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Originally Posted by 'Hamas' Jenkins

This is an easy issue become confused about because the language we use to describe it isn't very precise.

There are different strains of SARS-CoV-2, but different strains don't always mean you need different treatments. That depends on the difference from one virus to another. There is evidence that this particular disease does not mutate that much, which means that an effective treatment is likely to confer much broader protection than other viruses. This is also the rationale behind mass vaccination campaigns in general--if everyone is vaccinated for the measles and it can't establish a reservoir it can't mutate; if people don't get vaccinated the disease has an opportunity to mutate, which would then render the vaccine less effective.

In the case of the flu, there are almost 200 different subtypes and 131 types that have been found in people, but what you are commonly vaccinated against are H1N1, H3N2 (both flu A types) and two types of flu B. Within those viruses, there is enough genetic differentiation to make the vaccine a moving target--they try to zero in on the unique characteristics of the viruses of that year. The ability of flu to mutate rapidly is why treatments like amantadine is now functionally worthless (and why Tamiflu soon will be, too).

HIV is even more prone to mutation than the flu, but I don't like the analogy of it being a genius--it mutates so readily because its proofreading enzymes are really inaccurate. Nevertheless, that's why you need combination therapy to keep it in check; as it mutates so rapidly, the odds of resistance become virtually certain if on a single therapy. There are numerous different groups of HIV-1 (M, N, O, P) and within those groups there are subtypes, and within those subtypes there are numerous strains, and those strains can develop resistance to therapies over time, and sometimes clinicians even use that to their advantage. One of the reasons why many people starting out on anti-HIV therapy begin with a regimen with emtricitabine is because the mutation that confers resistance to it (M184, IIRC) actually make the virus less "fit".

What is the point of all this?

Viruses that are more likely to mutate are harder to treat because your initial therapies are less likely to work as the genetic code of the virus changes over time. Given that SARS-CoV-2 has shown little mutation to this point, the odds of a vaccine conferring superior protection in comparison to a flu vaccine are likely if we can find one that stimulates an adequate immune response.

Thanks for the breakdown! Cant wait for Pete to chime in with some response about us not knowing everything about this virus so who knows what it's really like and then claiming something about masks not working.