1970s and 'Patient 0' HIV-1 genomes illuminate early HIV/AIDS history in North America.
1970s and 'Patient 0' HIV-1 genomes illuminate early HIV/AIDS history in North America.
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1970年代和“患者0” HIV-1基因组阐明了北美早期的艾滋病毒/艾滋病历史。
DOI：
10.1038/nature19827
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发表时间：
2016-11-03
期刊：
影响因子：
64.8
通讯作者：
Jaffe HW
中科院分区：
文献类型：
--
作者：
Worobey M;Watts TD;McKay RA;Suchard MA;Granade T;Teuwen DE;Koblin BA;Heneine W;Lemey P;Jaffe HW
在北美男男性行为者（MSM）中出现艾滋病毒-1 M组B亚型是艾滋病毒/艾滋病大流行的一个关键转折点。系统发育研究表明，在整个20世纪70年代，美国（US）存在隐蔽的B亚型循环，在加勒比地区甚至更早。然而，这些时间和地理推断，基于部分HIV-1基因组，在1981年承认艾滋病之后，仍然存在争议，病毒在美国最早的运动是未知的。我们血清学筛选了bbb2000年至1970年的血清样本，并开发了一种高灵敏度的新方法，用于从降解的档案样本中恢复病毒RNA。在这里，我们报告了从1978-79年美国血清样本中获得的8个编码完整基因组——迄今为止9个最古老的HIV-1 M组基因组中的8个。这一早期的全基因组“快照”揭示了美国HIV-1流行病在20世纪70年代表现出惊人的广泛遗传多样性，但也提供了强有力的证据，证明它起源于先前存在的加勒比海流行病。贝叶斯系统发育分析估计在1970年左右跳跃到美国，并以0.99的后验概率支持将美国祖先病毒放在纽约市，强烈表明这是早期美国艾滋病毒/艾滋病多样化的关键枢纽。Logistic增长联合模型显示，美国和加勒比地区的流行病分别是0.86年和1.12年的两倍，这表明每个地区的早期扩张都很迅速。与最近的数据比较表明，如果没有存档的全基因组序列，许多这些见解是无法实现的。我们还从被称为“0号病人”的个体中恢复了HIV-1基因组，并显示既没有生物学证据也没有历史证据表明他是美国的主要病例，也没有证据表明他是整个B型的主要病例。我们根据这些进化论的见解来讨论这种信念的起源和持久性。
The emergence of HIV-1 group M subtype B in North American men who have sex with men (MSM) was a key turning point in the HIV/AIDS pandemic. Phylogenetic studies have suggested cryptic subtype B circulation in the United States (US) throughout the 1970s and an even older presence in the Caribbean. However, these timing and geographical inferences, based upon partial HIV-1 genomes that postdate the recognition of AIDS in 1981, remain contentious and the earliest movements of the virus within the US are unknown. We serologically screened >2000 1970s serum samples and developed a highly sensitive new approach for recovering viral RNA from degraded archival samples. Here, we report eight coding-complete genomes from US serum samples from 1978–79 – eight of the nine oldest HIV-1 group M genomes to date. This early, full-genome ‘snapshot’ reveals the US HIV-1 epidemic exhibited surprisingly extensive genetic diversity in the 1970s but also provides strong evidence of its emergence from a pre-existing Caribbean epidemic. Bayesian phylogenetic analyses estimate the jump to the US at ~1970 and place the ancestral US virus in New York City with 0.99 posterior probability support, strongly suggesting this was the crucial hub of early US HIV/AIDS diversification. Logistic growth coalescent models reveal epidemic doubling times of 0.86 and 1.12 years for the US and Caribbean, respectively, suggesting rapid early expansion in each location. Comparisons with more recent data reveal many of these insights to be unattainable without archival, full-genome sequences. We also recovered the HIV-1 genome from the individual known as ‘Patient 0’ and show there is neither biological nor historical evidence he was the primary case in the US or for subtype B as a whole. We discuss the genesis and persistence of this belief in the light of these evolutionary insights.