Spontaneous HCV clearance in a patient with HIV infection and a concurrent, never treated, evolutive HCV hepatitis, after over twenty years of chronic co-infection

The reciprocal virological-immunological interactions between HIV and HCV, as well as the reciprocal effect of the specific antiviral therapies, are still poorly known. A rare case report of spontaneous clearance of HCV occurred in an ex-IVDA co-infected with HIV-HCV since 20 years, and never treated for HCV, is presented.

A 49-year-old ex-IVDA patient (p) tested HIV-HCV positive since 1989, and was treated for HIV disease since 1990 with limited compliance until 2 years ago. He never attained undetectable HIV viremia until the last 6 months, although CD4+ T-lymphocyte count steadily remained >300 cells/μL.

Until this last semester, against medical recommendation, our p continued alcohol consumption and irregular drug addict, despite an ongoing methadone program. Serum transaminases showed fluctuating values, always >2-3.5-fold normal levels, while HCV replication was confirmed by values of 1,200-4,000 × 10³ IU/mL. During the last 6 months, our p first abandoned its former lamivudine-zidovudine-nevirapine therapy, leading to a combination including 2 novel nucleos(t)ide analogues (tenofovir-emtricitabine), associated to the protease inhibitors (PI) lopinavir-ritonavir, and finally in the last 3 months due to gastrointestinal intolerance-hypertriglyceridemia he introduced fosamprenavir-ritonavir on behalf of lopinavir-ritonavir. Already after lopinavir-ritonavir use, our p attained undetectable plasma HIV-RNA levels (always confirmed thereafter), while CD4+ count showed the greatest values even registered by our p (513-662 cells/μL). During 2 subsequent controls, qualitative HCV viremia tested negative for the first time, concurrently with normal transaminases.

Single cases of apparent disappearance of a chronic HCV infection in HIV-HCV co-infected p in absence of anti-HCV therapy have been described as anecdotal reports. In these episodes, a role of anti-HIV therapy (without reference to speficic drugs and associations), and that of a concurrent, significant immune recovery was often claimed. The eventual role of HIV PI, although a negligible direct anti-HCV is known, is still debated, depending on the direct-indirect role possibly played by PI in the dynemics of HIV-HCV co-infection. Fosamprenavir is a PI with contained liver toxicity, thus recommended just in p with a concomitant chronic hepatis/liver cirrhosis. A systematic revision of safety databases of fosamprenavir in HIV-infected p with chronic viral hepatitis (to detect eventual virological-immunological changes of the concomitant HCV hepatitis), and a systematic appraisal of all literature anecdotal case reports, may shed light on novel research targets in this relevant, but somewhat unexplored situation.