Hepatitis C virus–Epstein-barr virus interaction in patients with AIDS

✍ Scribed by Dominique Challine; Marlyse Buisson; Michel Cadilhac; Georgios Germanidis; Irene Joab; Muriel Eliaszewicz; Eric Caumes; Antoine Flahault; Anne-Marie Fillet; Jean-Michel Pawlotsky; Jean-Marie Seigneurin

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 78 KB
• Volume: 67
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.10130

✦ Synopsis

Abstract

Immortalization of B cells by Epstein‐Barr virus (EBV) and their subsequent proliferation leads to B‐cell non‐Hodgkin's lymphoma in immunocompromised patients. The role of hepatitis C virus (HCV) in B‐cell non‐Hodgkin's lymphoma has recently been raised, and an interaction between HCV and EBV is supported by recent in vitro experiments. The aim of this study was to investigate in vivo interactions between HCV and EBV in patients with AIDS, i.e., patients exposed to the risk of EBV‐related B‐cell non‐Hodgkin's lymphoma. A total of 135 patients were prospectively studied. Serological and molecular markers of HCV, EBV, and human immunodeficiency virus (HIV) infection were sought. All the patients harbored latent EBV infection, and 20% had detectable HCV RNA in serum. No significant relationship was found between HIV, HCV, and EBV viral load in peripheral blood mononuclear cells or plasma. There was no difference between anti‐HCV‐positive and ‐negative patients or between HCV RNA‐positive and ‐negative patients with regard to the prevalence of EBV markers, especially EBV replication markers. The presence of EBV replication markers was not related to HCV RNA seropositivity or to HCV viral load. Five patients subsequently developed B‐cell non‐Hodgkin's lymphoma, none of whom had markers of EBV or HCV replication. These results argue against an in vivo interaction between HCV and EBV in patients with AIDS, and against a role of HCV infection in the occurrence of B‐cell non‐Hodgkin's lymphoma in these patients. J. Med. Virol. 67:510–515, 2002. © 2002 Wiley‐Liss, Inc.