Wang A L, Zhou Y X, Yao Z Q
Department of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an.
Zhonghua Yi Xue Za Zhi. 1994 Mar;74(3):144-6, 190.
We examined the serum HBV DNA of the chronic hepatitis B patients with positive c-system by using polymerase chain reaction (PCR). Twenty samples of HBeAg(+)/anti-HBe(-) positive PCR products and 20 samples of HBeAg(-)/anti-HBe(+) positive PCR products were selected. These products were dot-hybridized by synthetic HBV pre-C region geno oligonucleotide probes M0 (non mutated), M1 (one) point-mutated), M2 (two point-mutated). The results thus obtained showed that for 85% (17/20) of the chronic hepatitis patients with HBeAg(-)/anti-HBe(+), point mutation occurred at the 1,896th nucleotide, resulting in the stop codon, and half (10/20) of the patients suffered two points mutation. The direct determination of the sequence of some mutation PCR products selected proved the existence of point mutation. The result indicated that the natural conversion of hepatitis patients' HBeAg(+) to anti-HBe(+) may have resulted from the genovariation in the pre-c region of HBVDNA rather than from the decreased of virus replication.
我们采用聚合酶链反应（PCR）检测了c系统阳性的慢性乙型肝炎患者的血清HBV DNA。选取了20份HBeAg(+)/抗-HBe(-)阳性的PCR产物样本和20份HBeAg(-)/抗-HBe(+)阳性的PCR产物样本。这些产物用合成的HBV前C区基因寡核苷酸探针M0（未突变）、M1（单点突变）、M2（双点突变）进行斑点杂交。结果显示，85%（17/20）的HBeAg(-)/抗-HBe(+)慢性肝炎患者在第1896位核苷酸发生了点突变，产生了终止密码子，且一半（10/20）的患者发生了双点突变。对部分选取的突变PCR产物序列的直接测定证实了点突变的存在。结果表明，肝炎患者HBeAg(+)向抗-HBe(+)的自然转换可能是由HBVDNA前C区的基因变异引起的，而非病毒复制减少所致。
