Spending a few days in Toronto with my kids, so I can go to the Darwin exhibit at the Royal Ontario Museum.1 Depending on when I get back, my next blog post may be a little delayed.)
Even though cytotoxic T lymphocytes are called “cytotoxic”, it was no surprise when new techniques in the mid-90s suggested that CTL might have other strings to their bows. (I talked about this the other day.) Some experiments were also pointing the same way. For example, Frank Chisari’s group offered evidence that CTL might be able to control hepatitis B virus without actually being cytotoxic.
Hepatitis B virus was a particularly difficult case for study in general, because it’s pretty much a human-specific virus. (HBV is a pain in tissue culture. There are a couple of animal models, but they’re hardly convenient. I mean, ducks? Woodchucks?) From studies of the natural disease, it seemed pretty clear that natural HBV infection was often handled by CTL; people who control HBV show a strong CTL response, those in whom HBV progresses and becomes chronic usually do not. But testing the function of CTL in HBV infection wasn’t easy without an animal model.
So Chisari made an animal model. He made transgenic mice that express the HBV genome (that is, the mouse genome contained the HBV genome) under a liver-specific promoter.2 There you go, hepatitis B virus in the mouse liver. It can’t spread and infect new cells as would normally happen in humans, but on the other hand you’re expressing the virus in essentially all the liver cells anyway, so you don’t need to infect new cells.
Even though cytotoxic T lymphocytes are called “cytotoxic”, it was no surprise when new techniques in the mid-90s suggested that CTL might have other strings to their bows. (I talked about this the other day.) Some experiments were also pointing the same way. For example, Frank Chisari’s group offered evidence that CTL might be able to control hepatitis B virus without actually being cytotoxic.
Hepatitis B virus was a particularly difficult case for study in general, because it’s pretty much a human-specific virus. (HBV is a pain in tissue culture. There are a couple of animal models, but they’re hardly convenient. I mean, ducks? Woodchucks?) From studies of the natural disease, it seemed pretty clear that natural HBV infection was often handled by CTL; people who control HBV show a strong CTL response, those in whom HBV progresses and becomes chronic usually do not. But testing the function of CTL in HBV infection wasn’t easy without an animal model.
So Chisari made an animal model. He made transgenic mice that express the HBV genome (that is, the mouse genome contained the HBV genome) under a liver-specific promoter.2 There you go, hepatitis B virus in the mouse liver. It can’t spread and infect new cells as would normally happen in humans, but on the other hand you’re expressing the virus in essentially all the liver cells anyway, so you don’t need to infect new cells.
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