Hepatitis Virus Diversity Research Programme (HVDRP), Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa; Kenya Medical Research Institute (KEMRI), Kenya; Jomo Kenyatta University of Agriculture and Technology (JKUAT), Kenya.
Infect Genet Evol. 2013 Dec;20:103-10. doi: 10.1016/j.meegid.2013.08.013. Epub 2013 Aug 23.
Hepatitis B virus (HBV) genotypes are important in both the clinical manifestation of disease and treatment response. Although Kenya belongs to the African Region (AFR-E) characterized by high mortality and hyperendemicity of HBV, there is a paucity of HBV genotyping data. The aim of this study was to molecularly characterize the basic core promoter/precore (BCP/PC) and complete surface (S) regions of HBV isolated from 61 HBsAg-positive liver disease patients attending Kenyatta National Hospital in Nairobi. HBsAg, HBeAg and viral loads were determined. HBV DNA was amplified and sequenced from 58/61 patients. In addition to the complete genome of two isolates, the BCP/PC and the complete S regions of 43 and 38 isolates, respectively were sequenced. Following phylogenetic analysis of the S region, 38 isolates clustered with subgenotype A1, whereas two isolates clustered with genotype D, one with subgenotype D1 and another as an outlier of the clade containing subgenotype D6 and the D/E recombinant. When the complete genome of the latter isolate was sequenced it clustered with D6. The majority of isolates belonged to serological subtype adw2 and only four to ayw2. Three distinct groups of subgenotype A1, distinguished by different amino acid motifs, circulate in Kenya: two in the African cluster and a monophyletic clade in the "Asian" cluster. HBeAg-negativity was a result of G1896A in genotype D isolates, whereas in subgenotype A1, the HBeAg-negativity was a result of mutations in the Kozak region (1809-1812) or precore start codon (1814-1816). Mutations at positions 1762 and 1764 occurred more frequently in HCC patients (p<0.05). In conclusion, subgenotypes A1, D1 and D6 circulate in liver disease patients in Kenya, with A1 predominating.
乙型肝炎病毒（HBV）基因型在疾病的临床表现和治疗反应中都很重要。尽管肯尼亚属于非洲区域（AFR-E），其 HBV 死亡率高且高度流行，但 HBV 基因分型数据却很少。本研究的目的是对来自内罗毕肯雅塔国家医院 61 名 HBsAg 阳性肝病患者的 HBV 基本核心启动子/前核心（BCP/PC）和完整表面（S）区进行分子特征分析。测定了 HBsAg、HBeAg 和病毒载量。从 58/61 例患者中扩增并测序了 HBV DNA。除了两个分离株的完整基因组外，还分别对 43 个和 38 个分离株的 BCP/PC 和完整 S 区进行了测序。对 S 区进行系统发育分析后，38 个分离株聚类为亚基因型 A1，而 2 个分离株聚类为基因型 D，其中 1 个分离株聚类为包含亚基因型 D6 和 D/E 重组的聚类的外群，另一个分离株聚类为包含亚基因型 D6 和 D/E 重组的聚类的外群。当对后者分离株的完整基因组进行测序时，它聚类为 D6。大多数分离株属于血清亚型 adw2，只有 4 个属于 ayw2。在肯尼亚，有 3 个不同的亚基因型 A1 组，它们通过不同的氨基酸基序区分：2 个在非洲群中，1 个在“亚洲”群中是单系群。基因型 D 分离株的 HBeAg 阴性是由于 G1896A 所致，而亚基因型 A1 的 HBeAg 阴性是由于 Kozak 区（1809-1812）或前核心起始密码子（1814-1816）的突变所致。位置 1762 和 1764 的突变在 HCC 患者中更常见（p<0.05）。总之，亚基因型 A1、D1 和 D6 在肯尼亚的肝病患者中传播，其中 A1 占主导地位。
