The biology of coronavirus COVID-19 - including research and treatments

Discussion in 'Epidemics (including Covid-19, not Long Covid)' started by Trish, Mar 12, 2020.

  1. Hutan

    Hutan Moderator Staff Member

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    From the information about the FLiRT variant above:
    So, that's alright then...
     
  2. Trish

    Trish Moderator Staff Member

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    According to News Medical Life Sciences, however, the symptoms do improve after two years.

    From the conclusion of the linked article:

     
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  3. Ash

    Ash Senior Member (Voting Rights)

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    :sick:
    :walkingdead:walkingdead:walkingdead:walkingdead+…?
     
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  4. rvallee

    rvallee Senior Member (Voting Rights)

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  5. rvallee

    rvallee Senior Member (Voting Rights)

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    What a cheap cop out, to use the "novelty" of the virus but to use 2 years, as a point where symptoms improve in some but not all, when it's already been 4. Which of course ignores the fact that this problem has been known for decades.

    Medicine is really putting out a masterclass in how to destroy the credibility of experts. Of all experts, sadly. This is explicitly using professional credibility to lie to and mislead people, with clear intent and purpose.
     
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  6. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    Preprint showing hydroxycholoroquine may have been a bad idea, upregulating endothelial ACE2 expression.

    Chloroquine Up-regulates Expression of SARS-CoV-2 receptor Angiotensin Converting Enzyme-2 in Endothelial Cells
    Hien C Nguyen; Shuhan Bu; Lynn Wang; Aman Singh; Krishna K Singh

    BACKGROUND AND PURPOSE
    The novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) posed a serious threat to global public health. Hydroxychloroquine (HCQ), which is a derivative of Chloroquine (CQ), was a WHO-recommended drug to treat COVID-19 with mixed effects. The purpose of the present study is to evaluate the plausible mechanisms of HCQ actions behind its observed mixed effect.

    KEY RESULTS
    We demonstrate that CQ-treatment significantly up-regulates mesenchymal markers and SARS-CoV-2 receptor ACE2 in cultured endothelial cells.

    CONCLUSIONS & IMPLICATIONS
    The detrimental effect of HCQ in seriously ill COVID-19 patients might be due to CQ-induced increased expression of endothelial ACE2 exacerbating the severity of SARS-CoV-2 infection. Our study warrants further investigation in animal models and humans and caution while prescribing HCQ to patients with an impaired renin-angiotensin-aldosterone system, such as in hypertension, cardiovascular diseases, or chronic kidney disease; particularly with ACE-inhibitors or statin therapy.


    Link | PDF (Preprint: BioRxiv) [Open Access]
     
  7. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    Sabine Hossenfender — Unapproved Trial for Discredited COVID Cure: Scandal In France

    "In 2020, French physician Didier Raoult claimed that hydroxychloroquine was a cure for Covid-19. The results could later not be reproduced, but tens of thousands of people died because they did not receive or not seek treatment that might actually have helped them. Unbelievable as it sounds, the story of his unethical practices continues to this day. I have the summary."
     
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  8. Wits_End

    Wits_End Senior Member (Voting Rights)

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    Mainly USA:

    https://www.huffingtonpost.co.uk/entry/covid-summer-2024-surge-symptoms_l_6679820de4b0d2f6354efe63

    "The FLiRT variants are offshoots of JN.1, which was the dominant variant in the U.S. this past winter.

    This family of variants appears to be very contagious, thanks to mutations in the spike protein that may improve the virus’s ability to bind to human cells. “When we look at their molecular profile, some of those mutations potentially could allow the [virus] to escape from previous immunity,” Hopkins explained."
     
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  9. wastwater

    wastwater Senior Member (Voting Rights)

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    Covid-19: First coronavirus was described in The BMJ in 1965

    The history of coronaviruses since 1931

    https://www.bmj.com/content/369/bmj.m1547/rr-2

    I also wondered if coronavirus have been modified for biological warfare if there maybe a mk1 and mk2 or just natural evolution

    What happens if you are modified with a coronavirus (like Cytomegalovirus causing birth defects)

    Does infection with coronavirus activate EBV to do endothelial damage
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10292739/
     
    Last edited by a moderator: Sep 9, 2024
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  10. Amw66

    Amw66 Senior Member (Voting Rights)

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    Could be a significant evolutionary mechanism .
    Reinstatement of previous deletions , not possible with stepwise evolution , but via a previous lineage without deleted variations .
    Does this happen in any other virus ?

    https://twitter.com/user/status/1736526826179092781


    The ∆69-70 pendulum is in the midst of yet another swing.
    What makes the alternation from ∆69-70 to S:H69+ S:V70 even more remarkable is that deletions are one-way mutations. They essentially cannot be reversed. There has never been an insertion at S:69-70 in SARS-CoV-2. 1/5

    So how, after repeated deletion of S:69-70, have S:H69 + V70 been restored? This cannot happen via stepwise evolution/antigenic drift.

    But it can if a new variant derives from an old, vanished lineage that's never had ∆69-70 & has spent months evolving in a single person. 2/5

    There has been great work on deletions in the NTD region of spike by @GuptaR_lab, @EnyaQing, @GroveLab, & others, some of which I tried to describe in the thread below.
    But a precise explanation for the ∆69-70 pendulum remains elusive. 3/5
    x.com/LongDesertTrai…. Thread link reference https://twitter.com/user/status/1569025039109873668


    Is SARS-CoV-2 the only virus in which successive dominant variants derive from long-term intrahost evolution in individual hosts?
    It seems so, but with better genetic surveillance, perhaps we'll find others—Norovirus is a candidate. Maybe noro guru @Chris3Ruis can elaborate? 4/5

    I wrote the thread below in April 2022, incorporating some history of science, in an attempt to decipher if the ∆69-70 pendulum was a real phenomenon that would continue or, like so many other things, just an odd, meaningless coincidence. 5/5
    x.com/LongDesertTrai…

    Related thread
    https://twitter.com/user/status/1722352486638354663
     
  11. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    Enhanced immune evasion of SARS-CoV-2 variants KP.3.1.1 and XEC through N-terminal domain mutations
    Jingyi Liu; Yuanling Yu; Fanchong Jian; Sijie Yang; Weiliang Song; Peng Wang; Lingling Yu; Fei Shao; Yunlong Cao

    P.3, a subvariant of JN.1, has rapidly emerged as the dominant strain of SARS-CoV-2 in several countries, and has been designated as a Variant Under Monitoring. Previous studies indicate that the unique Q493E substitution in KP.3 Spike glycoprotein enhances its receptor ACE2-binding affinity and immune evasion, enabling it to outcompete KP.2.1–6 Notably, KP.3.1.1, which only carries one additional S31 deletion compared to KP.3, has surpassed KP.3 to become the new dominant strain globally (figure A; appendix p 4).7 Meanwhile, XEC, a recombinant variant of KS.1.1 and KP.3.3, shows strong potential to become the next dominant strain, rapidly expanding across Europe and North America. Compared with KP.3, XEC has only two additional spike mutations, F59S and T22N (appendix p 4). Both S31del and T22N introduce potential glycosylation on the N-terminal domain. Consequently, there is an imperative need to characterise the antigenicity and infectivity of KP.3.1.1 and XEC.

    Link | PDF (The Lancet Infectious Diseases) [Open Access]
     
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  12. boolybooly

    boolybooly Senior Member (Voting Rights)

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    Probably.

    "Recombination in Coronaviruses, with a Focus on SARS-CoV-2" Focosi & Maggi
    https://www.mdpi.com/1999-4915/14/6/1239

    Speaking subjectively as a zoologist it seems inevitable really. If viruses persist in carriers with asymptomatic infection, who we know exist by the epidemiology of COVID spread, possibly in those who have long covid though there has been a failure to find active virus in long covid patients in the literature which may be due to a failure to identify refugia but it implies their immune system is active and they are not shedding viable virus. So it is a possibility that replicating strains of covid can coinfect the same cells in carriers.

    There are likely to be a great many such carrier individuals aka "Typhoid Marys", not a few, as viral carriage is likely to be an evolutionarily advantageous strategy as with grey squirrels, the strategy being to pass the virus on so that the individual concerned is not at a disadvantage and everyone else has the same infection to contend with. Grey squirrels have evolved to use the squirrelpox virus as a biological weapon in their competition with the red squirrel. This kind of evolutionary pressure could also well explain the evolution of sneezing which if you think about it is the perfect way to spread respiratory viruses and we all do that.

    In the intracellular environment containing coinfections by different variants which the carrier strategy probably creates, crossover events might occur, where one RNA strand is joined with another, most of which would not be viable but these would be naturally selected for viability and the viable recombinants would emerge from infected cells to replicate within the individual and then spread to others.
     
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