HEPATITIS-C (HCV) GENOTYPE AND VIRAL TITER DISTRIBUTION AMONG ARGENTINEAN HEMOPHILIC PATIENTS IN THE PRESENCE OR ABSENCE OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) COINFECTION

Hepatitis C (HCV) infection is frequent among hemophilic patients trea ted with non-inactivated factor-concentrates. Both HCV genotype and vi ral load have been suggested to be important prognostic markers of dis ease progression and treatment outcome. In addition, co-infection with the human immunodeficiency virus (HIV) has been associated with incre ased level of HCV replication and higher risk of developing liver fail ure. Thus, HCV genotype, viral load, and HIV co-infection are importan t factors in HCV infection. Using restriction fragment length polymorp hism analysis (RFLP) and the branched-DNA (bDNA) assay, we retrospecti vely investigated the HCV genotypes and viral loads present in 59 Arge ntinean hemophiliacs, in the presence or absence of HIV infection. HCV genotype 1 was the predominant viral variant detected among HIV-negat ive (HIV-) (76%) and HIV-positive (HIV+) (82.5%) patients, followed by genotypes 3 (10.4%), 2 (2%) and a small proportion of multiply co-inf ected patients including genotypes 4 and 5 (6.25%). HIV+ patients had higher plasma HCV RNA levels than HIV- patients (88.4 +/- 16.5 x 10(5) Eq/ml vs. 24.7 +/- 5.8 x 10(5) Eq/ml) (P < 0.001); however, no correl ation between HCV replication and level of immune suppression, evaluat ed by CD4(+) T-cell measurement, was observed among HIV+ patients (r = 0.017). Abnormal and higher ALT levels were more frequently detected among HIV+ (93%; 123.6 +/- 15.7 U/liter) than HIV-(41%; 70.2 +/- 24.2 U/liter) patients (P < 0.001; P < 0.05). Although we were able to conf irm previous reports suggesting the existence of increased HCV replica tion in HIV/HCV co-infected hemophiliacs, our data did not support the conclusion that HIV-induced immune suppression is directly responsibl e for this phenomena. It is possible that other factors induced by HIV are responsible for the increased levels in HCV replication observed. (C) 1997 Wiley-Liss, Inc.