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Ancient Covid?

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  • rogue06
    replied
    Originally posted by TheLurch View Post
    What is this "proof read" you speak of?
    I'm writing so much slower than I'm thinking forcing me to come back to what I'm writing. But when I come back I might change the pretenses or repeat myself in the sentence. One of the biggest tells for such a drifting is when I write something along the lines of "and now they are doing blah blah blah now."

    Then, in spite of telling myself for nearly two decades to check first, I still click "post reply" and only then I might check through it.

    Leave a comment:


  • TheLurch
    replied
    Originally posted by rogue06 View Post

    AMEN!
    And I'm too blasted lazy to proof-read before hitting "post reply"
    What is this "proof read" you speak of?

    Leave a comment:


  • Cow Poke
    replied
    Originally posted by TheLurch View Post
    Always happy to try to explain something better. My brain and keyboard don't always work at the same speed, so lots of things don't come out as clearly as i think they should.
    I was kidding... you do great, and I'm always glad to see you. When I have asked for further explanation or clarification, you have always come through.

    (unlike some who would retort "well, THAT wasn't what I was saying.... stop putting words in my mouth! )

    Leave a comment:


  • rogue06
    replied
    Originally posted by TheLurch View Post
    Always happy to try to explain something better. My brain and keyboard don't always work at the same speed, so lots of things don't come out as clearly as i think they should.
    AMEN!
    And I'm too blasted lazy to proof-read before hitting "post reply"

    Leave a comment:


  • TheLurch
    replied
    Originally posted by Cow Poke View Post
    Anyway, I enjoy reading your posts even if I don't understand half of what you type.
    Always happy to try to explain something better. My brain and keyboard don't always work at the same speed, so lots of things don't come out as clearly as i think they should.

    Leave a comment:


  • Cow Poke
    replied
    Originally posted by TheLurch View Post
    No, you haven't, which is my point. I'm not ignoring anything - i'm reading your sources more carefully than you do, in that i'm looking for supportive data in them.

    Your links have none. They earlier ones are all hypotheses. In most cases, they literally say "hypothesis". So, if you think they're evidence, you have to explain why a hypothesis now counts as data in your world instead of just dropping a link you don't seem to have read and pretending that's an argument.

    Your latest one actually summarizes data, which is a step in the right direction. It is, however, entirely about genetic changes in viruses, when your argument was that humans have adapted to the viruses. So, it's the converse of the evidence you'd actually need to support your argument.

    Other than the fact that you (apparently, by chance) are right more often than he is, you're as bad as Lee.
    Shuny is rather infamous for confirmation bias - so determined to find stuff that supports his beliefs that he doesn't even fully read the articles.

    Time and time again, he has unwittingly posted material that actually disputes his contention, thinking he's providing proof he's right.

    Anyway, I enjoy reading your posts even if I don't understand half of what you type.

    Leave a comment:


  • TheLurch
    replied
    Originally posted by shunyadragon View Post

    I have cited the references with evidence you choose to ignore.
    No, you haven't, which is my point. I'm not ignoring anything - i'm reading your sources more carefully than you do, in that i'm looking for supportive data in them.

    Your links have none. They earlier ones are all hypotheses. In most cases, they literally say "hypothesis". So, if you think they're evidence, you have to explain why a hypothesis now counts as data in your world instead of just dropping a link you don't seem to have read and pretending that's an argument.

    Your latest one actually summarizes data, which is a step in the right direction. It is, however, entirely about genetic changes in viruses, when your argument was that humans have adapted to the viruses. So, it's the converse of the evidence you'd actually need to support your argument.

    Other than the fact that you (apparently, by chance) are right more often than he is, you're as bad as Lee.

    Leave a comment:


  • shunyadragon
    replied
    Source: https://academic.oup.com/ve/article/7/1/veab020/6157737




    The evolutionary dynamics of endemic human coronaviruses

    Wendy K Jo, Christian Drosten, Jan Felix Drexler


    4. Discussion


    We evaluated the evolutionary dynamics of two ubiquitous endemic HCoV in comparison to IAV H3N2.

    We found several similarities between both HCoV and IAV H3N2, including tree shape and the location of both non-synonymous mutations and sites under positive selection. Genetic variability potentially compatible with antigenic drift has been described in preliminary studies analyzing the S genes of HCoV-229E (Chibo and Birch 2006) and HCoV-OC43 (Ren et al. 2015) individually. Our analysis of relatively larger HCoV and IAV datasets using identical methodology confirmed those preliminary studies and allowed direct comparisons between the viruses under study. Our data demonstrate considerably lower gene-wide change over time in HCoV than in IAV, which may imply a prolonged ability of vaccine-induced immune responses to neutralize coronavirus variants arising over time.

    However, even a single amino acid exchange can dramatically affect immune escape, as demonstrated for many viruses infecting humans. In IAV, the recently emerged HA mutation K166Q reduced HA inhibition titers by ≥two-fold (Linderman et al. 2014), prompting for modification of the H1N1 vaccine strain in 2017 (Raymond et al. 2018). In Polioviruses, immune escape mutations were associated with an outbreak of poliomyelitis in the Republic of Congo in 2010 (Drexler et al. 2014). Even in hepatitis B virus that evolves several orders of magnitude slower than IAV and Polioviruses (Muhlemann et al. 2018), vaccine breakthrough after mother-to-child transmission and subsequent immunization of the neonate was linked to a single mutation in the glycoprotein (Romano et al. 2015). It is therefore not unlikely that single amino acid changes can have a dramatic impact on HCoV antigenicity. Indeed, differential neutralization of HCoV-229E strains was linked to substitutions within the S1 receptor-binding loops within the RBD (Shirato et al. 2012; Wong et al. 2017). Moreover, it was recently demonstrated that historical human sera collected from 1985 to 1990 had lower neutralizing activity to pseudotyped viruses bearing the S of HCoV-229E strains isolated eight to seventeen years later (Eguia et al. 2020), suggesting antigenic drift.

    One year after SARS-CoV-2 was first reported in humans, several mutations in S leading to deletions or amino acid exchanges have emerged independently in several countries (e.g. UK, South Africa, and Brazil) and are becoming regionally predominant (Plante et al. 2020; Tegally et al. 2020; Faria et al. 2021; Volz et al. 2021). These amino acid exchanges or deletions in S can lead to increased transmission by increasing infectivity (e.g. D614G) (Plante et al. 2020), enhancing human ACE2-binding affinity (e.g. N439K and N501Y) (Starr et al. 2020; Thomson et al. 2020), or conferring partial immune escape by reduction of neutralizing activity to both human-derived polyclonal sera and monoclonal antibodies (e.g. N439K, E484K, K417N, N501Y, Δ69/70) (Kemp et al. 2021; Thomson et al. 2021; Weisblum et al. 2020; McCarthy et al. 2021; Wang et al. 2021). Most of these mutations are located within the RBD, which is indicative of the relevance of that genomic domain for viral adaptive evolution and consistent with our results and those of other studies (Wong et al. 2017; Weisblum et al. 2020). Some of the immune escape mutations were reported to emerge in immunocompromised individuals after treatment with monoclonal antibodies and convalescent plasma (Choi et al. 2020; Kemp et al. 2021). Although it is possible that prolonged within-host evolution of SARS-CoV-2 in immunocompromised individuals can enhance the emergence of mutations conferring immune escape, intense uncontrolled community transmission of SARS-CoV-2 will facilitate the emergence of escape variants irrespective of host immune status. Immune escape is all the more worrying because weak immune responses against SARS-CoV-2 have been reported to occur particularly in mild and asymptomatic infections (Okba et al. 2020; Wajnberg et al. 2020) and sporadically linked to re-infection with SARS-CoV-2 (Gupta et al. 2020; To et al. 2020; Tillett et al. 2021). Finally, neutralization assays of viruses pseudotyped with SARS-CoV-2 spike variants (e.g. UK-B.1.1.7 and South Africa-B.1.351) demonstrated reduced levels of neutralization by vaccinee-derived antisera (Madhi et al. 2021; Tada et al. 2021; Wu et al. 2021). COVID-19 vaccines may therefore require constant evaluation during pandemic SARS-CoV-2 spread.

    Limitations in our study include the small number of sequences per year and the different dataset sizes. Another limitation was the use of only S gene sequences, as T-cell reactivity has been reported for other SARS-CoV-2 proteins such as M, N and several non-structural proteins (Grifoni et al. 2020; Le Bert et al. 2020). However, the S protein is the main target of neutralizing antibodies (Premkumar et al. 2020), and therefore the main viral protein used for vaccine development (Jackson et al. 2020; Mulligan et al. 2020).

    Alike SARS-CoV-2, IAV H3N2 emerged relatively recently in 1968 from an animal reservoir (Smith et al., 2009). It seems plausible that the evolutionary trajectory of SARS-CoV-2 will bear similarities with that of IAV H3N2 during the pandemic phase and in the immediate aftermath, characterized by viral adaptation and accumulation of mutations in the RBD. Under this assumption, it seems plausible that the efficacy of COVID-19 vaccines against emerging SARS-CoV-2 variants requires careful validation and regular vaccine update during pandemic spread. In contrast, seasonal HCoV emergence likely dates back longer time spans, potentially implying several hundred years of purifying selection (Vijgen et al. 2006; Pfefferle et al. 2009; Corman et al. 2015) that limit comparability of HCoV evolution with pandemic SARS-CoV-2 evolution during intense transmission facilitated by global connectivity (Findlater and Bogoch 2018). Nonetheless, the unique presence of the highly conserved proofreading protein nsp14 across all coronaviruses implies that SARS-CoV-2 evolution will bear similarities with seasonal HCoV evolution in a post-pandemic scenario. Enhanced stability of COVID-19 vaccines in the post-pandemic stage can thus be expected compared to influenza vaccines, both due to viral properties and due to relatively stronger T-cell responses afforded by most COVID-19 vaccines (Corbett et al. 2020; Sahin et al. 2020) compared to current influenza vaccines (Kang et al. 2004).

    © Copyright Original Source

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  • shunyadragon
    replied
    Originally posted by TheLurch View Post
    No. I'm arguing from having done extensive reading of the academic literature on the pandemic. So my position is quite informed. And the information i have indicates that there is no evidence of any difference in the susceptibility of any populations so far.


    You can believe anything you want; the question is whether you have evidence that can convince other people. And so far, the sum total of the evidence you've presented here is a single correlation that doesn't even come with a mechanism to explain why the correlation exists.


    There's a key quote in the article that followed, a quote that you seem to be going right past: "we currently do not know whether selection has made a substantial contribution to the evolution of human genes that interact more specifically with coronaviruses."


    None of this is to say that there won't eventually be evidence of population level differences in the response to SARS-CoV-2. All i'm pointing out is that you seem to have convinced yourself this is true in the complete absence of that evidence.
    I have cited the references with evidence you choose to ignore.

    Leave a comment:


  • TheLurch
    replied
    Originally posted by shunyadragon View Post
    As before when you refused to respond I believe your playing the hostile witness 'arguing from ignorance.'
    No. I'm arguing from having done extensive reading of the academic literature on the pandemic. So my position is quite informed. And the information i have indicates that there is no evidence of any difference in the susceptibility of any populations so far.

    Originally posted by shunyadragon View Post
    I believe these papers and the evidence contribute to demonstrating inherited factors that contribute to the lowinfection and fatality rates in Southeast Asia, South Asia and to a lesser extent East Asia in general.
    You can believe anything you want; the question is whether you have evidence that can convince other people. And so far, the sum total of the evidence you've presented here is a single correlation that doesn't even come with a mechanism to explain why the correlation exists.

    Originally posted by shunyadragon View Post
    more to follow . . .
    There's a key quote in the article that followed, a quote that you seem to be going right past: "we currently do not know whether selection has made a substantial contribution to the evolution of human genes that interact more specifically with coronaviruses."


    None of this is to say that there won't eventually be evidence of population level differences in the response to SARS-CoV-2. All i'm pointing out is that you seem to have convinced yourself this is true in the complete absence of that evidence.

    Leave a comment:


  • shunyadragon
    replied

    Source: https://www.medicalnewstoday.com/articles/ancient-rna-virus-epidemics-occurred-frequently-during-human-evolution




    ‘Ancient RNA virus epidemics occurred frequently during human evolution’

    • Genome adaptations may offer insight into a viral epidemic as far back as 25,000 years.
    • Several lines of evidence point to a coronavirus or similar virus that emerged among the ancestors of East Asian people.
    • Identifying ancient viral activity may uncover the potential of evolutionary genomic methods to predict and combat future pandemics.

    A team of scientists, which researchers at the University of Arizona in Tucson and the University of Adelaide in South Australia co-led, delved into human genomes to find a correlation between ancient coronavirus epidemics and past adaptation in modern humans.

    They hope that understanding the effect of past pandemics on genetic mutations will give scientists more “ammunition” in the arms raceTrusted Source against SARS-CoV-2 variants.

    Stay informed with live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

    Yassine Souilmi, Ph.D., the lead author of the paper, is a postdoctoral research associate at the Australian Centre for Ancient DNA. He and his fellow researchers published their findings in the June 2021 edition of Current Biology.

    The authors explain in their article:

    “Here, we apply evolutionary analyses to human genomic datasets to recover selection events involving tens of human genes that interact with coronaviruses, including SARS-CoV-2, that likely started more than 20,000 years ago.”
    VIPs and RNA viruses
    Throughout human history, positive natural selection has often targeted virus-interacting proteins (VIPs). VIPs either work in building immunity or get hijacked by viruses.

    This natural selection has persisted over the past 50,000 years, especially around VIPs that react to RNA viruses, such as coronaviruses.

    According to Souilmi and his team:“The accumulated evidence suggests that ancient RNA virus epidemics have occurred frequently during human evolution; however, we currently do not know whether selection has made a substantial contribution to the evolution of human genes that interact more specifically with coronaviruses.

    ”The observed mutations may have steadily increased in frequency until about 200 generations, or an estimated 5,000 years, ago.Also, the CoV-VIP proteins demonstrate antiviral and proviral effects and variations that affect SARS-CoV-2 susceptibility and COVID-19 severity in the current British population.

    However, the paper notes that such adaptations in certain human populations do not imply that those populations are more susceptible to viral epidemics.

    Medical News Today asked Martin Bachmann, Ph.D., an immunologist and professor of vaccinology at the University of Oxford’s Jenner Institute in the United Kingdom and the University of Bern in Switzerland, for his perspective on this research:

    “For me, it is quite stunning that you can analyze epidemics from 20,000 years ago without actually looking at a sample that is older than a few years. It shows that there is an awful lot of information buried in the genome of the whole population rather than individual genomes.”

    © Copyright Original Source

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  • shunyadragon
    replied


    Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7159740/



    Role of viruses in human evolution

    Linda M. Van Blerkom

    Abstract


    The study of viral molecular genetics has produced a considerable body of research into the sequences and phylogenetic relationships of human and animal viruses. A review of this literature suggests that humans have been afflicted by viruses throughout their evolutionary history, although the number and types have changed. Some viruses show evidence of long‐standing intimate relationship and cospeciation with hominids, while others are more recently acquired from other species, including African monkeys and apes while our line was evolving in that continent, and domesticated animals and rodents since the Neolithic. Viral selection for specific resistance polymorphisms is unlikely, but in conjunction with other parasites, viruses have probably contributed to selection pressure maintaining major histocompatibility complex (MHC) diversity and a strong immune response. They may also have played a role in the loss in our lineage of N‐glycolylneuraminic acid (Neu5Gc), a cell‐surface receptor for many infectious agents. Shared viruses could have affected hominid species diversity both by promoting divergence and by weeding out less resistant host populations, while viruses carried by humans and other animals migrating out of Africa may have contributed to declines in other populations. Endogenous retroviral insertions since the divergence between humans and chimpanzees were capable of directly affecting hominid evolution through changes in gene expression and development. Yrbk Phys Anthropol 46:14–46, 2003. 2003 Wiley‐Liss, Inc.

    © Copyright Original Source


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  • shunyadragon
    replied
    Originally posted by TheLurch View Post
    You do realize that this and the ensuing one are both explicitly presented as hypotheses, right? The only evidence presented in the two is a single correlation.
    As before when you refused to respond I believe your playing the hostile witness 'arguing from ignorance.' I believe these papers and the evidence contribute to demonstrating inherited factors that contribute to the lowinfection and fatality rates in Southeast Asia, South Asia and to a lesser extent East Asia in general.

    more to follow . . .

    Leave a comment:


  • TheLurch
    replied
    Originally posted by shunyadragon View Post

    [cite=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7796072/]
    You do realize that this and the ensuing one are both explicitly presented as hypotheses, right? The only evidence presented in the two is a single correlation.

    Leave a comment:


  • rogue06
    replied
    Originally posted by shunyadragon View Post

    On th ground in the countries in the data is collected.

    Still waiting for you to document your objections. Your a scientist and it is best for you not to resort to the vague ambiguous 'argument from ignorance.'
    So they get their numbers from the folks who supply the official numbers for the country and are often effectively guessing.

    Leave a comment:

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