I just found this really interesting interview with Dr. Racaniello from Columbia University, a professor of virology. He touches on the vaccines only having the spike protein:
>>>I must say that early in the outbreak last year, when the vaccine development was just ramping up, we talked a lot about this idea that, should they really only be focusing on spike? Shouldn't they be putting some other viral proteins on, and in retrospect it was a good decision to get vaccines out in less than a year, because otherwise it might've been more complicated. But that's partly why all the variants are arising now, because we have only the spike epitopes in there. And so it's easy for the virus to get around that. So, it's two ways, that story. So those are the things that we've talked about. . . . Now for SARS-CoV-2, yes, having other proteins in the mix is a good idea. I think it depends on the severity of the disease. We did a paper 6 months ago which studied people who had died from COVID. So this was a very serious disease. And their lymph nodes had no germinal centers, which means no memory B cells to SARS-CoV-2. Even though they had antibodies, they had very low affinity antibodies. . . . So, on the one hand, yes, you make a lot of viral proteins and those are great epitopes for mainly T cells because I think most of the antibodies that are going to block infection are going to be spike directed. But any other viral protein could in theory be a T-cell target. So you'll get more epitopes.<<<
The discussion of T cells is also interesting:
>>>I think the T-cell immunity is substantial and really has been ignored. And the reason is, it's very easy to look for antibodies that block infection. You do a neutralization assay with virus in the lab and it's pretty straightforward. [You do a] T-cell assay if you want to know, do infected or vaccinated people make virus-specific T cells? It's harder. . . . And as I said earlier, the variants do not have changes in T-cell epitopes because -- and this is very interesting -- when you are infected and you make a variant that evades an antibody, that variant can go to someone else and evade their antibody too. So it spreads through the population. If you happen to make a variant that evades a T cell, it's not going to make a difference in the next person because everybody's T-cell epitopes are different. And so T-cell variants of viruses generally take many, many, many years to emerge. So it's not an issue. And so I think the T-cell immunity -- the last defense against an infection, right? To kill the infected cells. That can protect a lot of people in the face of even low antibody response. There are some agammaglobulinemic people who don't make antibodies who have been infected with a virus, and they don't have an unusually severe course, because I think the T cells are actually detecting them.
The discussion of antiviral drugs is also interesting:
>>>So this [molnupiravir] is what we would call a nucleoside analog. So it's a building block for the RNA of the virus and it inhibits the polymerase basically. And this is a great target because cells don't have such an enzyme. So it should be relatively low toxicity. I think molnupiravir is fabulous. It was shown to work really well at preventing transmission in ferrets last year, and now in the phase II [trial]. And this is exactly the drug we need because it's orally available. You just take a pill, and at your first positive test, you could take this and probably completely alter the course of not just disease, but also shedding. . . . And, of course, the other hand is we're going to get resistance to that drug immediately. So one drug is not enough. Nevertheless, I am very excited about it and I just hope we have some others, cause what we've learned from HIV antiviral therapy, one drug isn't enough. Two is not enough. Three is the magic number that you need to treat people with. . . . Now there are a lot of other drugs in the pipeline ... molnupiravir is a drug that existed before. But there are others that are being made that are purposefully selected for SARS-CoV-2. And I think it's important to push those forward in case we need to quell outbreaks and so forth. And we need to have a few of them. If we could make them more broadly acting, [that] would be great. Make an RNA inhibitor like molnupiravir that could inhibit many coronaviruses so that when the next one comes out of bats into people, which is going to happen probably in 10, 20 years, we'll be ready to take care of that. <<<
https://www.medpagetoday.com/blogs/marty-makary/92434