Switching to tenofovir suppresses hepatitis B in HIV/HBV co-infected people

Liz Highleyman
Published: 20 September 2012

People with HIV and hepatitis B virus (HBV) co-infection, who substituted tenofovir (Viread) for zidovudine (Retrovir) or abacavir (Ziagen) in their antiretroviral regimen, saw a reduction in hepatitis B viral load despite HBV being resistant to lamivudine (Epivir), according to a poster presented at the 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) last week in San Francisco.

Some antiretroviral drugs, including tenofovir and lamivudine, are also active against hepatitis B virus. European and US treatment guidelines recommend that people with HIV/HBV co-infection should include at least one of these drugs in their antiretroviral regimen. Hepatitis B virus rapidly develops resistance to lamivudine, however, which may compromise its effectiveness.

Kuan-Yeh Lee and colleagues from National Taiwan University Hospital prospectively evaluated clinical and virological response to combination antiretroviral therapy when people with HIV/HBV co-infection switched from zidovudine or abacavir – neither of which have anti-HBV activity – to tenofovir.

Between November 2010 and August 2012, researchers enrolled 30 people with co-infections who had lamivudine-resistant HBV. At study entry, all had been taking antiretroviral regimens containing lamivudine as the only drug with anti-HBV activity. The average duration of lamivudine use was about six years and the average period of resistance was about two years.

Almost all participants were men and the average age was 44 years; about three-quarters reported sex with men as their main HBV risk factor. They had well-preserved immune function, with a median CD4 count of 481 cells/mm3, and the median HIV viral load was below 50 copies/ml.

Most (87%) had HBV genotype B, approximately one-half were hepatitis B "e" antigen (HBeAg)-positive and the mean baseline HBV DNA level was 6.5 log10 copies/ml; one person was triply infected with hepatitis C.

The researchers measured HBV DNA viral load and hepatitis B surface antigen (HBsAg) levels at baseline and at regular intervals after switching drugs. They also periodically assessed HBV drug-resistance mutations, liver enzyme levels and serum creatinine (a potential marker of kidney toxicity).

Over an average follow-up period of 44 weeks, median HBV viral load decreases were larger with longer time on treatment: -2.210 log copies/ml at week 4, -3.010 at week 8, -2.910 at week 12, -3.810 at week 24, -4.410 at week 36 and -48 log10 copies/ml at week 48.

The proportion of participants who achieved undetectable HBV DNA (below 128 copies/ml) at these timepoints were 16.7%, 30.0%, 36.7%, 43.3%, 53.6% and 87.0%, respectively.

However, only one of eleven tested participants (9%) experienced HBeAg seroconversion, and changes in HBsAg levels were described as "negligible" over time.

The switch to tenofovir was generally safe and well-tolerated. One person experienced acute hepatitis due to new hepatitis C virus infection. No other study participants, however, experienced liver enzyme 'flares' or sudden large increases after changing therapy.

After 48 weeks of follow-up, switching to tenofovir/lamivudine in HIV/HBV co-infected patients with HBV resistance to lamivudine "was highly effective in achieving suppression of HBV replication", the researchers concluded.

Reference

Lee K et al. Clinical and virologic outcomes after switch to tenofovir/lamivudine of HIV-infected patients with hepatitis B virus (HBV) resistance to lamivudine in an hyperendemic area for HBV infection. 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy, San Francisco, abstract H-218, 2012. View the abstract on the conference website.

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