Polotan Francisco Gerardo M, Salazar Carl Raymund P, Morito Hannah Leah E, Abulencia Miguel Francisco B, Pantoni Roslind Anne R, Mercado Edelwisa S, Hué Stéphane, Ditangco Rossana A
Molecular Biology Laboratory, Research Institute for Tropical Medicine, 9002, Research Drive, Filinvest Corporate City, Alabang, Muntinlupa City, Metro Manila 1781, The Philippines.
Laboratory of Microbiology, Wageningen University and Research, Stippeneng 4, Wageningen 6700 EH, The Netherlands.
Virus Evol. 2023 Dec 7;9(2):vead073. doi: 10.1093/ve/vead073. eCollection 2023.
The Philippines has had a rapidly growing human immunodeficiency virus (HIV) epidemic with a shift in the prevalent subtype from B to CRF01_AE. However, the phylodynamic history of CRF01_AE in the Philippines has yet to be reconstructed. We conducted a descriptive retrospective study reconstructing the history of HIV-1 CRF01_AE transmissions in the Philippines through molecular epidemiology. Partial polymerase sequences (= 1144) collected between 2008 and 2018 from three island groups were collated from the Research Institute for Tropical Medicine drug resistance genotyping database. Estimation of the time to the most recent common ancestor (tMRCA), effective reproductive number (), effective viral population size (), relative migration rates, and geographic spread of CRF01_AE was performed with BEAST. and were compared between CRF01_AE and B. Most CRF01_AE sequences formed a single clade with a tMRCA of June 1996 [95 per cent highest posterior density (HPD): December 1991, October 1999]. An increasing CRF01_AE was observed from the tMRCA to 2013. The CRF01_AE reached peaks of 2.46 [95 per cent HPD: 1.76, 3.27] in 2007 and 2.52 [95 per cent HPD: 1.83, 3.34] in 2015. A decrease of CRF01_AE occurred in the intervening years of 2007 to 2011, reaching as low as 1.43 [95 per cent HPD: 1.06, 1.90] in 2011, followed by a rebound. The CRF01_AE epidemic most likely started in Luzon and then spread to the other island groups of the country. Both CRF01_AE and Subtype B exhibited similar patterns of fluctuation over time. These results characterize the subtype-specific phylodynamic history of the largest CRF01_AE cluster in the Philippines, which contextualizes and may inform past, present, and future public health measures toward controlling the HIV epidemic in the Philippines.
菲律宾的人类免疫缺陷病毒(HIV)疫情增长迅速,流行亚型已从B型转变为CRF01_AE型。然而,CRF01_AE在菲律宾的系统动力学历史尚未重建。我们进行了一项描述性回顾性研究,通过分子流行病学重建菲律宾HIV-1 CRF01_AE传播的历史。从热带医学研究所耐药基因分型数据库整理了2008年至2018年期间从三个岛屿组收集的部分聚合酶序列(= 1144)。使用BEAST对CRF01_AE的最近共同祖先时间(tMRCA)、有效繁殖数()、有效病毒种群大小()、相对迁移率和地理传播进行了估计。比较了CRF01_AE和B型之间的和。大多数CRF01_AE序列形成了一个单系分支,tMRCA为1996年6月[95%最高后验密度(HPD):1991年12月,1999年10月]。从tMRCA到2013年观察到CRF01_AE的增加。CRF01_AE在2007年达到峰值2.46[95% HPD:1.76,3.27],在2015年达到峰值2.52[95% HPD:1.83,3.34]。在2007年至2011年期间CRF01_AE出现下降,在2011年低至1.43[95% HPD:1.06,1.90],随后反弹。CRF01_AE疫情最有可能始于吕宋岛,然后蔓延到该国的其他岛屿组。CRF01_AE和B亚型随时间呈现出相似的波动模式。这些结果描述了菲律宾最大的CRF01_AE集群的亚型特异性系统动力学历史,为过去、现在和未来控制菲律宾HIV疫情的公共卫生措施提供了背景信息并可能提供参考。