Abstract

In HBV and HCV coinfection, there is usually a dominant virus with the other coinfected virus remaining undetectable. Previous treatment of HCV used PEG-IFN and RBV which also suppressed HBV. Recently, due to its success, direct-acting antiviral (DAA) therapy for HCV has become widely used; however, with coinfection, there is concern for reactivation because anti-HCV DAAs lack activity against HBV. Our first case shows reactivation of HBV after HCV treatment with ledipasvir and sofosbuvir, the first report using this regimen. The second and third cases show HCV reactivation after treatment of HBV. In the first case, a 45-year-old man with HCV and HBV coinfection presented for treatment of HCV. Initially, his HCV PCR was 600,000 IU/mL and he had an undetectable HBV DNA. He was started on ledipasvir and sofosbuvir for 12 weeks. After 4 weeks, his HCV viral load became undetectable; however, his HBV DNA increased to 1939 IU/mL. At 12 weeks, the HCV viral load remained undetectable, and the HBV DNA was also undetectable, without requiring HBV treatment. In the second case, a 37-yearold man also with coinfection of HCV and HBV presented for treatment of HBV with tenofovir. This patient had acute HBV suppressing chronic HCV. His HBV viral load trended down over 16 weeks of treatment; however, HCV RNA which was previously undetectable, became positive just as HBV DNA was decreasing to undetectable levels at 12 weeks. At 16 weeks, HBV DNA was trending towards being undetectable, and the HCV RNA was undetectable without requiring HCV treatment. In the third case, a 21-year-old man with coinfection of HCV and HBV presented for treatment of HBV with tenofovir. This patient had chronic HBV suppressing HCV. His HBV DNA trended down over 32 weeks of treatment; however, HCV RNA which was previously undetectable, became positive just as HBV DNA was decreasing to undetectable levels at 32 weeks. At 48 weeks, HBV DNA was undetectable, and HCV RNA was undetectable without requiring HCV treatment. There are no current guidelines regarding monitoring of non-dominant virus reactivation in these patients. Our patients had transient reactivation, but patients with other comorbidities may decompensate. Close follow-up laboratory studies for viral reactivation and liver function may be a necessary addition to current guidelines as detecting a second active hepatitis virus can prevent hepatic decompensation by allowing for the timely initiation of another antiviral agent.

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