Acute Non-AE Hepatitis in the United States and the Role of Hepatitis G Virus Infection
Miriam J. Alter, Ph.D., Margaret Gallagher, Ph.D., Timothy T. Morris, B.S., Linda A. Moyer, B.A., Emory L. Meeks, B.S., Krzysztof Krawczynski, M.D., Ph.D., Jungsuh P. Kim, Ph.D., Harold S. Margolis, M.D., for The Sentinel Counties Viral Hepatitis Study Team
Background Little is known about the relation of the newly discoveredhepatitis G virus (HGV) to the cause and clinical course ofacute and chronic viral hepatitis.
Methods We selected patients from a surveillance study of acuteviral hepatitis in four U.S. counties who had acute diseaseduring 1985 to 1986 or 1991 to 1995. Serum samples were testedfor HGV RNA by the polymerase chain reaction.
Results HGV RNA was detected in 4 of 45 patients with a diagnosisof non-AE hepatitis (9 percent), 23 of 116 patients withhepatitis C (20 percent), 25 of 100 patients with hepatitisA (25 percent), and 32 of 100 patients with hepatitis B (32percent) (P<0.05 for the comparison of hepatitis B with hepatitisnon-AE or C). The clinical characteristics of the acuteillness were similar for patients with HGV alone and those withhepatitis A, B, or C with or without HGV infection. During afollow-up period of one to nine years, chronic hepatitis didnot develop in any of the patients with HGV alone, but 75 percentwere persistently positive for HGV RNA, as were 87 percent ofthose with both hepatitis C and HGV infection. The rates ofchronic hepatitis were similar in patients with hepatitis Calone (60 percent) and those with both hepatitis C and HGV infection(61 percent).
Conclusions The evidence from this surveillance study does notimplicate HGV as an etiologic agent of non-AE hepatitis.Persistent infection with HGV was common, but it did not leadto chronic disease and did not affect the clinical course inpatients with hepatitis A, B, or C.
Source Information
From the Hepatitis Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta (M.J.A., M.G., T.T.M., L.A.M., E.L.M., K.K., H.S.M.); and Genelabs Technologies, Redwood City, Calif. (J.P.K.).
Address reprint requests to Dr. Alter at the Hepatitis Branch, Mailstop G37, Centers for Disease Control and Prevention, Atlanta, GA 30333.
Hepatitis G Infection
Kudo T., Morishima T., Shibata M., Goedert J. J., Steinmeyer L. A., Nakatsuji Y.
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N Engl J Med 1997;
337:276-277, Jul 24, 1997.
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