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8. Is there more than one type of hepatitis B virus?

There is more than one hepatitis B virus. The one I learned about in medical school we now call the wild type. This is the usual- what we now call “e-antigen positive hepatitis B”, these are individuals that have detectable DNA, have an e-antigen and do not have an e-antibody. This is the usual wild type. Now in a survey that I participated in, in the United States, 27% have a mutation called the Precore Mutation, and 44% of United States patients with hepatitis B have another mutation called the Core Promoter. In both cases, there is no e-antigen in the blood and there is an e-antibody, but the DNA is high, so these are active viruses. And this will confuse physicians because they all learned in medical school that if the e-antigen is not present then it’s inactive, but these two are exceptions. Now we do not have commercial tests that we can check off when we see you as a patient to get this done in the laboratory, so we have to make this judgment when we see that you do not have an e-antigen, you have an e-antibody but your DNA is high, and often your liver enzymes are high as well, we then diagnose “e-antigen negative chronic hepatitis B”. When I dictate my notes so I can remember, since I have a large practice, I always say “I just saw Mrs. Smith who has e-antigen positive chronic hepatitis B or e-antigen negative chronic hepatitis B,” so I can keep track of all of my patients. Now if that weren’t confusing enough, we’ve had two therapies that have come into the market in the last few years, one is called lamivudine, it was licensed in the US in 1998, and adefovir that was licensed in 2002, and both of these drugs when given to a patient over time can cause a drug-induced mutation. The one with lamivudine is called the YMDD mutation, it occurs at a relatively high rate, at about 20% per year. It’s sort of a partial failure of the therapy when this mutation occurs. And with adefovir, there was none at one year, 2% at two years, and the latest data published in Berlin is 4% at three years. So adefovir has a lower rate of forming mutations. They have different names, this will really blow your physician out of the water if you tell him, “I’m worried, Doc, about developing the N236T mutation and the A181V”. These occur fortunately at a lower rate with adefovir. Now it turns out that you’re not born with the precore and the core promoter mutation, patients who are infected early in life are infected with the wild type. When there is a phase that occurs in early adult life of beginning immune recognition of the virus, that’s the time that the virus can mutate, and rather than going from e-antigen positive to e-antigen negative and becoming quiescent, one of these two mutations form during the time of attempted spontaneous sero-conversion.