aCIC de Vaccinologie Cochin-Pasteur, INSERM CIC BT505
bDepartment of Clinical Pharmacology, Cochin Teaching Hospital, AP-HP, Université Paris Descartes
cInstitut Cochin, Université Paris-Descartes, CNRS (UMR 8104), INSERM U-1016, and Assistance Publique – Hôpitaux de Paris, Service d’Hépatologie, Hôpital Cochin, Paris, France.
Correspondence to Pierre Loulergue, MD, CIC de Vaccinologie Cochin-Pasteur, INSERM BT505, Cochin Teaching Hospital, AP-HP, Université Paris Descartes, 27, rue du faubourg Saint Jacques F75014 Paris, France. Tel: +33 158 419 36; fax: +33 158 41 29 10; e-mail: email@example.com
Received 9 January, 2012
Accepted 18 January, 2012
A 40-year-old man living with HIV since 1994 was diagnosed with acute hepatitis C virus (HCV) (genotype 3a) hepatitis in January 2011 after unprotected homosexual intercourse. His past history was otherwise unremarkable, and he denied using intravenous drugs. His co-medications at this time included raltegravir 400 mg b.i.d., darunavir 800 mg once daily, and ritonavir 100 mg daily. Hepatitis B virus serology was negative, and HIV viral load was below 20 copies/ml, with a CD4 cell count of 254/μl (18%). Liver function tests showed: serum glutamic oxaloacetic transaminase 61 UI/l, serum glutamic pyruvic transaminase 127 UI/l, bilirubin 9 μmol/l, gamma-glutamyl transferase 25 UI/l, alkaline phosphatases 63 UI/l, and HCV viral load was 68.106 IU/ml (7.84 log).
He was started on pegylated-interferon-α2a 180 μg/week and ribavirin 15 mg/kg/day on 23 March 2011. Immediate pretreatment HCV viral load was 5.2 106 IU/ml (6.72 log). The treatment was well tolerated with mild asthenia, and HCV viral load at week 4 of treatment was undetectable (<15 IU/ml or 1.2 log).
At week 12 of treatment, HCV viral load had risen to 11.2 106 IU/ml (7.05 log), with normal liver function tests. Pegylated-interferon injections were administered weekly at home by a nurse, excluding adherence issues. The patient admitted having had unprotected homosexual intercourse with a new sexual partner, but denied intravenous drug use at this time. Therefore, HCV genotype was determined again and was found to be 4a, 4c, 4d. The diagnosis of HCV super-infection was made, and the patient remained under pegylated-interferon and ribavirin until November 2011, in the absence of a validated therapeutic alternative. At week 12 of treatment, HCV viral load was 25 196 IU/ml (4.4 log).
The detection of multiple unique HCV viral strains is often designated as HCV mixed infection, and could result from simultaneous exposure or super-infection. HCV super-infection is defined as the presence of a new genotype, different to that observed at first.
Although re-infection following successful treatment for HCV can occur in up to 19% of patients , HCV super-infection during pegylated-interferon and ribavirin therapy is scarcely reported [2–5]. Most cases were described after blood transfusion, intravenous drug use, renal transplantation and colonoscopy . To the best of our knowledge, the present case is the second documenting HCV super-infection caused by unprotected sexual intercourse . Moreover, all cases but one reported super-infection with genotypes 1 and 3 .
Clinicians should be aware of the risk of HCV super-infection during pegylated-interferon and ribavirin therapy, and patients should be informed of this risk in case of unprotected sexual intercourse, given the severity of HIV–HCV co-infection.
Conflicts of interest
There are no conflicts of interest.
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