title: Molecular investigation of GB virus C RNA in hemodialysis and thalassemics patients from Brazil.
abstract: The GB virus C (GBV-C)/hepatitis G virus (HGV) is a member of the Flaviviridae family. Based on the clinical and epidemiological profiles, this virus could be acquired mainly by parenteral transmission through contaminated blood. We therefore investigated the presence of GBV-C/HGV and its relation with the other blood borne viruses as hepatitis B and C viruses (HBV, HCV) in hemodialysis and thalassemic individuals and blood donors from Ribeirão Preto-Brazil. Detection of blood borne virus markers including HBV surface antigen (HbsAg), HBV core antibody (anti-Hbc) and HCV antibody was carried out. HIV-1, HIV-2, HTLV-1 and HTLV-2 were also investigated. GBV-C/HGV RNA was detected by reverse transcriptase and polymerase chain reaction (RT-PCR). Ninety-four serum samples from patients with chronic renal failure were analyzed. GBV-C/HGV RNA was identified in 12 (12.8%) patients, anti-HCV antibodies in 28 (29.8%), anti-Hbc in 9 (9.6%), anti-HIV in 1 (1%), HBsAg in 33 (35.1%), and HBsAg/ anti-HBc was observed in 2 (2.1%) patients. Thirty-six (38.3%) samples were non-reactive. Seven of the 12 GBV-C/HGV RNA infected samples were co-infected with other viruses: 3 (25%) with HBsAg, 2 (16.7%) with anti-HCV and 2 (16.7%) with anti-HBc/anti-HCV/HBsAg. Among the 42 thalassemic patients GBV-C/HGV RNA was detected in 6/42 patients (14.2 %). Three patients presented GBV-C/HGV, with other blood borne markers. We also detected GBV-C/ HGV in 6/50 (12%) blood donors. In these GBV-C/HGV positive thalassemics patients, 50% (3/6) were young individuals (lesser 15 years old) and 67% (4/6) were female patients. The presence of GBV-C RNA in the absence of hepatitis B and C infection in the young patients and healthy donors could be indicate that this virus is capable of independent transmission and does not contribute to liver disease.
authors.affiliation: Department of Pathological Sciences, Londrina State University, Londrina, PR, Brazil. maewat@sercomtel.com.br
authors.forename: Maria Angelica Ehara
authors.initials: MA
authors.lastname: Watanabe
authors.forename: Cristiane Maria
authors.initials: CM
authors.lastname: Milanezi
authors.forename: Wilson Araújo
authors.initials: WA
authors.lastname: Silva
authors.forename: Ivan
authors.initials: I
authors.lastname: de Lucena Angulo
authors.forename: Gil
authors.initials: G
authors.lastname: Santis
authors.forename: Simone
authors.initials: S
authors.lastname: Kashima
authors.forename: José Abrão Cardeal
authors.initials: JA
authors.lastname: da Costa
authors.forename: Miguel Moisés
authors.initials: MM
authors.lastname: Neto
authors.forename: Dimas Tadeu
authors.initials: DT
authors.lastname: Covas
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001938:Brazil / Q000453:epidemiology; D005260:Female; D018178:Flaviviridae Infections / Q000097:blood / Q000175:diagnosis* / Q000276:immunology; D029407:GB virus C / Q000235:genetics / Q000276:immunology; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D006508:Hepatitis Antibodies / Q000097:blood / Q000276:immunology; D006509:Hepatitis B / Q000097:blood / Q000175:diagnosis / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology; D006526:Hepatitis C / Q000097:blood / Q000175:diagnosis / Q000276:immunology; D006525:Hepatitis, Viral, Human / Q000097:blood / Q000175:diagnosis* / Q000276:immunology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000276:immunology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D025202:Molecular Diagnostic Techniques; D015995:Prevalence; D012367:RNA, Viral / Q000097:blood / Q000276:immunology; D006435:Renal Dialysis; D013789:Thalassemia / Q000097:blood* / Q000276:immunology / Q000628:therapy; D065227:Transfusion Reaction
chemical_list: D015415:Biomarkers; D006508:Hepatitis Antibodies; D012367:RNA, Viral