With the approval of a new drug to treat chronic hepatitis B virus it is a good time to review HIV-HBV coinfection. It is also helpful that recommendations of a panel on HIV-HBV coinfection were published in the February 18 issue of the journal AIDS.
More has been said about HIVers coinfected with hepatitis C than with HBV, but worldwide, HBV is more common than HCV and causes more illness and death than HCV coinfection in both developed and developing countries.
There are about 400 million HBV carriers in the world, with the highest concentrations in the Far East and sub-Saharan Africa. HBV can be found in about 10% of HIV carriers. This is not surprising since HIV and HBV can be transmitted in the same ways: mother to baby, unsafe sex, injection-drug use, and blood transfusions. HIVers are 10 times more likely to carry HBV than the general population.
Typically infection with hepatitis B results in the classic symptoms of liver inflammation: nausea, fatigue, low-grade fever, jaundice, dark urine, and light stools. This can occur anywhere from six weeks to six months after contact. Hepatitis B resolves without treatment in 90% of infections, but in 10% the virus does not disappear. HBV becomes integrated into the genetic material of liver cells much like HIV in resting CD4 cells. These people become chronic carriers.
In HIV-negative HBV carriers about 25% to 30% will develop serious complications, such as cirrhosis, liver failure, or liver cancer. As in HCV-HIV coinfection, the risk of complications is higher in HBV carriers with HIV coinfection. HBV-HIV coinfected patients have higher levels of hepatitis virus, higher elevations of liver enzymes, and more liver damage upon completion of a biopsy. But the converse is not true: There is no data so far to indicate that HBV increases HIV disease progression.
Fortunately or unfortunately, some cases of hepatitis B are milder, and patients might think they have had only a 'stomach bug' for several days. If so, they might never go to a doctor nor know they have become a carrier. So in populations where HBV is common, such as gay men (10% of gay men carry HBV and slightly less than 10% of injection-drug users do), it is important that everyone get screened. If one is negative, then he or she should be vaccinated.
Because HBV is integrated like HIV, the goals of treatment are the same'to suppress the virus to delay or stop disease progression. As with HIV, we follow the HBV viral load as our primary marker of treatment success.
The first two drugs used to suppress HBV are well-known in HIV treatment circles. First was lamivudine. The second was adefovir. Adefovir started trials as an anti-HIV medication but was abandoned because of kidney toxicity. However, it was effective against HBV'in a smaller, safer dosage than that used for HIV. Adefovir sister compound tenofovir works similarly against HBV. Likewise, emtricitabine has anti-HBV activity similar to lamivudine.
Now there is entecavir (Baraclude), which was FDA-approved on March 29. It is taken once a day and has minimal side effects. Like adefovir, it has no effect on HIV; therefore, in a coinfected patient not yet on anti-HIV medications, either adefovir or entecavir would be the drug of choice'so as to avoid the development of HIV drug resistance possible with other agents. In patients on anti-HIV treatment it is recommended that the combination of tenofovir with either lamivudine or emtricitabine be used when appropriate for HIV. This is because of the development of lamivudine resistance in use for HBV, which occurs at a rate of 20% in the first year and 40% by the second.
All this activity is somewhat reminiscent of the early days of combination therapy in HIV. And with more than 15 other compounds under investigation for HBV activity, I think we are seeing the beginning of a new era in HBV treatment.
Bowers is board-certified in family practice and is a senior partner with Pacific Oaks Medical Group, one of the nation's largest practices devoted to HIV care.
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