Background & Aims
HIV/hepatitis B virus (HBV) coinfected subjects are thought to have faster progression to end‐stage liver disease (ESLD) than HBV mono‐infected subjects. We assessed whether this remains in the current cART‐era.
Methods
Data from subjects with follow‐up completion post‐2003 were compared between HIV/HBV coinfected subjects in the Dutch HIV Monitoring database and HBV mono‐infected subjects from two centres. The primary outcomes of composite ESLD included portal hypertension, decompensated cirrhosis, hepatocellular carcinoma, liver transplantation and liver‐related mortality. Outcomes were analysed using time‐dependent cause‐specific Cox regression models adjusted for follow‐up time and relevant covariates. Subset‐analyses were done in subjects with follow‐up pre‐2003.
Results
In the 1336 co‐ vs 742 mono‐infected subjects, coinfected subjects had no increased probability for ESLD compared to mono‐infected subjects (cHR 0.7 (95% CI 0.4‐1.1), but had increased probabilities for all‐cause (cHR 7.4 [4.9‐11.1]) and liver‐related mortality (cHR 3.4 [1.6‐7.5]). In the current combined cohort, treatment with tenofovir or entecavir was inversely associated with ESLD, all‐cause and liver‐related mortality (cHR 0.4 [95% CI 0.3‐0.7], cHR 0.003 [0.001‐0.01]), cHR 0.007 [0.001‐0.05]). Other predictors for ESLD were older age, being of Sub‐Sahara African descent, increased alanine aminotransferase levels and hepatitis C virus coinfection. While the probability for all‐cause mortality was increased in coinfected subjects, this rate decreased compared to pre‐2003 (HR 40.2 (95% CI: 8.7‐186.2).
Conclusions
HIV/HBV coinfected patients no longer seem to be at increased risk for progression to ESLD compared to HBV mono‐infected patients, likely due to widespread use of highly effective cART with dual HBV and HIV activity.
Although current therapies can be successful at suppressing hepatitis B viral load, long-term viral cure is not within reach. Subsequent strategies combining pegylated interferon alfa with nucleoside/nucleotide analogues have not resulted in any major paradigm shift. An improved understanding of the hepatitis B virus (HBV) lifec ycle and virus-induced immune dysregulation has, however, revealed many potential therapeutic targets, and there are hopes that treatment of hepatitis B could soon be revolutionized. This review summarizes the current developments in HBV therapeutics—both virus directed and host directed.
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