttal to this onslaught was signed by over 50 experts regarding the science of intelligence and published in The Wall Street Journal in December of 1994, as an op-ed entitled Mainstream Science on Intelligence. This article stated in part that Intelligence can be measured, and intelligence tests measure it well. (These IQ tests) are among the most accurate (in technical terms, reliable and valid) of all psychological tests and assessments.

Among the books that attacked The Bell Curve was an effort by Russell Jacoby and Naomi Glauberman, who published in 1995 The Bell Curve Debate. Their book contained two essays by Leon Kamin. In one of these essays, he engaged in some initial backpedaling. In The Pioneers of IQ Testing Kamin offered that, There is, of course, the theoretical possibility that the genetic theorists are correct. IQ is highly heritable and perhaps differences between races [] are in large measure due to heredity. There are serious scholars who have assumed this, and who have labored to adduce supporting evidence. Their data ought not to be ignored, and they deserve careful scrutiny.

Things remained relatively quiet until 2000 when the project to synthesize the human genome was completed (after which genetic research took off). Also, in 2003, A.W.F. Edwards struck an important blow against the nurture side of the genes/environment debate by publishing a scholarly paper entitled Human Genetic Diversity: Lewontins Fallacy. In this paper, he found that:

It is therefore been proposed that the division of Homo Sapiens into (ethnic or racial) groups is unjustified by genetic data. This conclusion, due to R.C. Lewontin in 1972, is unwarranted because the argument ignores the fact that most of the information that distinguishes populations is hidden in the correlation structure of the data and not simply in the variation of the individual factors.

This was followed in 2005 by Richard Dawkins writing in The Ancestors Tale that However small the racial partition of the total variation may be, if such racial characteristics, as there are, highly correlate with other racial characteristics, they are by definition informative, and therefore of taxonomic significance. And, thus, any vitality remaining in Lewontins 1972 paper was dissipated.

Then, in 2004, the highly regarded scientific journal, Nature Genetics, devoted an entire special edition (Genetics for the Human Race) to the question of whether human races exist, and the journal found that they did. Next, in a March, 2005 op-ed in The New York Times A Family Tree in Every Gene, Armand Marie Leroi asserted that the consensus regarding social constructs was unraveling and that the new genetic data show that races exist. (Note: Lerois book Mutants: On Human Variety and the Human Body, isby farthe very best book that I have read regarding the role of genes in human development. It is readable, short and persuasive.) One of the 2004 papers that appeared in the Nature Genetics special edition was by Lynn B. Jorde and Stephen P. Wooding entitled Genetic Variation, Classification and Race.' It found that Genetic variation is geographically structured, as expected from the partial isolation of human populations during much of their history. Because traditional concepts of race are in turn correlated with geography, it is inaccurate to state that race is biologically meaningless.

As quoted in Philosophy of Race Versus Population Genetics Round, this and countless other scientific findings led the President of the American Sociologicalin his 2005 presidential addressto call upon members to, Prepare to defend against the genomic data juggernaut heading their way down the pike.

The scientific evidence supporting nature over nurture continued to roll in. For example, in a 2007 article by Tarmo Strenze entitled Intelligence and Socioeconomic Success: A Meta-Analytic Review of Longitudinal Research, it was found that, The relationship between intelligence and socioeconomic success has been the source of numerous controversies. These results demonstrate that intelligence is a powerful predictor of success This sent the progressive lefts claim that economic success is due to privilege down in flames. Even African-American academics joined the fray. In the Winter 2008/2009 edition of The Journal of Blacks in Higher Education, the article Why Family Income Differences Dont Explain the Racial Gap in SAT Scores appeared, and it reported that, For Black and White students from families with incomes of more than $200,000 in 2008, there still remains a huge 149-point gap in SAT scores. Even more startling is the fact that in 2008 Black students from families with incomes of more than $200,000 scored LOWER (emphasis in the original) on the SAT test than did students from White families with incomes between $20,000 and $40,000.

In the interim, neuroscientists had joined the debate. Using functional MRI (fMRI), they were confirming what the geneticists had been discovering. In 2010, Ian J. Deary, Lars Penke, and Wendy Johnson published a paper entitled The Neuroscience of Human Intelligence Differences in the journal Nature Reviews: Neuroscience. They found that, Neuroscience is contributing to the understanding of the biological bases of human intelligence differences [] Quantitative genetic studies have established that there are additive genetic contributions to different aspects of cognitive abilityespecially general intelligenceand how they change through the lifespan. They continued, The brains of some people are more efficient than those of others. The biological foundations of these differences are of great interest to basic and applied neuroscience. There are already some well-replicated general findings. Thus, the differential neuroscience of human intelligence, therefore, has a strong mandate and a firm foundation from which to proceed. Later the authors added, The first adequately powered genome-wide studies of intelligence are in progress.

In 2014, a study by Mark Horowitz entitled Whither the Blank Slate? A Report on the Reception of Evolutionary Biological Ideas Among Sociological Theorists was published in the journal Sociological Spectrum. His paper caused quite a storm in the community of social scientists. Horowitz found that, Sociology is a house divided. Just over half of the (sociological) theorists in our sample deny the role of natural selection in shaping a range of human tendencies. Many more are unwilling to acknowledge the plausibility of evolutionary argument applied to sex differences. (Does this not sound at least a little bit like the beliefs held by Evangelical Christians who also deny evolution?) Progressive social scientists lashed out at this study, but both Jonathan Haidt and Steven Pinker rushed to Horowitzs defense. As Jonathan Haidt wrote in his article Political Diversity Will Improve Social Psychological Studies:

When facts conflict withsacred values, almost everyone finds a way to stick with their values and reject the evidence. On the Left, including the academic Left, the most sacred issues involve race and gender. So thats where you find most direct and I would say flagrant denial of evidence. I think the results of this study do clearly show that political concerns influence the willingness of sociologists to consider a major class of causal factors in human behavior.

To this point, Steven Pinker, in an op-ed in The Washington Post entitled Liberals Deny Science, Too, added that Im not surprised by the findings of this study. Sociology itself is a divided discipline, with radically diverging views on the role of science in general and of course evolution and genetics in particular. Nor am I surprised that gender is the bloodiest shirt. Together with race, gender has always been the biggest impetus for believing in the blank slate, and since the Larry Summers affair almost a decade ago, that has only intensified.

Another uproar came in 2014 with the publication of Nicholas Wades bookTroublesome Inheritances: Genes, Race, and Human History, which asserted that, race has a biological basis, one that is found in the subtle quality of allele frequency. This claim is far more likely than the alternative, that evolution has played no role whatever in shaping present-day societies. (Note: Wade clearly pointed out in the preface of his book that the first half was factual, and the second half was speculation. However, this did not stop 139 geneticists from signing a letter to the editor in The New York Times insisting that the latter portion of Wades book had not yet been demonstrated conclusively.)

A year later, science took a sharp turn away from nurture and toward an almost totally deterministic impact of genes. In an article entitled Meta-analysis of the heritability of human traits based on fifty years of twin studies, J.C. Polderman examined all of the twin studies from 1958 through 2012 (numbering 2,748 separate research projects that looked at 14,558,903 twin pairs, as well as 17,804 human traits). Poldermans meta-analysis was published in the journal Nature Genetics. These scientific researchers found that the observed pattern of twin correlations is consistent with a simple and parsimonious underlying model of the absence of environmental effects shared by twin pairs and the presence of genetic effects that are entirely due to additive genetic variation.

Richard Haier, former editor-in-chief of the scientific journal Intelligence, published a book entitled The Neuroscience of Intelligence in 2017, which found that researchers using functional MRI (fMRI) have concluded that:

Everyone has a notion about defining intelligence and an opinion about how differences among individuals may contribute to academic success and life achievement. Conflicting and controversial ideas are common about how intelligence develops. You may be surprised to learn that the scientific findings about these topics are more definite than you think. The weight intelligence from neuroscience research is rapidly correcting outdated and erroneous beliefs.

He continued, if you already believe that intelligence is due mostly to the environment, new neuroscience facts might be difficult to accept. Denial is a common response when new information conflicts with your prior beliefs. The older you are, the more impervious your beliefs may be. Santiago Casal, the father of neuroscience, once wrote: Nothing inspires more reverence and awe in me than the old man who knows how to change his mind.'

In 2018, Harvard geneticist David Reich published the book Who We Are and How We Got Here, bringing with it the following thoughts: Reich allows readers to discover how the human genome provides not only all the information a human embryo needs to develop but also the hidden story of our species. Reich delves into how the genetic revolution is transforming our understanding of modern humans and how DNA studies reveal deep inequalities among different populations, between the sexes, and among individuals. Even more compelling was the op-ed How Genetics is Changing Our Understanding of Race that Reich wrote for The New York Times in March of 2018. According to Reich, it was found that with Groundbreaking advances in DNA sequencing [we now know that] differences in genetic ancestry that happens to correlate to many of todays racial constructs are real. Later, Reich followed by writing, I have deep sympathy for the concern that genetic discoveries could be misused to justify racism. But as a geneticist, I also know that it is simply no longer possible to ignore average genetic differences among races.' He concluded: I am worried that well-meaning people who deny the possibility of substantial biological differences among human populations (races) are digging themselves into an indefensible position, one that will not survive the onslaught of science.

In 2018, a group of sociologists decided to confront head-on this question, and they published the book Reconsidering Race: Social Science Perspectives on Racial Categories in the Age of Genomics. The forward to this tome was penned by Henry Louis Gates, Jr., and it offered:

For decades most [social science] scholars and even the general publicat least in the United Statesgenerally accepted the story that races are socially constructed [but] after the initial completion of the genome [project] around the year 2000, some in the scientific community began unearthing vestiges of debates and questions around the science-race linkage. Even prominent scientific journals such as Science and Nature published articles that seemed to reassert the existence of categories that match the traditional understanding of racial groups. These developments have forced social scientists to reconsider race: To ask whether there is any credence to the natural science arguments that there might be a biological and genomic foundation to racial categories.

On January 28, 2020, Charles Murrays latest effort Human Diversity: The Biology of Gender, Race, and Class hit bookstore shelves, and another blow was struck against the soft sciences orthodoxy of social construction. According to Murray, All people are equal [but] all groups of people are not the same. Murray also writes:

advances in genetics and neuroscience are overthrowing an intellectual orthodoxy that has ruled the social sciences for decades. The core of the orthodoxy consists of three dogmas: gender is a social construct; race is a social construct and class is a function of privilege. The problem is that all three dogmas are half-truths. They have stifled progress in understanding the rich texture that biology adds to our understanding of the social, political, and economic worlds we live inWhy the resistance? Because social scientists have been in the grip of an orthodoxy (gender, race & class) that is sacred stiff of biologyThe core doctrine of the (gender, race & class) orthodoxy in the social sciences is a particular understanding of human equality.

It is not, for Murray, equality in the sense of Americas traditional idealall are equal in the eyes of God, have inherent dignity, and should be treated equally under the lawbut equality in the sense of sameness. in a properly run society, people of all human groupings will have similar life outcomes. (Emphasis in the original) Individuals might have differences in abilities but groups do not have inborn differences in the distribution of abilities. Inside the cranium, all groups are the same.

I firmly believe that all of the aforementioned scientific evidence, findings, and data lead to the conclusion that many members of the progressive left are failing to accept the clear cut truth on a number of issues, thereby doing precisely what they accuse their conservative counterparts of.

Climate Change

But what about climate change? I now turn to that topic, and readers will quickly see why I saved global warming until the end. First, here is an overview of the alleged scientific consensus regarding Anthropogenic Global Warming (AGW). Three surveys of climatologists have determined that 97% of these scientists believe in AGW. This finding has been repeatedly reported in the media. However, what many media outlets never mention is that a nationwide poll taken of meteorologists in 2016 found that Nearly half of weathercasters (46%) are convinced that the climate change over the past 50 years has been primarily or entirely due to human activity, and nearly one quarter (22%) think it is more or less equally caused by human activity and natural events. About one quarter (24%) think the change has been primarily or entirely due to natural events. But 46% is nowhere near 97%. And, far too frequently, media outlets fail to tell the complete story of scientific findings on climate change. As such, I have included below a non-exhaustive list of findings from climate science that might appear very surprising to those who have exclusively followed certain popular treatments of the issue.

Scafetta et al (2017) concluded that The severe discrepancy between observations and modeled predictions found during the 1922-1941 and 2000-2016 periods further confirms, according to the criteria proposed by the AGW theory advocates themselves, that the current climate models have significantly exaggerated the anthropogenic greenhouse warming effect. According to AGW theory advocates own criteria, a divergence between observations and climate models occurring at a bi-decadal scale would provide strong convincing evidence that the global climate models used to support the AGW theory are severely flawed. Thus the models are not able to reproduce the natural variability observed in the climate system and should not be trusted for future planning.

Cerrone & Fusco (2018) the results herein indicate that a progressive cooling has affected the year-to-year climate of the sub-Antarctic since the 1990s.

Kim et al (2018) the Yellow and East China Seas are widely believed to have experienced robust, basin-scale warming over the last few decades. However, this warming reached a peak in the late 1990s, followed by a significant cooling trend.

Morner (2018) The concept of an anthropogenic global warming (AGW) driven by the increase in atmospheric CO2 is compared to the concept of a natural global warming (NGW) driven by solar variability. The application of the AGW concept only rests on models, whilst the NGW concept rests on multiple observational and evidence-based facts. Even more so, the long-term solar variability predicts a new Grand Solar Minimum with severe climatic conditions (type Little Ice Age) to occur in 2030-2050. This violates all talk about an increasing, even accelerating, global warming. Similarly, there is no true treat of a future sea level rise flooding lowlands and islands.

Shen et al (2018) The results showed both future climate change (precipitation and temperature) and hydrologic response predicted by 20 global climate models were highly uncertain, and the uncertainty increased significantly over time.

Abbott & Marohasy (2018) While general circulation models are used by meteorological agencies around the world for rainfall forecasting, they do not generally perform well at forecasting medium-term rainfall, despite substantial efforts to enhance performance over many years. These are the same models used by the IPCC to forecast climate change over decades.

Scafetta et al (2018) Herein, the authors show that such a temperature peak is unrelated to anthropogenic forcing: it simply emerged from the natural fast fluctuations of the climate associated to the El Nio-Southern Oscillation (ENSO) phenomenon. By removing the ENSO signature, the authors show that the temperature trend from 2000 to 2016 clearly diverges from the general circulation model (GCM) simulations. Thus, the GCMs models used to support the AGWT are very likely flawed.

Lean (2018) Climate change detection and attribution have proven unexpectedly challenging during the 21st century. Earths global surface temperature rose less rapidly from 2000 to 2015 than during the last half of the 20th century, even though greenhouse gas concentrations continued to increase.

Scafetta & Wilson (2019) The climate warming hiatus observed since 2000 is inconsistent with CO2 AGW climate models [citations omitted].CO2 anthropogenic global warming (CAGW) climate models [citations omitted]. This points to a significant percentage of the observed 19802000 warming being driven by TSI variation [citations omitted]. A number of other studies have pointed out that climate change and TSI variability are strongly correlated throughout the Holocene including the recent decades [citations omitted].

Pei et al (2019) During the period of 0-10,000 years before present, Chinas temperature has closely followed the solar forcing. The correlation is as high as 0.800 (p less than 0.01) for Empirical Orthogonal Function-based reconstruction.

Paudel et al (2019) On a global scale changes in cloud cover were found to be significantly related to changes in solar activity through its effect on the flux of cosmic rays reaching the lower atmosphere [citations omitted] suggesting changes in solar emissions could be related to those in cloud cover and global radiation at the Earths surfaceAnalysis by stepwise regression indicated that since 1970 changes in cloud cover accounted for 61% of the changes in Egwhile the major increase in local fossil fuel consumption, serving as a proxy for anthropogenic aerosol emissions, only accounted for an additional 2% of the changes.

Varotsos & Efstathiou (2019) Based on these results and bearing in mind that climate systems are complicated and complex with existing uncertainties in the climate predictions, it is not possible to reliably support the view of the presence of global warming in the sense of an enhanced greenhouse effect due to human activities.

Kauppinen & Malmi (2019) The IPCC climate sensitivity is about one order of magnitude too high because the strong negative feedback of clouds is missing in climate models. If we pay attention to the fact that only a small part of the increased CO2 concentration is anthropogenic, we have to recognize that anthropogenic climate change does not exist in practice. The major part of the extra CO2 is emitted from oceans (cite omitted), according to Henrys Law. The low clouds practically control the global average temperature. The last 100 years the temperature was increased by about 0.1 degrees C because of CO2. The human contribution was about 0.01 degrees C.

Mao et al (2019) In science, when there are two or more ideas to be employed to explain the recent global warming, we always trust which can fit perfectly all the observed monthly anomaly of GLST from 1880 to now. Until now, no one claims that he can fit perfectly the observed monthly anomaly of GLST from 1880 to now as we do The function with best verification result has also been employed to predict the future behavior of the monthly anomaly of GLST; we can see that the downward trend for the monthly anomaly of GLST had already begun; it will reach the lowest point at 0.6051C in 2111.

Conclusion

Given all of this, it appears that both progressives and conservatives ignore or reject the facts and the science when it suits their ideological need to do so. That said, as I have argued, it appears that the Left is actually more guilty of these transgressions against the truth than the Right. Given this reality, perhaps certain Democratic politicians and media outlets should cease and desist slandering their political adversaries with the mostly false allegation that conservatives regularly reject or at least ignore the facts and the science. Regardless of what the Left decides on that matter, one should always remember what Neil DeGrasse Tyson said on Real Time with Bill Maher in April of 2011: The good thing about science is that it is the truth whether or not you believe it..

Richard W. Burcik is a retired economist and attorney.

See original here:
Conservatives Are Not the Only Ones Who Ignore Facts and the Science - Merion West

Wayengera is behind the country's effort to manufacture test kits. Courtesy photo

Testing is key for diagnosing and tracking the magnitude of the disease to know how many people have been infected or could infect others.

While people in Uganda have been asked to stay at home to contain the spread of the new coronavirus disease (COVID-19), a few others must continue working to find answers to the pandemic.

COVID-19 is wreaking havoc across the world. Uganda, just like most countries globally, is relying on aggressive screening and testing as the best approach to determine whether the virus is present in communities, and how far it has spread.

Testing is key for diagnosing and tracking the magnitude of the disease to know how many people have been infected or could infect others.

But, the high global demand for testing kits has strained supply.

Production and delivery of testing kits to meet demand is short. In turn, it has led to a rise in fake kits and a race to develop standardized, rapid, and accurate diagnostic tests.

Currently, Uganda is able to conduct over 2000 tests daily, and over 40, 000 tests have been carried out in total, which is much higher than tests conducted by any other East African country. But in South Korea alone, nearly 20,000 people are tested daily.

But not to worry, the number of tests could soon go much higher as Dr. Misaki Wayengera a Clinical Geneticist, Immunologist, and Virologist along with a team of other Ugandan scientists, are developing a cheaper COVID-19 testing kit that could deliver results in a minute or two. For him, it is about offering a homegrown solution to the testing gap.

Love For Science and Country

The innovation is not the first for Wayengera, he also developed the pan-filovirus rapid diagnostic test, a paper-strip test that can detect the Ebola and Marburg viruses in five minutes.

Wayengera is a towering and vibrant figure among his peers. He does not hesitate to share knowledge when he gives his time and is always happy to talk about science.

When I joined medical school, my friends were reading books to pass, I wanted to bring about change, he told a Ugandan television in an interview.

He is patriotic, and always talks about how his works should benefit the country, and develop Africa for Africans. His patriotism is rare to find among professionals, says Ian Peter Busuulwa a digital communications officer with Science Stories Africa and a biotechnologist who engages in agricultural research and science.

He is also passionate about sharing knowledge. He could be in some leading global pharmaceutical company earning lots of money, but Wanyengera finds it necessary to stay in Uganda, working with Makerere University to pass on knowledge to young scientists, he adds.

Who is Dr. Wanyengera

Wayengera is a medical doctor with graduate training, Masters of Science (MSc), Fellowship, and Doctorate of Philosophy (Ph.D.) in a diverse array of scientific fields including Immunology, Vaccinology, Clinical Microbiology, Genetics, and Filovirology.

It was in 2000 while a medical student, that he picked interest in studying filoviruses that can cause severe hemorrhagic fever in humans and non-human primates.

In 2007 while studying genomes of filoviruses, Wayengera focused his energy on the understanding of Ebola and Marburg viruses with targets for both vaccine and diagnostic development. He successfully developed a rapid testing kit for both viruses.

Wayengera also holds expert skills-training in Bioentrepeneurship and Research and Development.

Serving, Breaking Boundaries

Over the past 10 years, he has served as In-Charge of the Unit of Genetics and Genomics (a super-specialized referral centre for children and adults born with rare, Mendelian disease at the Mulago National Reference and Teaching Hospital Complex, Kampala, Uganda.

He is also In-Charge of the Unit of Genetic and Genomics, Department of Immunology and Molecular Biology at School of Biomedical Sciences, College of Health Sciences at Makerere University.

Wayengera is also a member of the African Society for Human Genetics (AfSHG) and Ex-Chair of the Education and Coordinated Working Group (ECTWG) of the H3Africa Consortium that empowers African Researchers to be competitive in genomic sciences and nurtures effective collaboration.

My research interests center on pathogens (virus, bacterium and other microorganisms that can cause disease) with a focus on identifying new its molecular targets (minute particles) for research and development of diagnostics, therapeutics, and vaccines, he says.

Together with his team, Wayengera has not only built the necessary expertise and experience but also established a network of partners from across the academia, industry, and public-private partnerships.

For this work and its impact on the 2013 to 2016 Ebola outbreak in West Africa, Wayengera was listed as the 57th of the 100 most influential Africans of 2015.

Last year (2019), his team won the 1st Prize for the World Health Organisation (WHO) innovation Challenge (Product Development), and he was nominated as REACH Award Finalist - Reaching the Last Mile (REACH/RLM).

Wayengera is currently (2019-2020) The World Academy of Sciences Sub Saharan Africa Regional Partner (TWAS-SAREP) Young Scientist award winner (Infectious Diseases).

He is also the Chair of the COVID-19 scientific committee in Uganda leading the response to the coronavirus.

Providing Solutions

I am excited Dr. Wayengera and his team are in the process of developing a testing kit for COVID-19. There is a huge challenge globally for testing kits. We look forward to this innovation closing this gap. He did the same for Ebola, says Professor Rhoda Wanyenze a Physician, Public Health Consultant, and Dean Makerere University School of Public Health.

It is always good to see scientists use their knowledge to develop innovations that address the critical aspects of health for our society. We keep getting epidemics. Right now besides COVID-19, neighbours DR Congo also have Ebola in the town of Beni, she says.

Professor Wanyenze says Wayengera is working on critical matters developing diagnostics. The STDS-Agx (swab tube dipstick agglutination) COVID-19 test kit developed by Wayengeras team can produce results in a minute or two, compared to the four-to-six hours it takes to get results from the WHO accredited Reverse transcription-polymerase Chain Reaction (RT-PCR) based tests that quantitate changes in gene expression, now in use.

Each kit will cost an estimated US$1.07 (about sh4,000), making testing affordable. It is intended for use in rural settings, which often lack laboratory capacity or expertise, says Wayengera.

It is a home-based solution to the evident scarcity of resources for the management of this pandemic globally. Everyone is running to the market and the difference in economic prowess means poor countries such as those in sub-Saharan Africa are left with nothing. We must innovate around these shortages to fight the pandemic, he says.

The Makerere University research team expects to have a prototype ready to be put into use next month, pending expert validations.

Three versions of the test kit are being developed. The tests will work by generating solid particles from the reaction of the virus with antibodies or vice versa.

The work has been seed funded by about US$22,000 from the Makerere University Research and Innovation Fund.

Wayengera says an estimated $272,000 will be required to develop a prototype and over $ 0.5million will be needed to mass-produce the kits.

Additional costs will also be incurred for regulatory approval, intellectual property protection, and commercialisation.

Continue reading here:
Dr. Misaki Wayengera: The Man Behind Uganda's Covid 19 Test Kits - New Vision

KEY POINTS

Health experts have been baffled as to why there are people infected with COVID-19 and yet barely feel the infection while others suffer life-threatening symptoms even if healthy and young. Scientists are looking for answers in the genes of patients, trying to discover mutations that affect the immune response, hoping that it could help in coming up with new treatments.

Profile Of A Severe Case

During the early days of the pandemic, a general profile of a severe case of coronavirus infection started to emerge. They are older adults with pre-existing medical conditions and are likely to be male. As the virus continued to infect more people, a small fraction started to deviate from the general profile.

Health experts are starting to see around 5% of those infected are under the age of 50 and do not have any underlying health conditions. These are the group of patients that interest Dr. Jean-Laurent Casanova, a geneticist and head of the St. Giles Laboratory of Human Genetics of Infectious Diseases.

Dr. Casanova told the AFP it is possible for someone who joined a marathon in October 2019 to find himself in intensive care, ventilated and intubated in April 2020. He revealed his desire to know if these types of patients have rare genetic mutations that have been triggered by the coronavirus infection. The assumption is that these patients have genetic variations that are silent until the virus is encountered, the doctor said. coronavirus silent mutation in human body may be the one exploited by the virus Photo: TPHeinz - Pixabay

A Huge Global Effort

The geneticist co-founded the COVID Human Genetics Effort, a collaborative work that seeks to know more about the genome of severely-ill young patients in several countries worldwide. These include patients in Europe, Japan, Iran, China, and the United States.

Dr. Casanovas group is also studying those who did not get infected despite being exposed many times. He said their main goal is to know why some are sicker than others, a knowledge that the geneticist said might help them in their quest to develop anti-viral therapies.

Gene Mutations Have A Long History

Scientists have long known that gene mutations can make people more susceptible to an array of infectious diseases, ranging from influenza to viral encephalitis. These gene mutations can also offer protection sometimes.

In the 1990s, a group of researchers found out that some rare mutations of a single gene successfully protected people against HIV infection. This discovery led to a betterunderstanding of how the virus worked and eventually paved the way for scientists to develop new treatments.

Read the original here:
Its In The Genes? Scientists Think Coronavirus Exploits Silent Hidden Mutations In The Body - International Business Times

MET 2020 Slot Booking: The Manipal Academy of Higher Education will be conducting the Manipal Entrance Test 2020 from July 24 to 27 and August 4 to 7, 2020. According to a recent announcement made, the Manipal Entrance Test 2020 will be conducted in the online mode. The slot bookings for the entrance tests will be open from July 15, 2020, onwards. Candidates who have applied for the entrance test can visit the official website for more details related to the entrance test.

The instructions to be followed by candidates during the slot booking process is available on the official website. Candidates are advised to read through the instructions provided carefully in order to complete the slot booking procedure without any mistakes.

MET 2020 Slot booking Guidelines

Candidates are advised to visit the official website - manipal.edu. To check the demo of the slot booking process for the Manipal Entrance Test 2020 candidates is advised to click on the link provided below.

MET Slot Booking Demo Direct Link

According to the notification available on the official website the MET 2020 examination is scheduled to be conducted in the decided number of cities and all the applications will be able to book their entrance test slots via the Online Test Booking System (OTBS) based on the availability of the seats. It must also be noted that in case a low number of applicants are seen in a particular city, the test centre will be shifted to the nearest city which is available on the OTBS.

The list of cities in each state where the Manipal Entrance Test 2020 will be conducted is available on the official website of MET. Candidates can also check the list of cities through the direct link provided below.

MET 2020 List of cities Direct Link

Manipal Academy of Higher Education conducts the Manipal Entrance Test 2020 for the admissions to the BTech, BTech (Lateral Entry Admissions), BPharm / PharmD, MTech, ME, MPharm / PharmD Post Baccalaureate, MSc Medical Biotechnology, MSc Molecular Biology & Human Genetics, MSc Systems Biology, MSc Genome Engineering, MSc by Research in Life Sciences programmes offered by the university.

Also Read: APSCHE to begin online GATE 2020 sessions for students during COVID-19 lockdown from today onwards

Read the original:
MET 2020 Slot booking to commence on July 15, Examination dates available at manipal.edu - Jagran Josh

LONDON When the first cases of a new coronavirus started to appear in China last December, the disease seemed to be a particularly aggressive respiratory infection. An "urgent notice" that month from the Wuhan health commission warned of "successive cases of unknown pneumonia".

Respiratory symptoms are still the first signs that doctors look for in suspected Covid-19 cases: cough, shortness of breath and fever.

But, less than five months after it was first identified, this new coronavirus is managing to throw up a series of medical mysteries - from blood clots and strokes to digestive problems - that are confounding the scientific community.

From head to foot, Covid-19 causes a fiendish variety of symptoms. Some are relatively mild, such as loss of smell and taste or chilblain-like sores on toes. But others may be fatal, such as when what doctors call an immune storm destroys vital organs. The more this virus is studied, the more complex it appears to be. "Every day we're learning of new tricks that the virus plays," Imperial College London's professor of experimental medicine Peter Openshaw says. "It is remarkable to see a disease unfolding in front of our eyes with so many twists and turns."

The proliferation of complex symptoms is not just a challenge for doctors treating the disease, but also for health systems trying to adapt to the pandemic. In the early months, the focus was on getting hold of ventilators that could help patients with severe respiratory problems. But now hospitals are also scrambling for more kidney dialysis machines and anticoagulant drugs.

A single individual can suffer the disease in more than one form, Prof Openshaw adds. "There are accounts of people experiencing one symptom, for example coughing, appearing to recover or go into remission and then returning with a more serious systemic disease."

With the worldwide death toll from Covid-19 already nearing 260,000 and confirmed cases close to exceeding 3.7 million, according to Johns Hopkins University, scientists have mobilised at a speed and on a scale unprecedented in the history of medicine, in an effort to understand the myriad ways in which the virus affects the human body. They hope that their research will not only improve clinical care of patients but also help the development of drugs and vaccines.

The initial diagnosis was that it was a respiratory infection, like its sister diseases Sars and Mers which are also caused by coronaviruses.

Respiratory symptoms remain the most common manifestations of Covid-19 in patients who go to hospital, according to a study of almost 17,000 people admitted to 166 UK hospitals carried out by a research consortium from Imperial College and Liverpool and Edinburgh universities. About two-thirds of patients in the study - the largest of Covid-19 hospital patients outside China - were admitted suffering from respiratory symptoms, says Dr Annemarie Docherty of Edinburgh, the lead author of the paper. But that proportion may have been raised by the fact that they reflect the official case definition of Covid-19.

But two other clusters of symptoms also dominate hospital admissions: systemic musculoskeletal symptoms (muscle and joint pain and fatigue) and enteric symptoms (abdominal pain, vomiting and diarrhoea). Many patients suffer from several symptoms simultaneously.

How the immune system reacts to Covid-19 is key to the course of the disease in adults. People who have been suffering with mild to moderate symptoms for a week or so often seem to hit a critical point: usually their immune system gets the virus under full control and sets them on a path to full recovery - but sometimes it goes into overdrive, triggering systemic inflammation and in severe cases a "cytokine storm" that destroys tissues and whole organs.

Inflammation also helps to explain why obesity makes people more susceptible to severe Covid-19. Seventy-three per cent of coronavirus patients in UK intensive care units are overweight or obese, with a body mass index above 25. "Fat cells secrete chemicals that increase the body's inflammatory response," says Liverpool University's professor of child health Calum Semple.

Kidney damage has emerged as another of the most frequent serious consequences of Covid-19, with 23 per cent of patients in intensive care requiring renal support. As with other organs, it is uncertain to what extent the virus is directly attacking the kidneys or whether the harm results more from generalised overactivity of the immune system and consequent changes in the patient's blood circulation.

Cardiovascular disease is the most common pre-existing health condition in people who die of Covid-19, ahead of lung and respiratory disorders such as asthma and chronic obstructive pulmonary disease. And many patients without a previous history of heart trouble develop severe cardiac symptoms while they are in hospital.

"When we first heard about the coronavirus we expected people with lung and breathing problems to be most at risk but that has not been the case," says the British Heart Foundation's medical director Nilesh Samani. "We need to understand why the virus is causing so many problems outside the lungs - and cardiovascular complications in particular."

The exaggerated immune response to the virus sometimes causes abnormal blood clotting. If this thrombosis happens in the brain, it may trigger a stroke. Neurologists at University College London (UCL) studied six Covid-19 patients who suffered acute stroke as a result of a large arterial blockage - in five of the cases more than a week after suffering headache, cough and fever and in one patient before other symptoms appeared.

The UCL researchers found all six patients had markedly raised blood levels of a protein fragment called D-dimer associated with abnormal clotting. The findings suggest that early testing for D-dimer could enable doctors to prescribe blood-thinning drugs to people at risk, reducing the chance of stroke or harmful clotting elsewhere in the body. "Early use of anticoagulant drugs might be helpful but this needs to be balanced against their brain bleeding risk," says study leader David Werring.

STRAITS TIMES GRAPHICS

"This study is consistent with the growing evidence that people hospitalised with Covid-19 are at risk from blood clots in multiple locations: the lungs (causing pulmonary embolus), the brain (causing stroke) and the veins (causing DVT)," says professor of cardiovascular medicine Tim Chico at Sheffield University. "The risk of blood clots with Covid-19 appears to be even greater than the increased risk of blood clots seen in other severe illnesses."

The coronavirus also seems capable of attacking the brain and nervous system directly, as well as indirectly through abnormal blood clotting, though the evidence for acute symptoms of neural infection is limited. The effects may show up in the longer term as post-viral fatigue.

Neurons in the olfactory bulb, which transmits information from the nose to the brain, are apparently infected by the virus. Indeed, anosmia - loss of the sense of smell - is one of the most frequently reported symptoms of mild infection, affecting about half of patients and lasting for several weeks in some cases.

The good news for those who develop anosmia is that they are much less likely to become seriously ill with Covid-19. Dr Carol Yan and colleagues at the University of California San Diego (UCSD) reported last week that patients reporting loss of smell were 10 times less likely to be admitted to hospital for Covid-19 than those without loss of smell.

The UCSD researchers suggest that a relatively small dose of virus delivered to the upper airway, where it causes anosmia, may be less likely to overwhelm the host immune response. "This hypothesis is in essence the concept underlying live vaccinations, where low dosage and a distant site of inoculation generates an immune response without provoking a severe infection," they say.

The declining strength of the immune system with age is a partial explanation for the increasing incidence of Covid-19 in older people. PHOTO: AFP

Besides anosmia, the most frequently seen minor symptoms are rashes, pustules and blisters on the skin - including lesions like chilblains that dermatologists are calling "Covid toe".

The results from the study led by Imperial College, Liverpool and Edinburgh universities echo other findings that the disease is much more common in men - who make up 60 per cent of UK Covid-19 hospital admissions - and its severity rises markedly with advancing years (the median age of patients is 72). The strong associations with the male sex and old age are a particular feature of Covid-19 compared with other infectious illnesses.

Data from the UK Intensive Care National Audit & Research Centre shows that men make up 71.5 per cent of patients whose disease becomes severe enough to require intensive care treatment. A comparable control group of patients critically ill with non-Covid viral pneumonia was just 54.3 per cent male.

"The reason behind this difference in Covid risk is unknown," says Dr James Gill, honorary clinical lecturer at Warwick Medical School. "There are several schools of thought on the matter, from the assumption that simply men don't look after their bodies as well, with higher levels of smoking, alcohol use, obesity and other deleterious health behaviours, through to immunological variations in genders. Women may have a more aggressive immune system, meaning a greater resilience to infections."

University of Oxford's professor of immunology Philip Goulder points out that several critical immune genes are located on the X chromosome - of which women have two copies and men one. "The immune response to coronavirus is therefore amplified in females," he says.

The declining strength of the immune system with age is also a partial explanation for the increasing incidence of the disease in older people, though it is not clear why this trend is more pronounced in Covid-19 than in many other viral infections.

Children are remarkably - but not completely - resistant to the disease. Just 3 per cent of UK hospital patients are under 18. Again no one knows quite why. But one answer may lie in the "keyhole" through which coronavirus enters human cells, known as the ACE2 receptor. In children these receptors have not developed to their full adult stage and therefore may not fit the "spike protein" that the virus uses to enter cells.

It is also possible that ACE2 develops more quickly in children's upper airways than their lower respiratory tract, allowing them to become infected - and thus able to transmit Covid-19 - without showing the same progression to severe symptoms.

The National Health System in London and the UK Paediatric Intensive Care Society recently alerted doctors to a rise in the number of children suffering from "a multi-system inflammatory state" similar to toxic shock, which might result from the immune system overreacting to viral infection. Italian and US paediatricians have noticed a similar body-wide inflammatory syndrome in children.

This paediatric condition is rare but researchers are investigating, says Prof Semple. "Some respiratory viruses are associated with a systemic inflammatory response, typically two weeks after infection. But this could be a phenomenon of heightened awareness."

Research also shows that children are remarkably - but not completely - resistant to the disease. PHOTO: AFP

For Prof Openshaw, the mysteries of Covid-19 recall the early days of the HIV/Aids outbreak in the 1980s - except that this time, they are unfolding much more quickly. "We need the answers also to appear far faster than they did with HIV," he says.

A global research effort is on to discover human genetic factors that would help to explain why Covid-19 infection varies so much in its symptoms.

Although much of the variation results from environmental and lifestyle factors, scientists are convinced that genetics play a significant role too.

"Experience with other viruses shows that genetics can explain some of the different responses to infection," says Dr Mark Daly, director of the Institute for Molecular Medicine Finland in Helsinki, who is coordinating the global response through the Covid-19 Host Genetics Initiative.

For example, genetic mutations on the CCR5 protein, which HIV uses to enter human cells, make rare individuals resistant to Aids. Researchers may find comparable variations in the human ACE2 protein, entry point of the coronavirus, designated as Sars-Cov-2, that causes Covid-19.

The Covid programme has two overlapping components. One uses human genomes already obtained for other research purposes from volunteers through bodies such as UK Biobank and Genomics England - and looks for differences in DNA between participants who become ill with Covid-19 and those who do not.

The other part obtains the fresh genomes from Covid-19 patients, looking for variations that might explain why some experience only mild symptoms while others become severely ill.

Genomics England, a public body owned by the UK Department of Health and Social Care, is involved in both approaches. Dr Mark Caulfield, its chief scientist, says it is too early to have obtained any results. "But I am confident that reading whole genomes will help to identify variation that affects response to Covid-19 and to discover new therapies."

Prof Daly hopes the initiative will have tens of thousands of human genomes to analyse. "We particularly want to identify a subset of younger individuals with no comorbidities who have a severe response to Sars-Cov-2 infection," he says.

FINANCIAL TIMES

Original post:
From blood clots to 'Covid toe': Experts confounded by series of medical mysteries - The Straits Times

An unprecedented amount of research has been focused solely on understanding the novel coronavirus that has taken nearly 150,000 lives across the globe. And while scientists have gotten to know some of the most intimate details of the virus called SARS-CoV-2, one question has evaded any definitive answers Where did the virus come from?

Live Science contacted several experts, and the reality, they said, is that we may never know where this deadly coronavirus originated. Among the theories circulating: That SARS-CoV-2 arose naturally, after passing from bats to a secondary animal and then to humans; that it was deliberately engineered and then accidentally released by humans; or that researchers were studying a naturally-occurring virus that subsequently escaped from a high-security biolab, the Wuhan Institute of Virology (WIV) in China. The head of the lab at WIV, for her part, has emphatically denied any link to the institute.

Just today (April 18), the vice director of WIV Zhiming Yuan CGTN, the Chinese state broadcaster, said "there is no way this virus came from us," NBC News reported. "We have a strict regulatory regime and code of conduct of research, so we are confident."

Furthermore, the notion that SARS-CoV-2 was genetically engineered is pure conspiracy, experts told Live Science, but it's still impossible to rule out the notion that Chinese scientists were studying a naturally-occurring coronavirus that subsequently "escaped" from the lab. To prove any of these theories takes transparent data and information, which is reportedly not happening in China, scientists say. Several experts have said to Live Science and other media outlets have reported that the likeliest scenario is that SARS-CoV-2 is naturally occurring.

Related: 13 coronavirus myths busted by science

"Based on no data, but simply [a] likely scenario is that the virus went from bats to some mammalian species, currently unknown despite speculation, [and] spilled over to humans," said Gerald Keusch, associate director of the Boston University National Emerging Infectious Diseases Laboratories. This spillover event may have happened before the virus found its way into a live animal market, "which then acted as an amplifying setting with many more infections that subsequently spread and the rest is history," Keusch said. "The timeline is fuzzy and I don't think we have real data to say when these things began, in large part because the data are being held back from inspection," Keusch told Live Science.

The SARS-CoV-2 virus is most closely related to coronaviruses found in certain populations of horseshoe bats that live about 1,000 miles (1,600 kilometers) away in Yunnan province, China. The first known outbreak of SARS-CoV-2 in humans occurred in Wuhan and initially was traced to a wet seafood market (which sold live fish and other animals), though some of the earliest cases have no link to that market, according to research published Feb. 15 in the journal The Lancet.

Related: 11 (sometimes) deadly diseases that hopped across species

What's more, despite several proposed candidates, from snakes to pangolins to dogs, researchers have failed to find a clear "intermediate host" an animal that would have served as a springboard for SARS-CoV-2 to jump from bats to humans. And if horseshoe bats were the primary host, how did the bat virus hop from its natural reservoir in a subtropical region to the bustling city of Wuhan hundreds of miles away?

These questions have led some people to look elsewhere in the hunt for the virus's origin, and some have focused on the Wuhan Institute of Virology (WIV).

In 2015, WIV became China's first lab to reach the highest level of bioresearch safety, or BSL-4, meaning the lab could host research on the world's most dangerous pathogens, such as Ebola and Marburg viruses. (SARS-CoV-2 would require a BSL-3 or higher, according to the Centers for Disease Control and Prevention.) Labs like these must follow strict safety guidelines that include filtering air, treating water and waste before they exit, and requiring lab personnel to shower and change their clothes before and after entering the facility, Nature News reported in 2017.

These types of labs do spur concerns among some scientists who worry about the risks involved and the potential impact on public health if anything were to go wrong, Nature News reported.

Related: The 12 deadliest viruses on Earth

WIV was not immune to those concerns. In 2018, after scientist diplomats from the U.S. embassy in Beijing visited the WIV, they were so concerned by the lack of safety and management at the lab that the diplomats sent two official warnings back to the U.S. One of the official cables, obtained by The Washington Post, suggested that the lab's work on bat coronaviruses with the potential for human transmission could risk causing a new SARS-like pandemic, Post columnist Josh Rogin wrote.

"During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory," the officials said in their cable dated to Jan. 19, 2018.

When reports of the coronavirus first popped up in China, the U.S. Deputy National Security Advisor Matthew Pottinger reportedly suspected a potential link to China labs. In mid-January, according to a New York Times report, Pottinger asked intelligence agencies like the C.I.A., particularly individuals with expertise on Asia and weapons of mass destruction, to investigate this idea. They came up empty-handed, the Times reported.

Meanwhile, the lab at the center of these speculations had long been sounding the alarm about the risk of the SARS-like coronaviruses they studied to spawn a pandemic.

The head of the lab's bat-coronavirus research, Shi Zhengli, published research on Nov. 30, 2017 in the journal PLOS Pathogens that traced the SARS coronavirus pandemic in 2003 to a single population of horseshoe bats in a remote cave in Yunnan province. The researchers also noted that other SARS-like coronaviruses discovered in that cave used the ACE2 receptor to infect cells and could "replicate efficiently in primary human airway cells," they wrote. (Both SARS and SARS-CoV-2 use the ACE2 receptor as the entry point into cells.)

Zhengli and her colleagues stressed the importance of monitoring and studying the SARS coronaviruses to help prevent another pandemic.

"Thus, we propose that monitoring of SARS-CoV evolution at this and other sites should continue, as well as examination of human behavioral risk for infection and serological surveys of people, to determine if spillover is already occurring at these sites and to design intervention strategies to avoid future disease emergence," they wrote.

Related: 20 of the worst epidemics and pandemics in history

The WIV lab, along with researchers in the U.S. and Switzerland, showed in 2015 the scary-good capability of bat coronaviruses to thrive in human cells. In that paper, which was published in 2015 in the journal Nature Medicine, they described how they had created a chimeric SARS-like virus out of the surface spike protein of a coronavirus found in horseshoe bats, called SHC014, and the backbone of a SARS virus that could be grown in mice. The idea was to look at the potential of coronaviruses circulating in bat populations to infect humans. In a lab dish, the chimeric coronavirus could infect and replicate in primary human airway cells; the virus also was able to infect lung cells in mice.

That study was met with some pushback from researchers who considered the risk of that kind of research to outweigh the benefits. Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, was one of those scientists. Wain-Hobson emphasized the fact that this chimeric virus "grows remarkably well" in human cells, adding that "If the virus escaped, nobody could predict the trajectory," Nature News reported.

None of this can show the provenance of SARS-CoV-2.

But scientists can start to rule out an idea that the pandemic-causing coronavirus was engineered in that lab or further created as a bioweapon. Researchers say the overwhelming evidence indicates this is a natural-borne virus that emerged from an animal host, likely a bat, and was not engineered by humans.

Related: 28 devastating infectious diseases

"This origin story is not currently supported at all by the available data," said Adam Lauring, an associate professor of microbiology, immunology and infectious diseases at the University of Michigan Medical School. Lauring pointed to a study published March 17 in the journal Nature Medicine, which provided evidence against the idea that the virus was engineered in a lab.

In that Nature medicine study one of the strongest rebukes of this idea Kristian Andersen, an associate professor of immunology and microbiology at Scripps Research, and his colleagues analyzed the genome sequences of SARS-CoV-2 and coronaviruses in animals. They found that a key part of SARS-CoV-2, the spike protein that the virus uses to attach to ACE2 receptors on the outsides of human cells, would almost certainly have emerged in nature and not as a lab creation.

"This analysis of coronavirus genome sequences from patients and from various animals suggests that the virus likely arose in an animal host and then may have undergone further changes once it transmitted and circulated in people," Lauring told Live Science.

That may rule out deliberate genetic engineering, but what about other scenarios that point to bats as the natural hosts, but WIV as the source of the outbreak?

Although researchers will likely continue to sample and sequence coronaviruses in bats to determine the origin of SARS-CoV-2, "you can't answer this question through genomics alone," said Dr. Alex Greninger, an assistant professor in the Department of Laboratory Medicine and an assistant director of the Clinical Virology Laboratory at the University of Washington Medical Center. That's because it's impossible to definitively tell whether SARS-CoV-2 emerged from a lab or from nature based on genetics alone. For this reason, it's really important to know which coronaviruses were being studied at WIV. "It really comes down to what was in the lab," Greninger told Live Science.

However, Lauring said that based on the Nature Medicine paper, "the SARS-CoV-2 virus has some key differences in specific genes relative to previously identified coronaviruses the ones a laboratory would be working with. This constellation of changes makes it unlikely that it is the result of a laboratory 'escape,'" he said.

As for what viruses were being studied at WIV, Zhengli says she did a thorough investigation. When she first was alerted to the viral outbreak in Wuhan on the night of Dec. 30, 2019, Zhengli immediately put her lab to work sequencing the genomes of SARS-CoV-2 from infected patients and comparing the results with records of coronavirus experiments in her lab. She also looked for any mishandling of viral material used in any experiments, Scientific American reported. She didn't find any match between the viruses her team was working with from bat caves and those found in infected patients. "That really took a load off my mind," she told Scientific American. "I had not slept a wink for days."

At the beginning of February, Zhengli sent a note over WeChat to reassure her friends that there was no link, saying "I swear with my life, [the virus] has nothing to do with the lab," the South China Morning Post reported Feb. 6. Zhengli and another colleague, Peng Zhou, did not reply to a Live Science email requesting comment.

The Wuhan lab does work with the closest known relative of SARS-CoV-2, which is a bat coronavirus called RaTG13, evolutionary virologist Edward Holmes, of the Charles Perkins Center and the Marie Bashir Institute for Infectious Diseases and Biosecurity at the University of Sydney, said in a statement from the Australian Media Center. But, he added, "the level of genome sequence divergence between SARS-CoV-2 and RaTG13 is equivalent to an average of 50 years (and at least 20 years) of evolutionary change." (That means that in the wild, it would take about 50 years for these viruses to evolve to be as different as they are.)

Though no scientists have come forth with even a speck of evidence that humans knowingly manipulated a virus using some sort of genetic engineering, a researcher at Flinders University in South Australia lays out another scenario that involves human intervention. Bat coronaviruses can be cultured in lab dishes with cells that have the human ACE2 receptor; over time, the virus will gain adaptations that let it efficiently bind to those receptors. Along the way, that virus would pick up random genetic mutations that pop up but don't do anything noticeable, said Nikolai Petrovsky, in the College of Medicine and Public Health at Flinders.

"The result of these experiments is a virus that is highly virulent in humans but is sufficiently different that it no longer resembles the original bat virus," Petrovsky said in a statement from the Australian Media Center. "Because the mutations are acquired randomly by selection, there is no signature of a human gene jockey, but this is clearly a virus still created by human intervention."

If that virus infected a staff member and that person then traveled to the nearby seafood market, the virus could have spread from there, he said. Or, he added, an "inappropriate disposal of waste from the facility" could have infected humans directly or from a susceptible intermediary, such as a stray cat.

Though we may never get a definitive answer, at least in the near-term, some say it doesn't matter.

"No matter the origin, evolution in nature and spillover to humans, accidental release from a lab, or deliberate release or genetic manipulation of a pathogen in the lab the way you develop countermeasures is the same," Keusch told Live Science. "Since one can never say 100% for anything, I think we always need to be aware of all possibilities in order to contravene. But the response to develop what is needed to respond, control and eliminate the outbreak remains the same."

Live Science senior writer Rachael Rettner contributed to this report.

Originally published on Live Science.

Read more:
Wuhan lab says there's no way coronavirus originated there. Here's the science. - Livescience.com

The novel coronavirus likely originated in bats, but the pathogen may have then hopped into dogs before infecting humans, a new study suggests.

But not everyone agrees with that hypothesis. One expert told Live Science that "there are a lot of weaknesses" in the study and that the data don't support the study's conclusions.

Before the new coronavirus SARS-CoV-2 made the jump to humans, two other coronaviruses, SARS-CoV and MERS-CoV, evolved in bats and passed through other animals on their way to people. SARS-CoV passed through civets and MERS-CoV through camels, and the molecular structure of SARS-CoV-2 suggests that the virus also passed through an intermediate animal, but scientists don't yet know which one.

In February, authors of a preliminary study published to the preprint database bioRxiv suggested that pangolins may bridge the gap between bats and humans, since SARS-CoV-2 and related coronaviruses that infect pangolins sport similar spike proteins a structure on the surface of the virus that allows it to infect cells. But other scientists argued that, despite their spike proteins, pangolin coronaviruses bear many differences to SARS-CoV-2 that make pangolins unlikely to be the source of infection, The New York Times reported.

With the mystery unresolved, biology professor Xuhua Xia of the University of Ottawa in Canada launched his own investigation into how the coronavirus passed from bats to people. His analysis, published April 14 in the journal Molecular Biology and Evolution, offered a new solution: dogs.

Xia reached his conclusion by scanning the genetic code of SARS-CoV-2 and other coronaviruses for a specific feature known as a CpG site, a sequence of genetic code in which the compound cytosine (C) is followed by the compound guanine (G). The human immune system sees CpG sites as a red flag, signaling that an invasive virus is present. A human protein called zinc finger antiviral protein (ZAP) latches onto the CpG sites on the viral genetic code and recruits help to break down the pathogen, according to UniProt, an online protein database. The theory follows that, the fewer CpG sites, the less vulnerable a virus will be to ZAP.

Related: 10 deadly diseases that hopped across species

Xia found that SARS-CoV-2 carries fewer CpG sites than the other known coronaviruses that first evolved in animals, including SARS-CoV and MERS-CoV. In addition, the closest known relative of SARS-CoV-2, the bat coronavirus RaTG13, contains fewer CpG sites than related bat coronaviruses, according to the analysis. "This suggests that SARS-CoV-2 may have evolved in a new host (or new host tissue) with high ZAP expression," which would place evolutionary pressure on the virus to shed CpG sites, Xia wrote.

Essentially, in order to survive and reproduce, a pathogen like SARS-CoV-2 needs to be able to evade the hosts immune fighters, and in this case it would mean getting rid of CpG sites that could alert ZAP proteins to the virus.

Unfortunately, little data exists on exactly how much ZAP appears in different animal tissues, Xia told Live Science. So he worked backwards, looking for animal coronaviruses with low CpG levels. He found a coronavirus that primarily infects the canine intestine, and thus inferred that the dog gut might contain adequate ZAP levels to drive viral evolution in this way.

"Only canids seem to have the tissue generating low-CpG CoVs during my study," Xia said. If a precursor to SARS-CoV-2 breached the canine intestine, then this would have "resulted in rapid evolution of the virus" to lose CpG sites and become better equipped to infect humans, he wrote in the paper. Beyond the low CpG levels, the paper did not note other genetic similarities between SARS-CoV-2 and the dog coronavirus, but suggested that the canine gut might provide the right environment for such viruses to evolve.

But why the dog intestine? Some research suggests that ZAP mRNA, which contains instructions to build the protein, appears in both the dog lung and colon but that higher concentrations accumulate in the lungs, Xia said. It may be that a glut of ZAP in the lungs guards the organ from coronaviruses, while the lower concentrations of ZAP in the colon leave the gut open to severe infection, though there are reasons to be cautious in coming to this conclusion, Xia said.

But does this hypothesis make sense?

"I think the data do not support these conclusions," Pleuni Pennings, an assistant professor of ecology and evolution at San Francisco State University, who was not involved in the study, told Live Science in an email. Pennings, whose research group has examined the CpG levels of many viruses, pointed out several weaknesses in the study's logic.

In a 2018 study published in the journal PLOS Genetics, Pennings surveyed CpG levels in the HIV virus and investigated how the pathogen evolves within individual people. She then led a similar study of several other viruses including Dengue fever virus, influenza, and hepatitis B and C to learn how often these bugs lose or gain CpG sites through mutations. Her group found that, in general, mutations that add CpG sites tend to be found in viral samples taken from people less often than mutations that remove CpG sites from the genome.

CpG-creating mutations may be costly to viruses in that they alert the body to infection, so over time, evolutionary forces minimize their appearance, Pennings said. That said, many viruses still carry CpG sites, so the mutations may carry some benefit "even if it comes with a slight cost," she added. So SARS-CoV-2 is not unusual in that way.

"There are many viruses with lower [CpG] values than SARS-CoV-2," Pennings said. "When you look at all viruses, the [CpG] value is not strange at all," she said.

Xia did find that SARS-CoV-2 contains fewer CpG sites than other animal-borne coronaviruses, and assuming that finding is correct, then it raises the question of why that came to be, she added.

But even if there is an evolutionary reason to explain why SARS-CoV-2 lost CpG sites, that evolutionary reason may not give the virus a special advantage for infecting humans, Pennings said.

In his paper, Xia noted that studies have "shown an association between decreased CpG in viral RNA genomes and increased virulence," meaning low-CpG viruses appear associated with more severe infection. However, although evolution favors mutations that delete CpG sites, and there's a general trend tying fewer CpG sites to more severe infection, "it doesnt mean that viruses with low numbers of CpG sites are necessarily more virulent," Pennings said. For example, the BK virus contains very few CpG sites and resides in the kidneys of an estimated 60% to 80% of adults, but typically only triggers symptoms in immunosuppressed people, she noted. (The virus was named the initials of the first person it was isolated from.)

If the CpG levels present in SARS-CoV-2 are somehow related to disease severity, "then this would provide an efficient way for vaccine development," Xia said. In this hypothetical scenario, scientists could eliminate CpG sites from the coronavirus genome in a lab dish, thereby weakening the bug to the point that it could safely be incorporated into a vaccine. But as of yet, no correlation has been drawn between CpG and the relative severity of SARS-CoV-2 infections.

Several pangolin coronaviruses included in Xia's study also contained few CpG sites, on par with SARS-CoV-2 and the bat virus RaTG13. Given other genetic differences between human and pangolin coronaviruses, however, the ancestor shared between this low-CpG pangolin coronavirus and SARS-CoV-2 would likely have existed over 130 years ago, Xia said. "We expect a SARS-CoV-2 progenitor to be much more recent," he said.

But did dogs serve as an intermittent host for the coronavirus? At this point, there's little evidence to suggest so.

Originally published on Live Science.

Here is the original post:
New study suggests COVID-19 hopped from dogs to humans. Here's why you should be skeptical. - Live Science