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Population dynamics of HIV-2 in rural West Africa: comparison with HIV-1 and ongoing transmission at the heart of the epidemic

de Silva, Thushan I.a,b,c,*; van Tienen, Carlaa,d,*; Onyango, Claytone; Jabang, Abdouliea; Vincent, Tima,g; Loeff, Maarten F. Schim van derh; Coutinho, Roel A.i; Jaye, Assana; Rowland-Jones, Sarahf; Whittle, Hiltona,j; Cotten, Matthewa,k; Hué, Stéphanec

doi: 10.1097/QAD.0b013e32835ab12c
Epidemiology and Social

Objectives: To compare the population dynamics of HIV-2 and HIV-1, and to characterize ongoing HIV-2 transmission in rural Guinea-Bissau.

Design: Phylogenetic and phylodynamic analyses using HIV-2 gag and env, and HIV-1 env sequences, combined with epidemiological data from a community cohort.

Methods: Samples were obtained from surveys in 1989–1991, 1996–1997, 2003 and 2006–2007. Phylogenies were reconstructed using sequences from 103 HIV-2-infected and 56 HIV-1-infected patients using Bayesian Evolutionary Analysis by Sampling Trees (BEAST), a relaxed molecular clock and a Bayesian skyline coalescent model.

Results: Bayesian skyline plots showed a strong increase in the 1990s of the HIV-1 effective population size (Ne) in the same period that the Ne of HIV-2 came into a plateau phase. The population dynamics of both viruses were remarkably similar following initial introduction. Incident infections were found more often in HIV-2 transmission clusters, with 55–58% of all individuals contributing to ongoing transmission. Some phylogenetically linked sexual partners had discordant viral loads (undetectable vs. detectable), suggesting host factors dictate the risk of disease progression in HIV-2. Multiple HIV-2 introductions into the cohort are evident, but ongoing transmission has occurred predominantly within the community.

Conclusion: Comparison of HIV-1 and HIV-2 phylodynamics in the same community suggests both viruses followed similar growth patterns following introduction, and is consistent with the hypothesis that HIV-1 may have played a role in the decline of HIV-2 via competitive exclusion. The source of ongoing HIV-2 transmission in the cohort appears to be new HIV-2 cases, rather than the pool of older infections established during the early growth of HIV-2.

aMedical Research Council (UK) Laboratories, Fajara, The Gambia

bDepartment of Infection and Tropical Medicine, Royal Hallamshire Hospital, Sheffield, UK

cDivision of Infection and Immunity, MRC/UCL Centre for Medical Molecular Virology, University College London

dErasmus Medical Centre, Rotterdam, The Netherlands

eKEMRI-Wellcome Trust Programme, Kilifi, Kenya

fNuffield Department of Medicine, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK

gProjecto de Saúde de Bandim, INDEPTH Network, Bissau Codex, Guinea-Bissau

hHealth Service of Amsterdam (GGD) and Academic Medical Centre, Amsterdam, The Netherlands

iCenter for Infectious Disease Control of the National Institute for Public Health and the Environment, Bilthoven and University Medical Center Utrecht, Utrecht, The Netherlands

jFaculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London

kWellcome Trust Sanger Institute, Hinxton, UK.

*Thushan I. de Silva and Carla van Tienen contributed equally to the writing of this article.

Correspondence to Thushan I. de Silva, Department of Infection and Tropical Medicine, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK. E-mail: thushandesilva@hotmail.com

Received 11 May, 2012

Revised 12 September, 2012

Accepted 24 September, 2012

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© 2013 Lippincott Williams & Wilkins, Inc.