CROI: Study fuels debate on role of GB virus C in HIV disease

A study presented on Tuesday at the Thirteenth Conference on Retroviruses and Opportunistic Infections in Denver has shown that levels of the harmless virus GB virus C rise after HIV treatment is started. The Swedish investigators claim that this shows that GB virus C is not responsible for slower HIV disease progression in co-infected patients.

GB virus C, sometimes referred to as hepatitis G virus, is found in the majority of patients with HIV. A number of observational studies have found that patients with higher levels of GB virus C have slower progression of HIV disease, leading many experts to conclude that the hepatitis virus slows down HIV replication.

Some researchers have even suggested deliberately infecting HIV-positive people with GB virus C - which does not cause disease in humans - in order to slow damage to their immune systems.

Despite the evidence of an interaction between the two viruses, it still is not clear whether higher GB virus C levels are a cause of slower HIV progression, or whether lower HIV levels allow GB virus C levels to increase.

Per Björkmann of Malmö University Hospital presented data at the Denver conference from patients infected with both HIV and GB virus C, whose virus levels were monitored before and after they began HIV treatment. The research team found that GB virus C levels rose after anti-HIV treatment was begun, and continued to rise while HIV levels were suppressed.

In a cohort of 28 patients, most of whom were white men, they saw that the median GB virus C viral load rose from 95 to 2000 copies/ml after starting antiretroviral therapy (p = 0.005). They rose further to 6000 copies/ml during stable HIV suppression, to a final level of 80,000 copies/ml after a median of 4.5 years of HIV treatment (p = 0.002).

In addition, the team found that GB virus C levels fell from a median of 12,500 copies/ml to less than 50 copies/ml during treatment interruptions in six patients (p = 0.03). GB virus C levels reappeared after treatment was started again.

Although Dr Björkmann claimed that his results demonstrate that GB virus C levels are a consequence, rather than cause of reduced HIV viral loads, audience members at Denver were more sceptical.

In the question session that followed his presentation, other experts agreed that the Swedish data confirmed the association between the two viruses. However, they pointed out that the association between HIV treatment and GB virus C levels does not prove that HIV levels determine GB virus C viral loads.

Future studies examining the potential mechanisms of interaction between the two viruses are awaited before this debate will be resolved. In the meantime, deliberate infection with GB virus C is unlikely to become an option for HIV-positive patients.