Re: Follow-up study of intrahost HIV type 2 variability reveals discontinuous evolution of C2V3 sequences.
Re: Follow-up study of intrahost HIV type 2 variability reveals discontinuous evolution of C2V3 sequences.
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回复：宿主内 HIV 2 型变异的后续研究揭示了 C2V3 序列的不连续进化。
DOI：
10.1089/08892220152644278
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发表时间：
2001
影响因子：
1.5
通讯作者：
Mullins,JI
中科院分区：
文献类型：
--
作者：
Gottlieb,GS;Mullins,JI
编辑：人们普遍认为，深入了解患者体内的遗传变异和进化动力学的艾滋病毒将提供重要的洞察艾滋病毒/艾滋病的发病机制。在MACS队列中对HIV-1 B亚型的研究表明，存在与疾病进展相关的一致的病毒进化变化，并且病毒多样性和分歧率遵循可预测的模式。[1]在这些研究之前，HIV-1多样性和差异性数据是一个不完整和混乱的阵列，受到来自不同疾病阶段的患者样本、短随访时间和对重新鉴定错误偏倚结果的担忧的困扰。2尚不清楚在HIV-1患者中观察到的发展为AIDS的病毒多样性和趋异性增加的模式以及CXCR 4嗜性病毒的出现是否发生在HIV-2感染患者中。以前很少有研究在疾病过程中患者体内HIV-2的演变。Sankale et al. 3的一份报告描述了5例患者中HIV-2 env V3环PBMC病毒序列的患者内变异性，显示无症状患者（0.6%）的病毒多样性低于有症状患者（2.0%），且多样性随时间推移而增加。他们还指出，HIV-2的患者内多样性低于HIV-1的报告。然而，目前尚不清楚这些观察到的差异是否是由于不同的病毒生物学，患者选择偏倚，或由于人口重新分配错误而低估了HIV-2的多样性。[2]因此，Esteves等人的研究引起了人们极大的兴趣。[4]他们在《AIDS Research and Human Retroviruses》中描述了两名患者gp 105的C2 V3区域在宿主内的HIV-2进化，其中一名患者也感染了HIV-1。有趣的是，在实验对象D中（HIV-1/2双重感染）据报道，HIV-2平均遗传多样性在5年内似乎急剧下降。（1992年为4.3%; 1995年为0.7%; 1997年，0.5%），而在主题C中，（仅HIV-2）据报道，HIV-2平均遗传多样性似乎先减少后增加（1992年，2.5%; 1995年，1.1%; 1997年，5.4%）。考虑到Sankale等人先前的报道和我们自己未发表的HIV-2进化观察结果，以及我们对HIV-1序列进化的了解，我们发现这些结果令人困惑。在检查作者提供的系统发育树时，似乎可能有一个reservation偏倚的问题。从受试者D，1997年的10个序列中的8个看起来相同，1995年的9个序列中的2个和9个序列中的3个也看起来相同。在受试者C中，1995年的11个序列中有3个也是相同的。因此，restestant错误可以解释的ob-
EDITOR: It is generally believed that a thorough understanding of intrapatient genetic variation and evolutionary dynamics of HIV will provide important insight into HIV/AIDS pathogenesis. Studies of HIV-1 subtype B in the MACS cohort suggest there are consistent viral evolutionary changes associated with the progression of disease and that rates of viral diversity and divergence follow a predictable pattern. 1 Before these studies there was an incomplete and confusing array of HIV-1 diversity and divergence data that was plagued by patient samples from different stages of disease, short follow-up times, and concerns of resampling errors biasing results. 2 It is unknown whether the pattern of increasing viral diversity and divergence, and the emergence of CXCR4-tropic viruses, that is observed in HIV-1 patients progressing to AIDS is occurring in patients infected with HIV-2. There have been few previous studies of intrapatient HIV-2 evolution during the course of the disease. A report by Sankale et al. 3 described the intrapatient variability of HIV-2 env V3 loop PBMC viral sequences in 5 patients and showed lower viral diversity in asymptomatic (0.6%) than in symptomatic (2.0%) patients and increasing diversity over time. They also noted that intrapatient diversity in HIV-2 was lower than that reported in HIV-1. However, it is unclear whether these observed differences were due to different virus biology, patient selection bias, or underestimation of HIV-2 diversity due to population resampling errors. 2 It is therefore with great interest that the study by Esteves et al. 4 appeared in AIDS Research and Human Retroviruses.They describe the intrahost HIV-2 evolution of the C2V3 region of gp105 over 5 years in two patients, one who was also infected with HIV-1. Interestingly, in subject D (HIV-1/2 dually infected) the HIV-2 mean genetic diversity reportedly appears to be decreasing dramatically over the course of 5 years (1992, 4.3%; 1995, 0.7%; 1997, 0.5%) whereas in subject C (HIV-2 only) the HIV-2 mean genetic diversity reportedly appears to be decreasing and then increasing (1992, 2.5%; 1995, 1.1%; 1997, 5.4%). Given what has been previously reported by Sankale et al. 3 and our own unpublished observations of HIV-2 evolution, and what is known about sequence evolution in HIV-1, we find these results puzzling. On inspection of the phylogenetic tree provided by the authors, it would appear there might be a problem with resampling bias. From subject D, 8 of the 10 sequences from 1997 appear identical, and 2 of 9 and 3 of 9 sequences from 1995 also appear identical. From subject C, 3 of the 11 sequences from 1995 also appear identical. Thus resampling error could explain the ob-