Tanaka M, Nishiguchi S, Tanaka T, Enomoto M, Fukuda K, Takeda T, Nakajima S, Shiomi S, Kuroki T, Monna T, Yano Y, Otani S
Second Department of Biochemistry, Osaka City University Medical School, Osaka, Japan.
J Hepatol. 1997 Dec;27(6):966-72. doi: 10.1016/s0168-8278(97)80138-9.
BACKGROUND/AIMS: Whether GB virus C and hepatitis G virus participate in fulminant hepatic failure is controversial. We studied the prevalence of the viral RNA in 48 patients. There were possible routes of infection, including blood transfusion, in 22 patients (group 1), and no risk factors in the other 26 (group 2).
We assayed serum viral RNA with reverse transcription and nested polymerase chain reactions. Serum was obtained at admission, and after transfusion in group 2.
Five (10%) serum samples from group 1 at admission had viral RNA of the 5'-untranslated region, and three of these samples had viral RNA of the NS3/helicase region. All five patients had transfusions before sampling. Two (4%) samples from group 2 were positive by both tests only after transfusion. Of two patients, one with non-A-E fulminant hepatic failure survived. Her serum alanine aminotransferase did not increase further after transfusion, but did stay above the reference range during follow-up. The other patient, with infection with hepatitis B virus detected at admission, died. After transfusion, his alanine aminotransferase did not increase further. Partial nucleotide sequences of GB virus C and hepatitis G virus from three fulminant hepatic failure patients and five control patients with chronic hepatitis C were compared with published sequences. A viral variant causing fulminant hepatitis, suggested elsewhere, was not found, nor was all of a characteristic pattern of six mutations found elsewhere.
GB virus C and hepatitis G virus may cause hepatitis, but probably not severe hepatitis such as fulminant hepatic failure.
背景/目的：庚型肝炎病毒（GBV-C）和G型肝炎病毒（HGV）是否参与暴发性肝衰竭仍存在争议。我们研究了48例患者中病毒RNA的流行情况。22例患者（第1组）存在包括输血在内的可能感染途径，另外26例（第2组）无危险因素。
我们采用逆转录和巢式聚合酶链反应检测血清病毒RNA。第2组在入院时及输血后采集血清。
第1组入院时5份（10%）血清样本检测到5'-非翻译区病毒RNA，其中3份样本检测到NS3/解旋酶区病毒RNA。所有5例患者在采样前均接受过输血。第2组2份（4%）样本仅在输血后两种检测均呈阳性。2例患者中，1例非甲-戊型暴发性肝衰竭患者存活。输血后其血清丙氨酸氨基转移酶未进一步升高，但在随访期间仍高于参考范围。另1例患者入院时检测到乙型肝炎病毒感染，死亡。输血后其丙氨酸氨基转移酶未进一步升高。将3例暴发性肝衰竭患者及5例慢性丙型肝炎对照患者的GBV-C和HGV部分核苷酸序列与已发表序列进行比较。未发现其他地方提示的导致暴发性肝炎的病毒变异体，也未发现其他地方报道的全部6个突变的特征性模式。
GBV-C和HGV可能引起肝炎，但可能不会引起暴发性肝衰竭等严重肝炎。
