Literature DB >> 9920171

Prevalence of GB virus type C/hepatitis G virus RNA and of anti-E2 in individuals at high or low risk for blood-borne or sexually transmitted viruses: evidence of sexual and parenteral transmission.

J J Lefrère1, F Roudot-Thoraval, L Morand-Joubert, Y Brossard, F Parnet-Mathieu, M Mariotti, F Agis, G Rouet, J Lerable, G Lefèvre, R Girot, P Loiseau.   

Abstract

BACKGROUND: The first epidemiologic evidence of GB virus type C (GBV-C)/hepatitis G virus (HGV) infection showed a high prevalence of asymptomatic carriers in blood donors and in populations at risk for blood-borne viruses. However, by using only viral RNA polymerase chain reaction, those studies underestimated the true spread of GBV-C/HGV infection. The combined detection of GBV-C/HGV RNA and of anti-E2 (which reflects recovery from infection) is necessary to define accurately the prevalence of GBV-C/HGV. STUDY DESIGN AND METHODS: The presence of both anti-E2 and GBV-C/HGV RNA was searched for in 1438 serum samples collected from various groups of individuals at low or high risk for blood-borne or sexually transmitted viruses (blood donors, organ donors, unselected pregnant women, immunocompetent or immunodepressed multiply transfused patients, HIV-positive or HIV-negative homosexual men, intravenous drug addicts).
RESULTS: The presence of GBV-C/HGV RNA and/or anti-E2 (exposure to GBV-C/HGV) was frequent in populations at risk for blood-borne or sexually transmitted viruses. GBV-C/HGV appeared also to be sexually transmitted, with transmission from male to female more efficient than vice versa. A particularly elevated level of exposure to GBV-C/HGV was observed in homosexual men. In immunocompetent individuals, the prevalence of anti-E2 was about twice that of GBV-C/HGV RNA, which suggests the frequency of recovery from GBV-C/HGV infection. Most of the GBV-C/HGV RNA-positive individuals had no biochemical evidence of liver damage.
CONCLUSIONS: GBV-C/HGV is frequent in populations at risk for blood-borne or sexually transmitted viruses. GBV-C/HGV is not a hepatitis virus, and it seems appropriate to rename it.

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Year:  1999        PMID: 9920171     DOI: 10.1046/j.1537-2995.1999.39199116899.x

Source DB:  PubMed          Journal:  Transfusion        ISSN: 0041-1132            Impact factor:   3.157


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