中山地区不同类型肝炎患者SEN病毒的感染状况

目的了解中山地区不同类型的病毒性肝炎患者SEN病毒的感染情况。方法设计合成SEN病毒D型和H型的型特异性引物,对乙肝病毒携带者73例、慢性乙肝124例、重症乙型肝炎58例、乙肝肝硬化63例、非甲-戊型肝炎患者57例和对照组健康体检者60人的血清进行套式PCR扩增。结果通过基因克隆和测序证实了基因扩增产物的特异性。非甲-戊型肝炎SEN病毒阳性率(66.67%)明显高于健康献血者(26.67%)(P<0.01)。慢性乙型肝炎患者(52.42%)、重症乙型肝炎患者(53.97%)、乙肝肝硬化患者(56.90%)和非甲-戊型肝炎患者(66.67%)SEN病毒阳性率之间无明显差异(P>0.05),但均显著高于乙肝病毒携带者(27.39%)和健康献血者(P<0.01)。乙肝病毒携带者SEN病毒阳性率与健康献血者之间无明显差异(P>0.05)。结论SEN病毒感染与非甲-戊型肝炎发病有一定的关系。SEN病毒感染可能与乙肝病毒感染的活动和加重有一定的关系。

Prevalence of SEN virus in patients with different subtypes of hepatitis in Zhongshan area

Objective To investigate prevalence of SEN virus in patients with different subtypes of hepatitis in Zhongshan area.Methods According to published gene sequences,Type specific primers to SENV-D and SENV H were designed and synthesized.SENV-D/H DNA were detected by nested-PCR in 60 samples from healthy voluntary blood donors,73 from hepatitis B virus carriers,124 from patients with chronic hepatitis B infection,58 from patients with severe hepatitis B infection,63 from patients with liver cirrhosis and 57 from patients with non-A-E hepatitis.PCR products of one SENV-D and one SENV H were cloned and sequenced.Results By sequencing,the specificity of genotype-specific PCR was confirmed.SENV-D/H DNA was detected in 66.67% of patients with non-A-E hepatitis,which was significantly higher than that in the healthy blood donors(26.67%)(P<0.01).The prevalence of SENV among patients with non-A-E hepatitis was similar to that among patients with chronic hepatitis B infection(52.42%),patients with server hepatitis B(53.97%)and patients with cirrhosis of liver(56.90%)(P>0.05),but significantly higher than that among the healthy blood donors and hepatitis B virus carriers(27.39%)(P<0.01).The prevalence of SENV among the hepatitis B virus carriers was no significant difference compared to that among blood donors(P>0.05).Conclusion The relationships of infection of SEN virus are associated in part with the development of non-A-E hepatitis.SEN virus may play a very important roles in activation and aggravation of infection of hepatitis B virus.