Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.

Phylogenies of highly genetically variable viruses such as HIV-1 are potentially informative of epidemiological dynamics. Several studies have demonstrated the presence of clusters of highly related HIV-1 sequences, particularly among recently HIV-infected individuals, which have been used to argue...

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Autores principales:	Erik M Volz, James S Koopman, Melissa J Ward, Andrew Leigh Brown, Simon D W Frost
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/861b5646151c4118869e85db5fd06c65
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spelling	oai:doaj.org-article:861b5646151c4118869e85db5fd06c652021-11-18T05:51:13ZSimple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.1553-734X1553-735810.1371/journal.pcbi.1002552https://doaj.org/article/861b5646151c4118869e85db5fd06c652012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22761556/pdf/?tool=EBIhttps://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358Phylogenies of highly genetically variable viruses such as HIV-1 are potentially informative of epidemiological dynamics. Several studies have demonstrated the presence of clusters of highly related HIV-1 sequences, particularly among recently HIV-infected individuals, which have been used to argue for a high transmission rate during acute infection. Using a large set of HIV-1 subtype B pol sequences collected from men who have sex with men, we demonstrate that virus from recent infections tend to be phylogenetically clustered at a greater rate than virus from patients with chronic infection ('excess clustering') and also tend to cluster with other recent HIV infections rather than chronic, established infections ('excess co-clustering'), consistent with previous reports. To determine the role that a higher infectivity during acute infection may play in excess clustering and co-clustering, we developed a simple model of HIV infection that incorporates an early period of intensified transmission, and explicitly considers the dynamics of phylogenetic clusters alongside the dynamics of acute and chronic infected cases. We explored the potential for clustering statistics to be used for inference of acute stage transmission rates and found that no single statistic explains very much variance in parameters controlling acute stage transmission rates. We demonstrate that high transmission rates during the acute stage is not the main cause of excess clustering of virus from patients with early/acute infection compared to chronic infection, which may simply reflect the shorter time since transmission in acute infection. Higher transmission during acute infection can result in excess co-clustering of sequences, while the extent of clustering observed is most sensitive to the fraction of infections sampled.Erik M VolzJames S KoopmanMelissa J WardAndrew Leigh BrownSimon D W FrostPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 8, Iss 6, p e1002552 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Erik M Volz James S Koopman Melissa J Ward Andrew Leigh Brown Simon D W Frost Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.
description	Phylogenies of highly genetically variable viruses such as HIV-1 are potentially informative of epidemiological dynamics. Several studies have demonstrated the presence of clusters of highly related HIV-1 sequences, particularly among recently HIV-infected individuals, which have been used to argue for a high transmission rate during acute infection. Using a large set of HIV-1 subtype B pol sequences collected from men who have sex with men, we demonstrate that virus from recent infections tend to be phylogenetically clustered at a greater rate than virus from patients with chronic infection ('excess clustering') and also tend to cluster with other recent HIV infections rather than chronic, established infections ('excess co-clustering'), consistent with previous reports. To determine the role that a higher infectivity during acute infection may play in excess clustering and co-clustering, we developed a simple model of HIV infection that incorporates an early period of intensified transmission, and explicitly considers the dynamics of phylogenetic clusters alongside the dynamics of acute and chronic infected cases. We explored the potential for clustering statistics to be used for inference of acute stage transmission rates and found that no single statistic explains very much variance in parameters controlling acute stage transmission rates. We demonstrate that high transmission rates during the acute stage is not the main cause of excess clustering of virus from patients with early/acute infection compared to chronic infection, which may simply reflect the shorter time since transmission in acute infection. Higher transmission during acute infection can result in excess co-clustering of sequences, while the extent of clustering observed is most sensitive to the fraction of infections sampled.
format	article
author	Erik M Volz James S Koopman Melissa J Ward Andrew Leigh Brown Simon D W Frost
author_facet	Erik M Volz James S Koopman Melissa J Ward Andrew Leigh Brown Simon D W Frost
author_sort	Erik M Volz
title	Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.
title_short	Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.
title_full	Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.
title_fullStr	Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.
title_full_unstemmed	Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.
title_sort	simple epidemiological dynamics explain phylogenetic clustering of hiv from patients with recent infection.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/861b5646151c4118869e85db5fd06c65
work_keys_str_mv	AT erikmvolz simpleepidemiologicaldynamicsexplainphylogeneticclusteringofhivfrompatientswithrecentinfection AT jamesskoopman simpleepidemiologicaldynamicsexplainphylogeneticclusteringofhivfrompatientswithrecentinfection AT melissajward simpleepidemiologicaldynamicsexplainphylogeneticclusteringofhivfrompatientswithrecentinfection AT andrewleighbrown simpleepidemiologicaldynamicsexplainphylogeneticclusteringofhivfrompatientswithrecentinfection AT simondwfrost simpleepidemiologicaldynamicsexplainphylogeneticclusteringofhivfrompatientswithrecentinfection
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Simple epidemiological dynamics explain phylogenetic clustering of HIV from patients with recent infection.

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