Alter H J, Nakatsuji Y, Melpolder J, Wages J, Wesley R, Shih J W, Kim J P
Department of Transfusion Medicine, National Institutes of Health, Bethesda, MD 20892, USA.
N Engl J Med. 1997 Mar 13;336(11):747-54. doi: 10.1056/NEJM199703133361102.
The role of hepatitis G virus (HGV) in transfusion-associated infection and its relation to liver disease are not well understood.
Serum samples collected between 1972 and 1995 from 357 transfusion recipients, 157 controls who did not receive transfusions, 500 randomly selected volunteer blood donors, and 230 donors of blood received by HGV-infected patients were tested for HGV RNA by qualitative and quantitative polymerase-chain-reaction assays. Samples obtained before transfusion and serially after transfusion from 79 of the 81 transfusion recipients who had transfusion-associated non-A, non-B hepatitis were available for testing.
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 acute hepatitis could not be determined; of the remaining 13 patients, 3 had acute HGV infection, and 10 were infected with unidentified agents. Six of the 63 patients with HCV infection who were tested (10 percent) were also infected with HGV. The three patients infected only with HGV had mild hepatitis (mean peak alanine aminotransferase level, 198 U per liter; none had jaundice); the levels of alanine aminotransferase and HGV RNA were not well correlated. The combined HCV and HGV infections were no more severe than HCV infections alone; the alanine aminotransferase values paralleled the levels of HCV RNA, but not those of HGV RNA. There were 35 HGV infections among the 357 transfusion recipients; only 3 had hepatitis with HGV as the sole viral marker. One of the 157 controls and 7 of the 500 randomly selected blood donors (1.4 percent) had detectable HGV RNA. In all eight instances in which a transfusion recipient had acute HGV infection after transfusion and samples from all donors could be tested, at least one HGV-positive donor was identified.
HGV was common in a group of volunteer blood donors, and it can be transmitted by transfusion. Most HGV infections were not associated with hepatitis. HGV did not worsen the course of concurrent HCV infection. No causal relation between HGV and hepatitis has been established.
庚型肝炎病毒（HGV）在输血相关感染中的作用及其与肝脏疾病的关系尚未完全明确。
采用定性和定量聚合酶链反应检测法，对1972年至1995年间采集的血清样本进行检测，这些样本来自357名输血受者、157名未接受输血的对照者、500名随机选取的志愿献血者以及230名接受HGV感染患者所献血液的献血者。对81名发生输血相关性非甲非乙型肝炎的输血受者中的79名，在输血前及输血后连续采集样本进行检测。
在79例输血相关性肝炎患者中，63例（80%）感染了丙型肝炎病毒（HCV），3例既往感染HCV，其急性肝炎病因无法确定；其余13例患者中，3例为急性HGV感染，10例感染了不明病原体。在检测的63例HCV感染患者中，有6例（10%）同时感染了HGV。仅感染HGV的3例患者患有轻度肝炎（平均谷丙转氨酶峰值水平为每升198 U；均无黄疸）；谷丙转氨酶水平与HGV RNA水平无明显相关性。HCV和HGV合并感染并不比单独的HCV感染更严重；谷丙转氨酶值与HCV RNA水平平行，但与HGV RNA水平无关。357名输血受者中有35例HGV感染；仅3例以HGV作为唯一病毒标志物患有肝炎。157名对照者中有1例，500名随机选取的献血者中有7例（1.4%）检测到HGV RNA。在所有8例输血受者输血后发生急性HGV感染且可对所有献血者样本进行检测的情况下，均至少鉴定出1名HGV阳性献血者。
HGV在一组志愿献血者中很常见，且可通过输血传播。大多数HGV感染与肝炎无关。HGV并未使同时存在的HCV感染病情加重。尚未确立HGV与肝炎之间的因果关系。
