首页> 美国卫生研究院文献>Journal of Clinical Microbiology >Strong Association between Genotype F and Hepatitis B Virus (HBV) e Antigen-Negative Variants among HBV-Infected Argentinean Blood Donors
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Strong Association between Genotype F and Hepatitis B Virus (HBV) e Antigen-Negative Variants among HBV-Infected Argentinean Blood Donors

机译:基因型F与HBV感染的阿根廷献血者之间的乙型肝炎病毒(eV)抗原阴性变异之间的强关联

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摘要

A number of reports have indicated an increased risk of cirrhosis and hepatocellular carcinoma in hepatitis B virus (HBV)-infected individuals carrying HBV e antigen (HBeAg)-negative variants. Although distinct core promoter and precore mutations distributed according to geographical locality and viral genotype have been reported, epidemiological data from South America are still scarce. The prevalences of HBV genotypes and core promoter and precore polymorphisms in 75 HBeAg-negative Argentinean blood donors were surveyed. The observed frequencies of HBV genotypes were 64.0% for genotype F, 17.3% each for genotypes A and D, and 1.3% for genotype C. Genotype F strains were widely distributed and significantly more prevalent in the northern region of the country (P < 0.001). An overall high proportion of a stop codon mutation (UAG) at precore codon 28 (66.7%) was observed. Wild-type codon 28 (UGG) was present in 29.3% of the samples, and the remaining 4.0% of samples had mixed variants. The combination of A at nucleotide (nt) 1762 and G at nt 1764 of the core promoter was found in 58.7% of the samples. The variant profiles—T at nt 1762 and A at nt 1764 or A at nt 1762 and A at nt 1764—were detected in 28.0 and 1.3% of the samples, respectively. The observed core promoter polymorphisms could not be related to the ratio of HBeAg to anti-HBeAg antibody, HBV genotype, or precore codon 28 status. Nevertheless, a clear association of genotype F and a precore stop codon mutation was found (P < 0.05). In conclusion, HBV genotype F and mutant codon 28 strains predominated and were strongly associated in a geographically broad Argentinean blood donor population.
机译:许多报告表明,携带乙肝病毒e抗原(HBeAg)阴性变异的乙型肝炎病毒(HBV)感染的个体,发生肝硬化和肝细胞癌的风险增加。尽管已经报道了根据地理位置和病毒基因型分布的不同核心启动子和前核心突变,但是来自南美的流行病学数据仍然很少。调查了75名HBeAg阴性的阿根廷献血者中HBV基因型,核心启动子和核心前多态性的患病率。观察到的HBV基因型频率为F基因型为64.0%,A基因型和D基因型分别为17.3%,C基因型为1.3%。F基因型菌株广泛分布,在该国北部地区更为普遍(P <0.001 )。观察到在前核心密码子28处终止密码子突变(UAG)的总体比例很高(66.7%)。 29.3%的样品中存在野生型密码子28(UGG),其余4.0%的样品具有混合变体。在58.7%的样品中发现了核心启动子的核苷酸(nt)1762处的A和核苷酸1764处的G的组合。分别在28.0%和1.3%的样品中检测到了变异谱-在1762核苷酸处的T和在1764核苷酸处的A或在1762核苷酸处的A和在1764核苷酸处的A。观察到的核心启动子多态性与HBeAg与抗HBeAg抗体的比率,HBV基因型或前核心密码子28状态无关。然而,发现基因型F与前核心终止密码子突变之间存在明确的关联(P <0.05)。总之,HBV基因型F和突变密码子28株占主导地位,并与地理上广泛的阿根廷献血者群体密切相关。

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