morrobay said:
Not quite: The ubiquitous first line defense by T cells that target non mutating viral proteins and up to 30 epitopes on virus most likely account for exposures by infected family members that do not result in seroconversion/antibodies. Or mild/asymptomatic infections , with antibodies. I am unvaccinated for SARS-CoV-2. However Im sure have been exposed many times especially in these crowded wet markets.
https://www.science.org/doi/10.1126/science.abh1823
You are of course right, our immune system targets a wide range of viral proteins which influence our responses to future exposures. Some of these viral proteins can indeed be shared with other virus's, particularly those closely related to the SARS-Cov2, and these include several coronaviruses that cause cold like symptoms. It's interesting that the huge research effort that COVID-19 stimulated even identified parts of the immune responses that had previously unrecognised, and we know that any recent viral infection can activate a general immune response that increases resistance. We have also become increasingly aware of the way in which different antibodies can interact and effect the functioning of others, in some cases adversely, as happens in what is called, the original antigenic sin. I will however stick with my statement, it was confirmed in early research that it was the antibodies that targeted the spike protein, used to gain cell entry, that had the most important effect on preventing disease progression. It was this finding that was used in the development of all the vaccines, if the virus can't gain entry to the cells, it can't reproduce and cause disease. While with Covid the initial viral load seems able to overwhelm this protection, it does seem that a wider range of antibodies with different targets increases protection, often acting during different stages of the infection.
I am aware of the way in which people try to use the raw data available to draw conclusions about prevention and disease severity / mortality, often comparing COVID-19 with influenza. I think that both of these infections are seasonal, respiratory infections, this means that the numbers of cases vary dramatically depending on the time of year and the presence of other seasonal virus's. Viruses appear to be rather well-mannered, they, for whatever reason, appear to take turns causing infections in the population. Being respiratory virus's it does make sense that masks will affect transmission, though Covid does appear to be far more transmissible, this means that the effectiveness is much more dependent on the type of mask and how it's worn. The raw data on the risk of serious disease or death is much more misleading, while it clearly shows that Covid presents a greater risk, flu like many other infections has its greatest effect on the very young and the very old. In the case of Covid, the very young appear to have some inherent resistance to the disease, so mortality for example is concentrated in the elderly, using the raw data from population studies significantly underestimates the risk to the elderly. I am aware of the very real issues that people have with mandated vaccination and personal autonomy, few people appear to address this issue in relation to health care staff who work with vulnerable populations. In the UK it is already the case that vaccination against specific diseases is required to work in a clinical setting, depending on risk, this includes having had the routine vaccines given in childhood, the Hep.B vaccination, Chickenpox, possibly BCG for TB is there is a risk of exposure and of course COVID-19.
) against Omicron only, what do you think about the efficiency I can expect?