Squadrito Giovanni, Orlando Maria Elena, Pollicino Teresa, Raffa Giuseppina, Restuccia Tea, Cacciola Irene, Di Marco Vito, Picciotto Antonio, Colucci Giuseppe, Craxì Antonio, Raimondo Giovanni
Dipartimento di Medicina Interna, Università di Messina, Italy.
Am J Gastroenterol. 2002 Jun;97(6):1518-23. doi: 10.1111/j.1572-0241.2002.05707.x.
The virological profiles of hepatitis B and C viruses (HBV and HCV) and their interplay in cases of coinfection are undefined. A suppressed and occult HBV infection may occur in hepatitis B surface antigen (HBsAg) negative patients with chronic hepatitis C. The HCV core protein is able to inhibit HBV "in vitro," and serines at positions 99 and 116 are essential for such inhibition. We aimed to assess the HBV and HCV virological profiles in cases of coinfection and to evaluate the relationship between HCV core gene variability and HBV activity.
Eighty-two anti-HCV positive patients were examined: 35 cases were HBsAg positive, 24 were HBsAg negative with "occult" HBV infection, and 23 were HBV negative. HBV and HCV viremia levels were evaluated in all cases. HCV genomic region coding for the aminoacid sequence 99-116 of core protein was amplified and sequenced in all HCV RNA positive cases. The entire core gene was amplified and sequenced in three randomly selected cases.
Serum HCV RNA was detected in all cases but 13, all HBsAg positive individuals; HCV viremia levels of the other 22 HBsAg positive subjects were similar to those detected in HBsAg negative patients with or without occult HBV infection. Among the 35 HBsAg positive patients both HBV DNA and HCV RNA were detected in five cases, HCV RNA alone in 17, and HBV DNA alone in six, whereas seven cases had undetectable levels of both viruses. Sequencing analyses showed that the HCV core gene was highly preserved in all patients.
A wide spectrum of HCV and HBV virological patterns may occur in a case of coinfection. HCV core variability is not related to HBV activity "in vivo."
乙型肝炎病毒（HBV）和丙型肝炎病毒（HCV）的病毒学特征及其合并感染时的相互作用尚不清楚。慢性丙型肝炎患者中可能发生乙肝表面抗原（HBsAg）阴性的隐匿性HBV感染。HCV核心蛋白在“体外”能够抑制HBV，且99位和116位的丝氨酸对于这种抑制作用至关重要。我们旨在评估合并感染时的HBV和HCV病毒学特征，并评估HCV核心基因变异性与HBV活性之间的关系。
对82例抗-HCV阳性患者进行检查：35例HBsAg阳性，24例HBsAg阴性且伴有“隐匿性”HBV感染，23例HBV阴性。对所有病例评估HBV和HCV病毒血症水平。在所有HCV RNA阳性病例中，扩增并测序HCV基因组中编码核心蛋白氨基酸序列99 - 116的区域。随机选择3例病例扩增并测序整个核心基因。
除13例HBsAg阳性个体外，所有病例均检测到血清HCV RNA；其他22例HBsAg阳性受试者的HCV病毒血症水平与有或无隐匿性HBV感染的HBsAg阴性患者中检测到的水平相似。在35例HBsAg阳性患者中，5例同时检测到HBV DNA和HCV RNA，17例仅检测到HCV RNA，6例仅检测到HBV DNA，而7例两种病毒水平均未检测到。测序分析表明，所有患者的HCV核心基因高度保守。
合并感染时可能出现多种HCV和HBV病毒学模式。HCV核心基因变异性与“体内”HBV活性无关。
