Differences in vaccination efficacy can be caused by many things. The infectious organism itself is a major factor. Many diseases, such as influenza, require frequent vaccination due to the constantly changing nature of the influenza virus from year to year. Secondly the type of vaccine is another factor. Vaccines can be live organsim, killed organism, or subunit types. A live vaccine typically mimics a real infection and they tend to provide the most long lasting immunity (think MMR). Killed organism vaccines generally work well, but do not mimic the infectious state and usually do not last as long. Subunit vaccines provide immunity that is as long lasting as killed vaccines. However, back to point one, if the organism changes in an appropriate way it may then avoid the vaccine induced immunity. Killed vaccines and subunit vaccines are usually scheduled for boosters every 5-10 years to maintain immunity. We are also finding that due to the near eradication of many diseases there is no more "boost" of immunity from the community. Therefore even some live virus vaccines need to be boosted every 20 years or so. In summary, there are a lot of factors that affect vaccine immunity both from the infectious agent and the body.

Hi James,

I do agree with you that both the antigen and the host immune system determine the outcome of vaccine immunity. Nature, amount & presentation of the antigen, adjuvants, route of immunization, boosting, and age, health status of the host, stress, etc. influence the immune responses and protection against homologous challenge with the pathogen.

I was rather trying to look into factors contributing to the window of protection after the neutralizing/protective antibody levels would have declined to undetectable levels. In the absence of antibodies, 'long-lived' memory B cells are believed to be major players in protection against pathogen challenge. Whether Ag1 (e.g. FMD VP1 neutralizing epitope)-specific memory B cells have longevity equal to or different from that of Ag2 (e.g. vaccinia virus Ag)? There must be differences in the cues or microenvironment responsible for variation in the longevity. Too difficult to determine!

I think I see what you are getting at. I believe the number of "long-lived" memory B-cells is correlated to the amount of T-cell help present during the initial infection/vaccination. Live virus vaccines generate more T-cell help, therefore, more memory B-cells. That is probably only part of the story. In the early days of mass vaccination using live virus vaccines there was still plenty of infectious disease in the community. This served to boost the immunity of those already vaccinated. This boost would increase the number of memory cells (both T and B). We see the results of not having this boost with the occurrence of measles in supposedly vaccinated individuals (many years after the vaccination). This is why it is now recommended to get a booster for many live virus vaccines after 20 years or so, especially if you live in a country with high vaccine coverage. I cannot say for certain that memory B-cells generated in response to a subunit vaccine will last longer or shorter than memory cells generated to a live vaccine or natural infection. However, without teasing out the frequency of the memory cell response combined with even an equal half-life you will have difficulty getting at your question of true differences in the memory B-cells. It is a difficult problem. I worked on something similar many years ago looking at the immune memory in bone marrow transplant recipients. A similar population may be a place to start looking at things.

Obviously yes

Obviously yes

Dear Mohemid Al-Jebouri,

I think you mean to say 'yes' to existence of variation in longevity of memory B cells that would be likely contributing to the differences in duration of protective immunity by different vaccines.

I would wonder if there are some ways to considerably enhance the longevity and number of memory B cells against vaccinal antigens. It could be a step forward to achieving the aim of constructing ideal one-shot vaccine.