Molecular Investigation of GB Virus C Infection in Hemophiliacs in Japan

Kinoshita, Tadatoshi; Miyake, Kensuke; Nakao, Haruhisa; Tanaka, Takeshi; Tsuda, Fumio; Okamoto, Hiroaki; Miyakawa, Yuzo; Matsui, Makoto

doi:10.1093/infdis/175.2.454

Cited by 36 publications

(19 citation statements)

References 15 publications

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“…Several studies of GBV-C/HGV prevalence in HIV-infected patients have been published; a high frequency of GBV-C/HGV genome detection was also found: 10/55 (18.2%) in individuals with HIV-infection, but HIV risk groups weren't specified [Feucht et al, 1997b], 9/100 (9%) in intravenous drug users and homosexual men [Nü bling and Löwer, 1996], 8/33 (24%) in HIV-infected hemophiliacs [Kinoshita et al, 1997], 3/17 (17.6%) in HIVinfected pregnant women [Feucht et al, 1996], 2/20 (10%) in another series of HIV-seropositive hemophiliacs [Jarvis et al, 1996], and 11/41 (26.8%) in Japanese hemophilia patients with HIV coinfection [Toyoda et al, 1998]. …”

Section: Discussionmentioning

confidence: 99%

“…However, it seemed that HIV by itself did not increase GBV-C/HGV prevalence. For instance, Stark et al [1996] did not find any association of GBV-C/HGV prevalence with HIV antibodies in intravenous drug users and homosexual men; 24% of hemophiliacs with HIV antibodies, vs. 23% without HIV antibodies, were GBV-C/ HGV-positive for Kinoshita et al [1997]; Jarvis et al [1996] found GBV-C/HGV RNA in 10% of HIV-infected hemophiliacs vs. 11/75 (14.7%) of HIV-negative hemophiliacs; GBV-C/HGV RNA status was not associated with HIV in 246 intravenous drug users (OR, 0.9 ; 95% CI; 0.4-2.0) [Thomas et al, 1997]; GBV-C/HGV RNA was detected in 11% and 8%, respectively, of HIVpositive and HIV-negative patients (81 hemophiliacs) [Goedert et al, 1997].…”

Section: Discussionmentioning

confidence: 99%

“…However, many epidemiological studies have been undertaken, usually by serum RNA detection, showing a high prevalence of this virus in humans: 0.8-13% in blood donors Linnen et al, 1996;Stark et al, 1996;Feucht et al, 1997a;Wang and Jin, 1997], much more higher rates in patients with parenteral exposures (intravenous drug users Linnen et al, 1996;Schreier et al, 1996;Stark et al, 1996;Feucht et al, 1997b;Fong et al, 1997;Thomas et al, 1997], transfusion recipients [Linnen et al, 1996;Alter HJ et al, 1997;Feucht et al, 1997b;Sampietro et al, 1997;Skidmore et al, 1997], hemophiliacs [Jarvis et al, 1996;Linnen et al, 1996;Nü bling and Löwer, 1996;Alter HJ et al, 1997;Feucht et al, 1997b;Kinoshita et al, 1997], and patients on chronic hemodialysis [Masuko et al, 1996;Tsuda et al, 1996;Feucht et al, 1997b;Lampe et al, 1997;Ross et al, 1998]). Sexual transmission also occurred [Stark et al, 1996;Rubio et al, 1997], as well as vertical transmission [Feucht et al, 1996;Fischler et al, 1997;Hino et al, 1998].…”

Section: Introductionmentioning

confidence: 99%

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High prevalence of GB virus C/hepatitis G virus RNA in patients infected with human immunodeficiency virus

et al. 1999

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Prevalence of GBV-C/HGV was determined in a cohort of HIV-infected patients, via a reverse transcription-polymerase chain reaction detection of RNA in serum, amplifying the NS5 region of GBV-C/HGV genome. GBV-C/HGV RNA was detected in 143 (37.7%) of 379 patients, with similar results in the different HIV risk groups: 25/56 (44.6%) in intravenous drug users, 66/161 (41%) in homo- and bisexual men, 35/108 (32.4%) in heterosexual patients, 6/20 (30%) in transfusion recipients (P=0.41). There was no difference according to the presence or absence of hepatitis C virus infection. In univariate analysis, GBV-C/HGV genome prevalence was lower in patients over 50 years old (18.2%), compared to other age groups (20-29 years: 34.2%; 30-39 years: 44.3%; 40-49 years: 36.7%, P=0.03), as well as in patients with normal CD4 cell count (29.2% vs. 45.4% between 200-500/mm3, and 35.3% below 200 CD4/mm3, P=0.012) and individuals with a chronic hepatitis B. However, in the multivariate analysis, the only prognostic factor of GBV-C/HGV RNA positivity was the presence of a chronic hepatitis B, compared to the absence of any HBV marker, or a previous exposition to HBV (presence of anti-HBc and/or anti-HBs, absence of HBsAg), or the presence of anti-HBs alone.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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High prevalence of GB virus C/hepatitis G virus RNA in patients infected with human immunodeficiency virus

et al. 1999

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“…Though HGV infection is common worldwide, the prevalence is high in Thailand (4.3%) [14], Vietnam (5.7%) [15], Germany (4.7%) [16], South Africa (10.4-12.9%) [10] and West Africa (14.2%) [17], but low in Japan (0.6-0.9%) [18][19][20], China (0.7-2.0%) [21][22][23] and the United States (0.8-1.7%) [5,17].…”

Section: Hgv Infection In the General Population And Blood Donorsmentioning

confidence: 99%

GB Virus C/Hepatitis G Virus

Kiyosawa

Tanaka²

1999

Intervirology

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Hepatitis G virus (HGV) is a positive, single-strand RNA virus that has been classified in the family Flaviviridae. The 5′-untranslated region (UTR) of the HGV genome is lengthy and does not share any significant primary and secondary RNA structures with the 5′-UTR of hepatitis C virus (HCV). The internal ribosome entry site has extraordinarily weak activity. The HGV genome does not seem to encode a nucleocapside protein analogous to HCV. Blood-borne transmission is presumed to be the commonest mode of transmission of the virus. Current infection with HGV is diagnosed by detection of HGV RNA by the polymerase chain reaction (PCR), and past infection with HGV is detectable by testing anti-HGV E2. HGV is distributed worldwide, but its prevalence varies widely from one population to another. Although the prevalence of HGV in association with acute and chronic hepatitis is higher than that in the general population, further prospective studies are needed to demonstrate its relative significance in causing hepatitis and other disease. The major unresolved biological issue at the moment is its hepatotropsim and site of propagation. Recent progress demonstrates that HGV replicates in lymphocytes rather than hepatocytes. HGV may be pathogenic under special conditions, but does not influence carcinogenesis.

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“…Determinadas populações de pacientes têm alta prevalência do GBV-C, a saber, portadores de insuficiência renal crônica em hemodiálise (ZHU et al, 2003;MASUKO et al, 1996;DE LAMBALLERIE;CHARREL;DUSSOL, 1996), hemofílicos (KINOSHITA et al, 1997) e usuários de drogas injetáveis (STARK;BIENZLE;. O presente estudo investiga a presença do RNA GBV-C no plasma de doadores de sangue saudáveis.…”

Section: Introductionunclassified

Detecção do RNA HGV/GBV-C em Indivíduos Saudáveis não Portadores de HBV, HIV-1/2 e HCV

Amarante

Miranda

Oliveira

et al. 2004

Semin. Cienc. Biol. Saude

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ResumoO vírus da hepatite G (HGV ou GBV-C) é um membro da família Flaviviridae. Baseado no perfil clínico e epidemiológico, este vírus pode ser adquirido principalmente por transmissão parenteral, por meio de sangue contaminado. Nós investigamos a presença do RNA do GBV-C/HGV em amostras de sangue periférico de doadores normais na ausência de marcadores como antígenos de superfície do HBV (HBsAg), anticorpos anti-HBc (anti-HBc), anticorpos anti-HCV e anticorpos anti-HIV-1/HIV-2. O RNA GBV-C foi detectado por reação de transcriptase reversa e reação em cadeia catalisada pela polimerase (RT-PCR). Foram analisadas 50 amostras de plasma e identificados 6 (12%) amostras positivas para o RNA do GBV-C. A presença de RNA GBV-C na ausência de hepatite B e C em doadores saudáveis pode indicar que este vírus é capaz de transmissão independente e não contribui para doença hepática. Palavras-chaves: GBV-C. Doadores de sangue. PCR. AbstractThe 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 can be acquired mainly by parenteral transmission through contaminated blood. It was therefore investigated the presence of GBV-C/HGV RNA in the peripheral blood from healthy blood donors in the abscence of virus markers including HBV surface antigen (HBsAg), HBV core antibody (anti-HBc) and HCV antibody. HIV-1, HIV-2, were also investigated. GBV-C RNA was detected by reverse transcriptase and polymerase chain reactions (RT-PCR). It was detected GBV-C RNA in 6/50 (12 %) blood donors. The presence of GBV-C RNA in the abscence of hepatitis B and C infection in young patients and healthy donors could indicate that this virus is capable of independent transmission and does not contribute to liver disease.

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Molecular Investigation of GB Virus C Infection in Hemophiliacs in Japan

Cited by 36 publications

References 15 publications

High prevalence of GB virus C/hepatitis G virus RNA in patients infected with human immunodeficiency virus

High prevalence of GB virus C/hepatitis G virus RNA in patients infected with human immunodeficiency virus

GB Virus C/Hepatitis G Virus

Detecção do RNA HGV/GBV-C em Indivíduos Saudáveis não Portadores de HBV, HIV-1/2 e HCV

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