Something that has popped in and out of my head as I've been reading some the vaccine news is: if part of a virus and a cold virus from a chimp are shot into people's blood, can it also lead to some of the C19 side effects we are seeing (heart, lung, neuro.?)? If its strong enough to get an immune response is it strong enough to trigger the side effects? Are chimp viruses safe for us or are those going to lead to other issues? The RNA methods seems similarly loaded to me as well.
If you're referring to the Oxford trial, which uses a viral vector from chimps, then no, the vector won't cause any side effects. A vector is basically a large piece of DNA into which is inserted coding regions for proteins that are supposed to trigger antibody formation, in this case, the spike protein of SARS-CoV-2. The advantage is that you can just inject a patient with the vector, and it will seek out cells that it can enter into with its payload.
This particular vector has been used in many other vaccine trials, though I don't believe that any approved vaccines make use of it. It has been engineered so that it can't replicate itself, and therefore can't cause any infection. That doesn't mean their can't be any side effects, but AFAIK, the use of this vector doesn't present any particular hazards. But I'm no expert in vaccines.
RNA vaccines, such as the one Moderna is working on, use the genetic code to produce protein fragments, or peptides, that activate the immune system. The RNA is packaged in a way that allows it to be injected into the person, and possibly, that will allow it to target certain cells, fuse with them, and get inside, where it will be translated into protein.
The main side effect I would worry about is that most of these vaccines are based on the spike protein, which SARS-CoV-2 uses to enter cells. The spike protein binds to a specific receptor, ACE2, on cells. If you make a spike protein, or fragment of the spike protein, and it doesn't trigger an immune response, it will probably be rapidly degraded. But if it weren't, it could bind to cells and block the ACE2 receptor. Many drugs work like this, e.g., beta-blockers for heart patients, and naloxone, the antidote to morphine and other opioids. A protein like this could thus interfere with normal cell function, though it would also prevent the virus itself from entering cells.
In fact, there are known drugs that block the ACE2 receptor, ARBs, that have important medical uses, and I now see that in fact some researchers have suggested they might be used to treat C19:
https://www.ersnet.org/covid-19-blog/ace2-receptor-blockers--a-novel-therapeutic-approach-for-covid-19#:~:text=Therefore, angiotensin receptor blockers (ARBs,their infection to host cells.
https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656
One problem, as I alluded to before, is that in the process, the antagonist will interfere with normal cell function. Since the main function of ACE2 is to produced angiotensin, maybe use of an ARB could be done in conjunction with a treatment to elevate angiotensin levels. At the very least, this might be a short-term solution, for someone who might have come into contact with an infected person, and wants to stop the virus immediately. It might also be used in the short term to slow down viral replication, giving the immune system time to get up to speed.
However, there is another major problem with ARBs. If you block a receptor like ACE2, the body quite frequently will compensate by increasing synthesis of that receptor (this is the same kind of feedback mechanism which results when a cyclist transfuses blood, and inhibits reticulocyte formation, only in reverse). So taking ARBs could make a viral infection even worse. In fact, patients often take ARBs for precisely the kind of comorbidities that are associated with increased risk from the virus, and there has been concern that they face a dilemma: they need the ARB for their condition, but it could increase their susceptibility to the virus. Medicine is complicated and messy.
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