Prevalence of TT virus infection in US blood donors and populations at risk for acquiring parenterally transmitted viruses.
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Two overlapping sets of TT virus (TTV)-specific polymerase chain reaction primers were used to test for presence of TTV, which was found in approximately 10% of US volunteer blood donors, 13% of commercial blood donors, and 17% of intravenous drug abusers. The rate of TTV infection among US non-A, non-B, non-C, non-D, non-E hepatitis patients was only 2%. Among commercial blood donors and intravenous drug abusers, only 1%-3% of the TTV-positive individuals were coinfected with GB virus C (GBV-C), a parenterally transmitted virus. This suggests that GBV-C and TTV may have different routes of transmission. Comparison of the sensitivities of 2 TTV polymerase chain reaction (PCR) primer sets showed that the majority of samples were detected with only 1 of the 2 sets. Therefore, previous studies in which only a single PCR primer pair was used may have significantly underestimated the true prevalence of TTV. (+info)
A high prevalence of serum GB virus C/hepatitis G virus RNA in children with and without liver disease.
(10/233)
The role of GB virus C/hepatitis G virus (GBV-C/HGV) in adult and pediatric liver disease is unclear. We detected serum GBV-C/HGV RNA by reverse transcriptase polymerase chain reaction in 1 (3%) of 38 cholestatic infants, in 4 (4%) of 95 children without liver disease, and in none of 30 children with autoimmune hepatitis. One cholestatic infant had antibodies, presumably maternal, to GBV-C/HGV. Sequence analysis of a nonstructural 3 region fragment suggested that mother-to-infant transmission was the route of infection for the cholestatic infant. The four infected children without liver disease had normal liver function test results and lacked risk factors for bloodborne infections. Thus, the detection of GBV-C/HGV RNA among children with and without liver disease suggests that chronic GBV-C/ HGV infections may be established early in life, possibly by mother-to-infant transmission. This may explain in part the high prevalence of serum GBV-C/HGV RNA and antibodies in healthy adults. (+info)
In vitro infection of human peripheral blood mononuclear cells by GB virus C/Hepatitis G virus.
(11/233)
GB virus C (GBV-C), also known as hepatitis G virus, is a recently discovered flavivirus-like RNA agent with unclear pathogenic implications. To investigate whether human peripheral blood mononuclear cells (PBMC) are susceptible to in vitro GBV-C infection, we have incubated PBMC from four healthy blood donors with a human GBV-C RNA-positive serum. By means of (i) strand-specific reverse transcription-PCR, cloning, and sequencing; (ii) sucrose ultracentrifugation and RNase sensitivity assays; (iii) fluorescent in situ hybridization; and (iv) Western blot analysis, it has been demonstrated that GBV-C is able to infect in vitro cells and replicate for as long as 30 days under the conditions developed in our cell culture system. The concentration of GBV-C RNA increased during the second and third weeks of culture. The titers of the genomic strand were 10 times higher than the titers of the antigenomic strand. In addition, the same predominant GBV-C sequence was found in all PBMC cultures and in the in vivo-GBV-C-infected PBMC isolated from the donor of the inoculum. GBV-C-specific fluorescent in situ hybridization signals were confined to the cytoplasm of cells at different times during the culture period. Finally, evidence obtained by sucrose ultracentrifugation, RNase sensitivity assays, and Western blot analysis of the culture supernatants suggests that viral particles are released from in vitro-GBV-C-infected PBMC. In conclusion, our study has demonstrated, for the first time, GBV-C replication in human lymphoid cells under experimental in vitro infection conditions. (+info)
Age-dependent acquisition of hepatitis G virus/GB virus C in a nonrisk population: detection of the virus by antibodies.
(12/233)
Until now there have been few seroepidemiological data for hepatitis G virus/GB virus type C (HGV/GBV-C). A four-antigen HGV/GBV-C immunoblot was established to examine 446 serum specimens from healthy individuals without risk factors for parenteral viral transmission. These individuals were divided into seven groups according to age. Seroprevalence rates were low for children and adolescents (5.6%) and increased for the age groups assumed to be the most sexually active (15.3 to 26.8%). Remarkably, none of the 80 individuals who tested positive for HGV/GBV-C antibodies were simultaneously positive for HGV/GBV-C viremia. From our data we conclude that HGV/GBV-C infection is widespread in the general population (16 to 25%). The development of an antibody response is associated with clearance of HGV/GBV-C viremia. Due to the lack of risk factors for HGV/GBV-C infection of blood, other efficient transmission routes must exist. It must be assumed that HGV/GBV-C transmission may be linked to sexual activity. (+info)
GB virus C/hepatitis G virus groups and subgroups: classification by a restriction fragment length polymorphism method based on phylogenetic analysis of the 5' untranslated region.
(13/233)
A phylogenetic tree based on 150 5' untranslated region sequences deposited in GenBank database allowed segregation of the sequences into three major groups, including two subgroups, i.e., 1, 2a, 2b, and 3, supported by bootstrap analysis. Restriction site analysis of these sequences predicted that HinfI and either AatII or AciI could be used for genomic typing with 99.4% accuracy. cDNA sequencing and subsequent alignment of 21 Argentine GB virus C/hepatitis G virus strains confirmed restriction fragment length polymorphism patterns theoretically predicted. This method may be useful for a rapid screening of samples when either epidemiological or transmission studies of this agent are carried out. (+info)
High prevalence of GB virus C in Brazil and molecular evidence for intrafamilial transmission.
(14/233)
The prevalence of GB virus C (GBV-C) in candidate Brazilian blood donors with normal and elevated alanine aminotransferase levels was found to be 5.2% (5 of 95) and 6.5% (5 of 76), respectively. Among Brazilian patients, GBV-C was found in 9.5% (13 of 137) of cases of hepatitis not caused by hepatitis A virus (HAV), HBV, HCV, HDV, or HEV (non-A-E hepatitis) and in 18.2% (8 of 44) of individuals infected with HCV. Molecular characterization of GBV-C by partial sequencing of the NS3 region showed clustering between members of a single family, implying intrafamilial transmission. In conclusion, these results together suggest that contagion mechanisms which facilitate intrafamilial transmission of GBV-C may partially explain the high prevalence of viremic carriers worldwide. (+info)
GB virus C/hepatitis G virus infection in HIV infected patients with haemophilia despite treatment with virus inactivated clotting factor concentrates.
(15/233)
AIM: To determine the frequency of GB virus C (GBV-C)/hepatitis G virus (HGV) infection before and after switch to the use of virus inactivated concentrates in haemophiliac patients infected with human immunodeficiency virus (HIV). PATIENTS AND METHODS: Initial and follow up sera from 49 children with haemophilia were analysed for the presence of GBV-C/HGV RNA and antibodies to HGV (anti-HGV). All patients had been infected with HIV while receiving concentrates without virus inactivation before 1984 and were subsequently treated with virus inactivated concentrates. RESULTS: In the first available serum sample (1987 or later), two of 49 patients were GBV-C/HGV RNA positive and two further patients were anti-HGV positive. During follow up (mean, 6 years), 14 patients developed markers of GBV-C/HGV infection. Eleven of these had received no blood products except clotting factor concentrates that had been prepared with virus inactivation. CONCLUSIONS: Despite being treated with virus inactivated clotting factor concentrates, HIV positive patients with haemophilia are at an increased risk of manifesting GBV-C/HGV infection. We hypothesise that GBV-C/HGV is transmitted by these clotting factor concentrates. However, we cannot rule out the emergence of markers of GBV-C/HGV infection as a result of the progression of immune impairment in the course of HIV infection. (+info)
Outcome of mother to infant acquired GBV-C/HGV infection.
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Twelve children born to hepatitis C virus antibody GBV-C/HGV RNA positive mothers who acquired GBV-C/HGV infection by the vertical or perinatal route were studied. Most (91%) were persistently GBV-C/HGV RNA positive up to 12 months of age. Four out of six cases who acquired GBV-C/HGV alone had normal alanine amino transferase activities. Long lasting evidence of hepatocellular injury was detected only in children with GBV-C/HGV and hepatitis C virus and HIV coinfection. (+info)