This article is dedicated to the memory of Dr. Raffaella Rosso who for years cared for this patient.
Article first published online: 18 JUL 2012
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Medical Virology
Volume 84, Issue 9, pages 1340–1343, September 2012
How to Cite
Mikulska, M., Taramasso, L., Giacobbe, D. R., Caligiuri, P., Bruzzone, B., Di Biagio, A. and Viscoli, C. (2012), Case report: Management and HBV sequencing in a patient co-infected with HBV and HIV failing tenofovir. J. Med. Virol., 84: 1340–1343. doi: 10.1002/jmv.23338
The authors declare that there were no conflicts of interest.
- Issue published online: 18 JUL 2012
- Article first published online: 18 JUL 2012
- Manuscript Accepted: 3 MAY 2012
- R192PR mutation;
- TDF resistance
Nucleos(t)ide analogs such as tenofovir, lamivudine, or emtricitabine are active against both HBV and HIV. Tenofovir confers potent and durable HBV-DNA suppression but the best strategy in case of resistance of HBV to tenofovir remains unknown. A case of a 22-year-old patient with co-infection with HBV and HIV transmitted perinatally is reported. After prolonged and intermittent treatment of HIV with lamivudine and tenofovir, HBV became resistant to lamivudine. Subsequently, clinical resistance to tenofovir occurred, manifesting as HBV-DNA breakthrough. The non-compliance was reasonable excluded and HIV-RNA remained constantly suppressed. Entecavir (1 mg daily) was added and the combination therapy resulted in a rapid and continuous suppression of HBV-DNA for over 12 months. The treatment was well-tolerated and safe. No known mutations, such as rtA181T/V associated with rtN236T or A194T that are associated with reduced susceptibility or resistance to tenofovir were detected. However, a unique and complex HBV substitution pattern was found: with a development of rtR192PR mutation at the time of virological failure. Adding entecavir to failing therapy with tenofovir and emtricitabine was feasible, well-tolerated and resulted in virological success. The rtR192PR, which is located in the B domain near the rtA194T, occurring in a context of a very complex substitutions patterns, might be associated with resistance to tenofovir. J. Med. Virol. 84:1340–1343, 2012. © 2012 Wiley Periodicals, Inc.