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Vaccines are targeted at surface structures of the micro organisms that you want to vaccinate against. For viruses you want to target structures on the viral surface that not only allows the antibody to bind to the viruses surface, but you also want it to prevent the virus from binding to their cell surface target and thus block the viruses ability to enter the cell.For bacteria the vaccine can have two different purposes, the first is to inactivate bacterial toxins that may be the reason for us becoming very sick, such as the diphtheria toxins that causes the severe diarrhea that is associated with the disease. The other purpose is to mark the tharget for other cells in our immune system such that they can bind on to the bacteria and kill them.The fact that antibodies bind onto the surface of pathogens allows our immune cells such as granulocytes and macrophages to identify those as foreign. Our immune cells has evolved react to things like LPS molecules that are unique and central to bacteria as a life form. This means that certain parts of our immune response to pathogens are “hard coded” into our immune system. But these inate immune cells have also evolved to cooperate with our adaptive immune system. Making the whole system even more effective in combating infectious diseases. So the cells in our inate immune system carry Fc receptors that bind antibodies and thus allows them to use those antibodies produced by our adaptive immune system to more effectively identify things we have encountered in the past. Basically the antibodies will paint a big bullseye on the bacteria.The antibodies that bind to the surface of bacteria allow opsonization to occur whereby specific proteins in our blood become actated and covers the target with molecular hand holds for our immune system to make the process of grabbing and deactivating bacteria more effective.

Thank you for the A2A:Although, down regulation of HLA class I is certainly a possibility for immune escape for both tumors and viruses for that matter our immune system would be fairly worthless if it was that simple to fool it. As this is a fairly obvious immune escape mechanism our immune system does use a lack of HLA class I as a none self signal for for our immune system. However, those receptors aren’t found on T-cells but on NK-cells that are responsible for eliminating the cell that displays this “danger signal”.Our immune system is primed with several such danger signals such as LPS that’s found on gram negative bacteria, double stranded RNA that isn’t natural in our body, flagellin which is specific to bacteria, in methylated DNA and so on, which are nonspecific but general signals of none self that can trigger our immune system to react to something as foreign. These are referred to as PAMPs and DAMPs for pathogens and general danger signals associated with cell damage respectively. However, the immune response may be none specific and may not lead to a specific immune response unless this also results the release of something that our B- and T-cells can recognize as none self.If these sigals are effective enough to eliminate a small amount of viruses or bacteria before they get a foothold then it might be enough that our innate immune system cleans it up and there’s no need to involve the specific immune system. There are quite a few organisms that survive without such a immune systems in nature such as starfish. Our cellular and humoral immunity is fairly specific to vertebrates and even though all multicellular organisms need some form of immune system to survive shows how far you can get based on a inate immune system for creatures like starfish.

The main difference is that the vaccine is just the antigen, and nothing else. This means the immune system can just hum along as normal, do its thing, and if there was enough of a pulse of the antigen from the vaccine, you should be good to go for sometime.I suspect that the vaccine immunity will be longer lasting, not just because they intentionally designed it to give a stronger antigenic “pulse” than you could ever get from the real virus, but also because the virus itself probably does things to reduce your ability to develop immunity against it.It is often portrayed that a virus just waltzes into your cells and then hijacks your machinery for replication, but that is a VERY simplified version of events. Your cells are not sheep for the picking, and many viruses are quite a bit more sophisticated than is typically explained.Innate immunity against virusesYour cells have a variety of innate immune mechanisms that make it very difficult for a virus to get in and hijack your cells in the first place. Your cells have a variety of “Pattern Recognition Receptors” (PRRs) that recognize things considered to be “Pathogen Associated Molecular Patterns” (PAMPS). These are things that “aren’t quite right” in a human/mammalian context. This can be anything from unusually large amounts of double stranded RNA to incorrectly “capped” RNA, at least in the case of viruses. Either way, that will trip a PRR, which will likely result in a signal cascade that among other things, will attract immune attention.Your cells also express enzymes that mutate and alter RNA and DNA that don’t appear to belong, such as APOBECs. The expression of these is often upregulated in an inflammatory condition (such as the one created by a PRR detecting a PAMP). APOBECs will then go in and hopelessly mutate any exposed RNA or DNA in the cytoplasm, to the point that it can no longer create a viable virus.All of this is passive and is already present in your cells, independent of the “adaptive” immune system (cellular and antibody based immunity) that you’re used to hearing about.However, if everything worked out that perfectly, Coronavirus wouldn’t be a problem.Viral inhibition of the Immune SystemMany subunits of the virus appear to actively disrupt and block PRRs before they can set off a great enough alarm. Other parts of the virus appear to be able to “proofread” their own replicating RNA, and so hypothetically they may “undo” any APOBEC induced changes, if APOBEC ends up being expressed at all. Its possible this expression gets blocked or otherwise inhibited as well.Just look at this excerpt of a fun list of SARS-CoV-2 non-structural proteins and what scientists suspect they do:Coronavirus RNA Proofreading: Molecular Basis and Therapeutic TargetingTable 1Summary of the Coronavirus Nonstructural ProteinsFunction in Virus Life CycleInate host responseNsp1: cellular mRNA degradation and preventing host mRNA translation through ribosome bindingCottam et al., 2011; Narayanan et al., 2015; Thoms et al., 2020Nsp2: proposed to disrupt host intracellular signalingNsp6: implicated in the generation of autophagosomes for the degradation of immunomodulatory proteins….Replication and transcription…Nsp14: exonuclease (ExoN) domain that proofreads the nascent RNA strand and excises the misincorporated nucleotides….So you can see, the SARS-CoV-2 does a lot to suppress your immune system from the outset.You can see NSP14 “undoing” any anti-viral RNA editting by APOBEC enzymes, and you can see how many of the initially expressed viral proteins (NSP1, NSP2, NSP6) are directed against disrupting and preventing the host cell from responding against it.In nearly every infection, the symptoms are based on the immune response. Many people already have immune systems that are less than finely tuned (we all know someone who gets EXTRA sick all the time), and then Covid comes in and royally derails (the technical term is “dysregulates”) your immune responses. This will result not only in reduced effectiveness, but more intense immune responses to escalate.This is where that “cytokine storm” you’ve heard about comes from.This dysregulation has a strong chance of also disrupting the formation of your memory B cells that create long term immunity. The paper linked below reports on such a mechanism.Loss of Bcl-6-Expressing T Follicular Helper Cells and Germinal Centers in COVID-19Essentially, the virus creates enough dysregulation that certain classes of T Helper Cells do not form, and this results in the failure of memory B-cells to mature properly, resulting in short lived antibody immunity.Antibody producing “plasma cells” derived from Memory B-cells, and these Plasma cells tend to last about as long as the reported length of natural covid immunity. Memory B-cells need to undergo a highly regulate process called “Affinity Maturation” in order to form long lasting memory B-cells that further Plasma cells can be derived from. This process takes place in the “germinal centers” of lymph nodes.No T-Follicular helper cells means dysregulated Germinal centers, which means no affinity maturation, and no long term immunity.To circle back, the vaccine DOES NOT do any of thisIt just introduces the antigen without any of those immune system disrupting proteins.Since the immune system can just hum along and do what it normally does, its just a question of introducing enough antigen in the right way to form some memory B cells.Unless the vaccine is just not as immunogenic as they have lead us to believe, I can’t see why the vaccine immunity wouldn’t last.If there is no Covid dysregulating your immune system, the vaccine should work just fine.