SARS-CoV-2 Thoughts

As SAGE implied in their 20th Technical Update's note 1.8.1 , we have effectively multiple serotypes of SARS-CoV-2 already, as Delta antisera doesn't neutralize B.1.351 nor B.1.621 virus meaningfully. That makes South Africa a potentially interesting case, because B.1.351 and C.1.2 emerged there. B.1.621 emerged in Colombia and has accounted for a significant percentage of cases, but Delta caused a serious wave in only South Africa. Beta was never recorded in Colombia and Delta barely touched them, and interestingly, they are now far below their record high infections, indicating that B.1.621 antisera is effective against its respective virus. https://origin-coronavirus.jhu.edu/region/colombia The lack of Delta's emergence could be geographic and political, but it may also mean that B.1.621 antisera is effective against Delta, which would be very encouraging news. https://outbreak.info/situation-reports?pango=B.1.621&selected=COL&loc=IND&loc=ZAF...

Vaccinated people infected by Delta are more likely to be hospitalized than unvaccinated people by Alpha. The statistical power of this study isn't great, but it implies that vaccinated people are more likely to need hospitalization. Ware the confounders. https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(21)00475-8/fulltext Reading the full paper, we find 1.9% of unvaccinated Alpha infectees required hospital admission. 2.2% of unvaccinated versus 2.3% of vaccinated Delta infectees required it, and 3.4% of vaccinated Alpha infectees required it. Thus, strangely, vaccination appears in these findings to increase the risk of hospitalization or emergency treatment required. The statistical power of these findings isn't very great because of too few hospital admissions amongst vaccinated infectees, and bear in mind we vaccinated people at higher underlying risk first and more thoroughly and the propensity of people who have been vaccinated to also be more l...

Original antigenic sin(OAS) has not yet been demonstrated in SARS-CoV-2 . However, I strongly believe that OAS will manifest itself, and it will be a bad and worsening problem over time. If I am correct, it may mean that getting vaccinated will become actively dangerous, depending on antibody-dependent enhancement(ADE) and its degree. OAS occurs when an immune response is produced by the body to a closely related pathogen or vaccine(such as a different strain of a virus) instead of generation of a novel immune response . This is because of homology between the two intruders' epitopes and resulting cross-reactive immune activity. SARS-CoV-2 has clearly demonstrated induction of variably cross-reactive antibodies with strain-variable neutralization potential. It has been demonstrated in many viruses ranging from Dengue Fever to influenza to HIV-1 . The set of viruses is not arbitrary: OAS abuse is a particularly effective strategy in viruses that mutate quickly, like influe...

Summary: The "efficacy" of a vaccine(VE) is a convenient number, but it's often provided without vital context that would ensure it is interpreted correctly. There are different kinds of efficacy that matter, and the numbers reported are often at peak levels following vaccination. It is in the commercial, professional, and political interest of drugmakers, the media, virologists, and policymakers to emphasize the highest number to demonstrate the power of the vaccines. The 3 primary outcomes that vaccination is intended to prevent are severe disease, infection, and transmission. The number for severe disease is likely to be highest, while the number for transmission is likely to be lowest. This is because different aspects of the immune response affect each. There are 3 main takeaways: VE is usually reported in terms of prevention of severe disease, VE can change against infection and severe disease independently, and SARS-CoV-2 is likely to escape from today...

SARS-CoV-2 is known to be a seasonal virus because the amount of viral transmission depends critically on the temperature . There are higher loads of viral inoculum that are transmitted greater distances when it's cold and absolute humidity is lower, and people are more likely to gather inside together for warmth. https://www.frontiersin.org/articles/10.3389/fpubh.2021.650493/full This is true of all strains, and we are entering autumn with a higher case count than we had last year. Also, last winter, Alpha was dominant nearly entirely alone, and it's not antigenically very distant from the original S protein. Instead, today, we now have many antigenically distant strains and variants of concern(VoCs). Check the dot plot for cross-immunoreactivity between strains in the following article. https://www.sciencemag.org/news/2021/08/new-sars-cov-2-variants-have-changed-pandemic-what-will-virus-do-next Through those two factors, we should see new domestic highs in case co...

SARS-CoV-2 caught most experts off guard with its evolutionary alacrity , but it always should have been expected to be very good at evolution despite a relatively low mutation rate . The progenitor virus(or, at least, the majority of its genome) came from bats. Bats have amazing immune systems due to their colony lifestyle in cramped quarters and their high metabolic rate. Further, coronaviruses have the longest genomes of any known +ssRNA viral family, and viruses are under constant evolutionary pressure to keep their genomes small. The genome of SARS-CoV-2 is about 30kb in length. The value of the genome was evidently great enough to compensate for that pressure. There is more highly conserved genetic material in coronaviruses than others, which in SARS-CoV-2's case means a lot of finely tunable accessory genes that screw up the immune system badly and even vicious microRNA's outside the coding regions of actual genes . SARS-CoV-2 has absolutely ingenious replicatio...

The Delta strain of SARS-CoV-2 has a longer asymptomatic period than earlier strains: around a day more. This is because it becomes detectable by PCR in 1.5 fewer days than previous strains, on average, but that is slightly counterweighted by faster symptom onset. Thus, although overall, symptoms present themselves slightly more quickly than in other strains, this still allows for longer aymptomatic transmission. https://www.nature.com/articles/d41586-021-02259-2 Although these mutations probably just generally facilitate spread, they demonstrate that the virus has the ability to adapt itself to our quarantine strategies. SARS-CoV-2 has now demonstrated that it can modify both of these timepoints -- seroconversion and symptom onset -- independently, and it can probably modify each timepoint in either direction. It's not clear just how long it can make its incubation or asymptomatic phases, though, because extension of that time could come at the cost of pathogenicity over...