Take Me Now! 101 Reasons You Are Single Ladies’ Edition (Monkey University Lecture Series #2)

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I would love to hear your thoughts on all of this. Great podcast! Your podcast is great at rounding out my knowledge of the virus I work on, and of course many other viruses as well. Your discussion left me with a bunch of questions regarding B cells and antibodies.

As I was listening to the discussion of affinity maturation, I kept trying to think of how this process interacts with existing memory B cells, and in particular, how it interacts with original antigenic sin. What happens when you already have a good population of memory B cells to an antigen.

Do you get new germinal centers forming and the affinity maturation process going on again? And if so, does it start with the B cells that have already been through that process, or does it start with new, immature B cells that responded to the soluble antigen? Does that depend on how much new antigen is available if you have an effective antibody response, does that keep this process from restarting?

Do some mutations in the affinity maturation process close off the possibility of mutating back in some way that would be helpful later, or is all the raw material still around in a functional B cell after affinity maturation, so that you can get from a good antibody to the flu strain to a good antibody for the one you get in ? Is this process the reason why some vaccines require three shots to get protection?

I recall getting the Hep B vaccine many years ago in three doses—the second shot a month after the first, the third six months later. Or is this more a matter of getting enough antibodies, rather than getting higher affinity antibodies? Is there some mechanism to recycle the antigen?

Is the supply of antigen the limiting factor in this process, or is there plenty—maybe my intuitions at this scale are just all wrong? Please congratulate you listener, these are all excellent questions. Vaccine development has historically been mostly empirical, and regimes are usually based on what works best rather than on immunological considerations most vaccines were actually developed by microbiologists.

Part of the difficulty in addressing these issues is technical — it would be very difficult and costly to serially determine the affinities and specificities of B cells responding to antigen during consecutive immunizations of the same individual or animal. The novel ignored determinant would not be capable of priming naive B cells because it would be bound by circulating antibody and complement and eliminated before it ever had a chance to do so.

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I would expect that a secondary GC would therefore contain a mixture of B cells derived from naive and memory precursors. Many factors could influence the composition of this putative mixture, including competition between B cell clones for limiting amounts of antigen or T cell help. However, naive B cells are constantly being turned over dying and being re-generated in the bone marrow. But theoretically it is possible that an unswitched memory cell could re-enter a GC in response to viruses, and in this case, it is conceivable that some cells could be impaired by specific mutations, but these would be unlikely to last in the highly competitive environment of the GC.

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Serum antibody affinity already increases quite dramatically up to 10, fold within the first immunization, although serum antibody titers a composite measure of affinity and amount of antibody only really really go sky high after one or two booster shots. What the role in vaccination is of GCs emerging during booster doses is not clear at least as far as I know , but could conceivably involve the recycling of unswitched memory B cells back into GCs for further affinity maturation.

Antigen appears not to be limiting, since it can be detected on FDCs many months after the GC reaction has faded, though how available this antigen is at this point is not clear. Many hypothesis exist for why the GC response ends; these include competition between B cells and circulating antibody which would sequester the antigen available on FDCs and exhaustion of GC T cells perhaps through their regulation by GC-resident regulatory T cell populations.

I tend to favor the latter, but this is still a topic of fervent investigation. Attached are my two questions. She died 14 Oct 09 from bilateral pneumonia as a result from a confirmed case of H1N1. I prefer my medical advice from a doctor, imagine that! I am a grad student studying influenza here in Singapore.

The pink bar pandemic H1N1 shows a decrease in size over time, corresponding to the end of the pandemic. I am curious as to whether or not the same trend is observed in the US. You guys seem to suggest that after the pandemic the incidences of seasonal flu and flu B were not as prevalent, this is obvioulsy not the case here in Singapore.