Challenges and Controversies

A decline in HBV DNA from 10 million IU/mL to 500-1000 IU/ml over two years is excellent. And argues for likely and eventual progression to complete HBV viral suppression (HBV not detected). The kinetics of HBV decline can be much slower than HIV or HCV, particularly in the second phase of decay when there may still be persistent viremia lingering months into therapy. That being said, there is data to suggest that HBV viremia, perhaps even as low at 200 IU/ml, is associated with longterm complications like HCC (see citation). So the motivation to achieve more prompt and complete HBV viral suppression is one that should be acknowledged. I am not sure however that adding entecavir will result in significantly faster achievement of complete HBV suppression at this stage of viral suppresion... such that we can prevent such clinical complications. The benefit may be marginal. In addition, entecavir is really our only remaining alternative HBV antiviral, and not necessarily more potent than tenofovir. I generally like to reserve this if I can for situations where I have no other choice.

The patient is clearly taking his ART, as evidenced by an undetectable HIV viral load. So that takes out the possibility of poor adherence. I worry that the low level viremia can lead to development of viral resistance (especially to a lower barrier antiviral like emtricitabine) and also lead to transmission if partners are not vaccinated. I’ve seen this “plateau” of viral load occur in patients who have a high viral load at baseline. When I’ve added entecavir, the patients always achieve undetectable viral load. It’s generic and has low toxicity so not a lot of downside.