title: Hepatitis C (HCV) genotype and viral titer distribution among Argentinean hemophilic patients in the presence or absence of human immunodeficiency virus (HIV) co-infection.
abstract: Hepatitis C (HCV) infection is frequent among hemophilic patients treated with non-inactivated factor-concentrates. Both HCV genotype and viral load have been suggested to be important prognostic markers of disease progression and treatment outcome. In addition, co-infection with the human immunodeficiency virus (HIV) has been associated with increased level of HCV replication and higher risk of developing liver failure. Thus, HCV genotype, viral load, and HIV co-infection are important factors in HCV infection. Using restriction fragment length polymorphism analysis (RFLP) and the branched-DNA (bDNA) assay, we retrospectively investigated the HCV genotypes and viral loads present in 59 Argentinean hemophiliacs, in the presence or absence of HIV infection. HCV genotype 1 was the predominant viral variant detected among HIV-negative (HIV-) (76%) and HIV-positive (HIV+) (82.5%) patients, followed by genotypes 3 (10.4%), 2 (2%) and a small proportion of multiply co-infected 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 +/- 10(5) Eq/ml) (P < 0.001); however, no correlation between HCV replication and level of immune suppression, evaluated 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 confirm previous reports suggesting the existence of increased HCV replication in HIV/HCV co-infected hemophiliacs, our data did not support the conclusion that HIV-induced immune suppression is directly responsible for this phenomena. It is possible that other factors induced by HIV are responsible for the increased levels in HCV replication observed.
authors.affiliation: Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA. gaspicc@inetworld.net
authors.forename: G R
authors.initials: GR
authors.lastname: Picchio
authors.forename: M
authors.initials: M
authors.lastname: Nakatsuno
authors.forename: C
authors.initials: C
authors.lastname: Boggiano
authors.forename: R
authors.initials: R
authors.lastname: Sabbe
authors.forename: M
authors.initials: M
authors.lastname: Corti
authors.forename: J
authors.initials: J
authors.lastname: Daruich
authors.forename: R
authors.initials: R
authors.lastname: Pérez-Bianco
authors.forename: M
authors.initials: M
authors.lastname: Tezanos-Pinto
authors.forename: R
authors.initials: R
authors.lastname: Kokka
authors.forename: J
authors.initials: J
authors.lastname: Wilber
authors.forename: D
authors.initials: D
authors.lastname: Mosier
mesh_terms: D000293:Adolescent; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001118:Argentina; D018791:CD4 Lymphocyte Count; D002648:Child; D002675:Child, Preschool; D004279:DNA, Viral / Q000097:blood; D005838:Genotype; D015658:HIV Infections / Q000150:complications*; D006467:Hemophilia A / Q000150:complications*; D016174:Hepacivirus / Q000235:genetics*; D006526:Hepatitis C / Q000097:blood / Q000150:complications* / Q000821:virology*; D006801:Humans; D008875:Middle Aged; D012189:Retrospective Studies; D019562:Viral Load
chemical_list: D004279:DNA, Viral; D000410:Alanine Transaminase