Emerging Challenges in Managing Hepatitis B in HIV Patients

Abstract

Roughly 10 % of HIV-positive individuals worldwide have concomitant chronic hepatitis B virus (HBV) infection, with large differences between geographical regions and/or risk groups. Hepatitis B is a preventable infection with vaccines. However, it cannot be eradicated once acquired, resembling HIV and in contrast with HCV. In developed countries, hepatitis B exhibits particular features in the HIV population. First, HBV infection is less frequently misdiagnosed than in the general population. Second, nucleos(t)ide analogs active against HBV are widely used as part of antiretroviral combinations and are taken by most HIV patients. Lastly, as the HIV population ages given the success of antiretroviral therapy, non-AIDS co-morbidities are becoming a major cause of disease, for which specific drugs are required, increasing the risk of interactions and hepatotoxicity. Furthermore, concern on HBV reactivation is rising as immunosuppressive drug therapies are increasingly been used for cancers and other non-malignant conditions. In this scenario, new challenges are emerging in the management of hepatitis B in HIV-positive individuals. Among them, major interest is focused on failures to suppress HBV replication, HBV breakthroughs and reactivations, the meaning of isolated anti-HBc, screening for liver cancer, and the complexity arising when hepatitis viruses C and/or D are additionally present. This review will focus on these challenges and the major advances in HBV coinfection in HIV.

Hepatitis B reactivation after HCV treatment with sofosbuvir/ledipasvir in a HIV-coinfected patient with previous positive anti-HBs antibody: a case report and a review of literature

“…Liu [30]. Although the potential protective role of the anti-HBs antibodies is controversial, the risk of HBV reactivation is considered lower than in those without HBsAb [21,30]. Our case and case 7, both describe HBV reactivation in HBsAb positive patients, which means that clinicians should moni-positive patients had a reactivation [29].…”

“…Hepatitis B reactivation after treatment of chronic hepatitis C with pegylated-interferon and ribavirin has been described and was mostly attributed to the end of the HCV suppressive effect on HBV replication after SVR achievement [4,21]. Some authors believe that this phenomenon was less likely to occur with the interferon-based treatments due to the anti-HBV effect of these drugs that DAAs do not possess [21].…”

“…Hepatitis B reactivation after treatment of chronic hepatitis C with pegylated-interferon and ribavirin has been described and was mostly attributed to the end of the HCV suppressive effect on HBV replication after SVR achievement [4,21]. Some authors believe that this phenomenon was less likely to occur with the interferon-based treatments due to the anti-HBV effect of these drugs that DAAs do not possess [21]. Besides not being active against HBV, DAAs achieve high SVR12 rates and very steep decreases in HCV RNA [7,22], which may predispose to an increase in the number of HBV reactivations occurring after HCV treatment.…”

“…Due to the persistence of HBV in the form of cccDNA in hepatocytes and other tissues, the reactivation of hepatitis B is tor patients with serological markers of "resolved" HBV infection. In both cases of reactivation with anti-HBs antibody, patients were HIV-coinfected, and studies have shown that HIV-related immunosuppression plays a deleterious role on HBV infection with higher rates of chronicity, positive antigenemia, chronic liver disease, and even HBV reactivation [21,31]. Fabbri et al (case 7) describe a case of an immunocompromised HIV patient with low values of anti-HBsAb when he started ART without any HBV active drug (boosted darunavir and etravirine).…”

“…We know from literature that the interaction between HCV and HBV is complex and not completely understood [2,21]. With the tolerability of DAAs and their high SVR rates, many HCV/HBV-coinfected patients will be cured of HCV infection and therefore, as an unintended consequence, the immunosuppressive effects of HCV on HBV will be lost and there will be room for HBV reactivation.…”