Characterization of HIV diversity, phylodynamics and drug resistance in Washington, DC

Washington DC has a high burden of HIV with a 2.0% HIV prevalence. The city is a national and international hub potentially containing a broad diversity of HIV variants; yet few sequences from DC are available on GenBank to assess the evolutionary history of HIV in the US capital. Towards this gener...

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Bibliographic Details
Published in:PloS one 2017-09, Vol.12 (9), p.e0185644-e0185644
Main Authors: Pérez-Losada, Marcos, Castel, Amanda D, Lewis, Brittany, Kharfen, Michael, Cartwright, Charles P, Huang, Bruce, Maxwell, Taylor, Greenberg, Alan E, Crandall, Keith A
Format: Article
Language:English
Subjects:
Acquired immune deficiency syndrome
Adult
AIDS
Amino acids
Bayesian analysis
Biodiversity
Biology and Life Sciences
Cluster analysis
Clustering
Cohort Studies
Computer and Information Sciences
Data processing
Demographics
Disease transmission
District of Columbia
DRM protein
Drug resistance
Drug Resistance, Viral
Drug therapy
Epidemiology
Evolution (Biology)
Female
Gene sequencing
Genotypes
HIV
HIV infections
HIV Infections - transmission
HIV Infections - virology
HIV-1 - classification
Human immunodeficiency virus
Humans
Male
Medicine and health sciences
Middle Aged
Mutation
Phylogeny
Population genetics
Population number
Research and Analysis Methods
Risk analysis
Risk factors
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Summary:Washington DC has a high burden of HIV with a 2.0% HIV prevalence. The city is a national and international hub potentially containing a broad diversity of HIV variants; yet few sequences from DC are available on GenBank to assess the evolutionary history of HIV in the US capital. Towards this general goal, here we analyze extensive sequence data and investigate HIV diversity, phylodynamics, and drug resistant mutations (DRM) in DC. Molecular HIV-1 sequences were collected from participants infected through 2015 as part of the DC Cohort, a longitudinal observational study of HIV+ patients receiving care at 13 DC clinics. Sequences were paired with Cohort demographic, risk, and clinical data and analyzed using maximum likelihood, Bayesian and coalescent approaches of phylogenetic, network and population genetic inference. We analyzed 601 sequences from 223 participants for int (~864 bp) and 2,810 sequences from 1,659 participants for PR/RT (~1497 bp). Ninety-nine and 94% of the int and PR/RT sequences, respectively, were identified as subtype B, with 14 non-B subtypes also detected. Phylodynamic analyses of US born infected individuals showed that HIV population size varied little over time with no significant decline in diversity. Phylogenetic analyses grouped 13.5% of the int sequences into 14 clusters of 2 or 3 sequences, and 39.0% of the PR/RT sequences into 203 clusters of 2-32 sequences. Network analyses grouped 3.6% of the int sequences into 4 clusters of 2 sequences, and 10.6% of the PR/RT sequences into 76 clusters of 2-7 sequences. All network clusters were detected in our phylogenetic analyses. Higher proportions of clustered sequences were found in zip codes where HIV prevalence is highest (r = 0.607; P
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0185644