I'm just writing to clarify my question about the production of the flu vaccine if one of the other seasonal strains was removed as there seemed to be a bit of confusion about the point of it.
As I understand it one of the biggest holdups in seasonal flu vaccine production is getting enough eggs of the right quality to grow the vaccine in. This is effectively a fixed amount that gets split three ways between the three seasonal strains. So this would mean for 100 units of possible production each strain gets 33.3 units made.
What if the WHO decided that Swine Origin H1N1 had not only displaced the previous seasonal H1N1 but also one of the other seasonal strains and thus the next seasonal vaccine, for whichever hemisphere is next, only needs a bivalent vaccine instead of the previous trivalent vaccine. To my understanding this would mean that for 100 units of available production you could make 50 units of each strain.
This would have two immediate advantages. Either you can make the same number of seasonal flu vaccines as in previous in less time. Or for the same amount of time you can get more doses. The main logistical advantage of this would be that you could vaccinate more people faster then is currently possible.
This of course would require the WHO to decide that Swine Origin H1N1 to have displaced two seasonal strains which seems to be unlikely from my outside view.
James from Wellington
Thanks for this wonderful podcast.
I found two of your stories in TWIV #82 really fascinating, and wanted to ask a couple questions. Forgive me if these are dumb questions--I'm a computer scientist with little formal biology background, so I may be missing all kinds of stuff.
First, from your dengue story, I was trying to get my head around antibody-dependent enhancement of infection.
How is ADE related to original antigenic sin? Is it just a worse variant of it? In both cases, you get infected with strain #1 of the virus, you develop an immune response to it, and then when you're exposed to strain #2, you respond as though it were strain #1. In the original antigenic sin case, you produce relatively ineffective antibodies, so you don't get as effective an immune response as you should. In the ADE case, the ineffective antibodies provide an opportunity for the virus to gain entry to macrophages via the Fc receptor, along with failing to neutralize the virus. Is that basically right, or have I misunderstood?
What I'm trying to understand is why this doesn't happen all the time. I mean, if the viral infection is still present when my antibody response starts ramping up, shouldn't I start having virions getting bound to by some of those early antibodies at a level where they're not neutralized, but they can get inside the macrophages using the Fc receptor? (Perhaps most viruses just can't benefit from being engulfed by the macrophage, but dengue can?)
How is the T-cell response involved in all this? If I already have cytotoxic t-cells that recognize what infected cells look like, shouldn't they be killing the infected macrophages? (Or maybe that's why the second bout of dengue makes you so sick?)
After you've had the second bout of dengue, assuming you survive, do you end up with antibodies that protect you from both strains you've been exposed to? Or are you stuck with the antibody response to the first strain?
Second, when you were talking about the different MHC molecules associated with people whose bodies control HIV for a long time without getting sick, I was curious about whether these MHC molecules were associated with different levels of autoimmune disease. On one side, I'd expect MHC molecules that don't bind well to many self antigens to be less likely to cause autoimmune disease. On the other side, I'd expect a wider range of antigens that could be bound by the MHC to be associated with more ways for something to go wrong, leading to your immune system attacking healthy host cells. Or does the process of selection in the thymus keep those MHC differences from having much effect?
The Jul/Aug 2010 issue of Discover Magazine addresses faulty research in an article by David H. Freeedman, called "The Streetlight Effect", which is based on his new book, entitled "Wrong".
The NY Times had a column that discussed this book and included the following comment:
"Mr. Freedman, the author of “Wrong,” is a science and business journalist...
"He points out that most expert wisdom, especially about health issues, isn’t just sometimes but nearly always ultimately proved wrong. He is diligent about explaining the “disconcerting reasons” why this is so. He examines how the sausage that is major health studies is actually made. It’s not pretty.
"Mr. Freedman observes the way that very small (and hence unreliable) surveys, often based solely on animal testing, are used to make extravagant claims about cancer or our diets. He notes how scientists discard data that doesn’t fit their theses. He talks about measurement errors and the academic pressures of publish-or-perish."
His concerns and those addressed by the cancer doctor about journalism seems to present issues for anyone interested in a research career might need to know about.
Jim from VA