The Incidence of Transfusion-Associated Hepatitis G Virus Infection and Its Relation to Liver Disease
Harvey J. Alter, M.D., Yoshiyuki Nakatsuji, M.D., Jacqueline Melpolder, M.T.(A.S.C.P.), John Wages, M.S., Robert Wesley, Ph.D., J. Wai-Kuo Shih, Ph.D., and Jungsuh P. Kim, Ph.D.
Background The role of hepatitis G virus (HGV) in transfusion-associatedinfection and its relation to liver disease are not well understood.
Methods Serum samples collected between 1972 and 1995 from 357transfusion recipients, 157 controls who did not receive transfusions,500 randomly selected volunteer blood donors, and 230 donorsof blood received by HGV-infected patients were tested for HGVRNA by qualitative and quantitative polymerase-chain-reactionassays. Samples obtained before transfusion and serially aftertransfusion from 79 of the 81 transfusion recipients who hadtransfusion-associated non-A, non-B hepatitis were availablefor testing.
Results Of the 79 patients with transfusion-associated hepatitis,63 (80 percent) had infections related to the hepatitis C virus(HCV) and 3 had preexisting HCV and the cause of their acutehepatitis could not be determined; of the remaining 13 patients,3 had acute HGV infection, and 10 were infected with unidentifiedagents. Six of the 63 patients with HCV infection who were tested(10 percent) were also infected with HGV. The three patientsinfected only with HGV had mild hepatitis (mean peak alanineaminotransferase level, 198 U per liter; none had jaundice);the levels of alanine aminotransferase and HGV RNA were notwell correlated. The combined HCV and HGV infections were nomore severe than HCV infections alone; the alanine aminotransferasevalues paralleled the levels of HCV RNA, but not those of HGVRNA. There were 35 HGV infections among the 357 transfusionrecipients; only 3 had hepatitis with HGV as the sole viralmarker. One of the 157 controls and 7 of the 500 randomly selectedblood donors (1.4 percent) had detectable HGV RNA. In all eightinstances in which a transfusion recipient had acute HGV infectionafter transfusion and samples from all donors could be tested,at least one HGV-positive donor was identified.
Conclusions HGV was common in a group of volunteer blood donors,and it can be transmitted by transfusion. Most HGV infectionswere not associated with hepatitis. HGV did not worsen the courseof concurrent HCV infection. No causal relation between HGVand hepatitis has been established.
Source Information
From the Departments of Transfusion Medicine (H.J.A., Y.N., J.M., J.W.-K.S.) and Information Systems (R.W.), Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Md.; and Genelabs Technologies, Redwood City, Calif. (J.W., J.P.K.).
Address reprint requests to Dr. Alter at the Department of Transfusion Medicine, Bldg. 10, Rm. 1C-711, National Institutes of Health, Bethesda, MD 20892.
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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