Wei Q, Fultz P N
Department of Microbiology, University of Alabama School of Medicine, Birmingham 35294, USA.
J Virol. 1998 Apr;72(4):3005-17. doi: 10.1128/JVI.72.4.3005-3017.1998.
A chimpanzee (C-499) infected for more than 9 years with two subtype B isolates of human immunodeficiency virus type 1 (HIV-1), one (HIV-1(SF2)) that replicates poorly and one (HIV-1(LAV-1b)) that replicates efficiently in chimpanzees, died of AIDS 11 years after initial infection (F. J. Novembre et al., J. Virol. 71:4086-4091, 1997). Nucleotide sequence and phylogenetic analyses of the C2 to V5 region of env (C2-V5env) in proviral DNA from peripheral blood lymphocytes obtained 22 months before death revealed two distinct virus populations. One of these populations appeared to be a recombinant in env, having the V3 loop from HIV-1(SF2) and the V4-V5 region from HIV-1(LAV-1b); the other population had evolved from HIV-1(LAV-1b). In addition to C2-V5env, the entire p17gag and nef genes were sequenced; however, based on nucleotide sequences and phylogeny, whether the progenitor of the p17gag and nef genes was SF2 or LAV-1b could not be determined. Compared to the two original viruses, the divergence of all clones of C2-V5env ranged from 9.37 to 20.2%, that of p17gag ranged from 3.11 to 9.29%, and that of nef ranged from 4.02 to 7.9%. In contrast, compared to the maximum variation of 20.2% in C2-V5env for C-499, the maximum diversities in C2-V5env in proviruses from two chimpanzees infected with HIV-1(LAV-1b) for 9 and 10 years were 9.65 and 2.48%, respectively. These results demonstrate that (i) two distinct HIV-1 populations can coexist and undergo extensive diversification in chimpanzees with progressive HIV-1-induced disease and (ii) recombination between two subtype B strains occurred even though the second strain was inoculated 15 months after the first one. Furthermore, evaluation of env genes from three chimpanzees infected with the same strain suggests that the magnitude of HIV-1 diversification could be related to higher viral burdens, manifestations of disease, and/or dual infection.
一只黑猩猩(C-499)感染两种1型人类免疫缺陷病毒(HIV-1)B亚型分离株超过9年,其中一种(HIV-1(SF2))在黑猩猩体内复制能力差,另一种(HIV-1(LAV-1b))在黑猩猩体内复制效率高,该黑猩猩在初次感染11年后死于艾滋病(F. J. 诺温布雷等人,《病毒学杂志》71:4086 - 4091, 1997)。对死亡前22个月采集的外周血淋巴细胞原病毒DNA中env基因的C2至V5区域(C2-V5env)进行核苷酸序列和系统发育分析,发现了两个不同的病毒群体。其中一个群体在env基因中似乎是重组体,其V3环来自HIV-1(SF2),V4-V5区域来自HIV-1(LAV-1b);另一个群体由HIV-1(LAV-1b)进化而来。除了C2-V5env,还对整个p17gag和nef基因进行了测序;然而,基于核苷酸序列和系统发育,无法确定p17gag和nef基因的祖先是SF2还是LAV-1b。与两种原始病毒相比,C2-V5env所有克隆的差异范围为9.37%至20.2%,p17gag的差异范围为3.11%至9.29%,nef的差异范围为4.02%至7.9%。相比之下,与C-499的C2-V5env最大变异20.2%相比,两只感染HIV-1(LAV-1b) 9年和10年的黑猩猩原病毒中C2-V5env的最大多样性分别为9.65%和2.48%。这些结果表明:(i)在患有进行性HIV-1诱导疾病的黑猩猩中,两种不同的HIV-1群体可以共存并经历广泛的多样化;(ii)尽管第二种毒株在第一种毒株接种15个月后接种,但两种B亚型毒株之间仍发生了重组。此外,对三只感染相同毒株的黑猩猩的env基因评估表明,HIV-1多样化的程度可能与更高的病毒载量、疾病表现和/或双重感染有关。