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Elife. 2014 Sep 12;3:e03821. doi: 10.7554/eLife.03821.

HIV-1 DNA predicts disease progression and post-treatment virological control.

Collaborators (178)

Breckenridge A, Clayden P, Conlon C, Conradie F, Kaldor J, Maggiolo F, Ssali F, Cooper DA, Kaleebu P, Ramjee G, Schechter M, Tambussi G, Miro JM, Weber J, Fidler S, Babiker A, Peto T, McLaren A, Beral V, Chene G, Hakim J, Babiker A, Porter K, Thomason M, Ewings F, Gabriel M, Johnson D, Thompson K, Cursley A, Donegan K, Fossey E, Kelleher P, Lee K, Murphy B, Nock D, Phillips R, Frater J, Ohm Laursen L, Robinson N, Goulder P, Brown H, McClure M, Bonsall D, Erlwein O, Helander A, Kaye S, Robinson M, Cook L, Adcock G, Ahmed P, Paton N, Fidler S, Kelleher A, Moore R, McFarlane R, Roth N, Finlayson R, Kiem Tee B, Read T, Kelly M, Doong N, Bloch M, Workman C, Grey P, Cooper DA, Kelleher A, Law M, Schechter M, Gama P, Mercon M, Barbosa de Souza M, Beppu Yoshida C, Grangeiro da Silva JR, Sampaio Amaral A, Fernandes de Aguiar D, de Fatima Melo M, Quaresma Garrido R, Tambussi G, Nozza S, Pogliaghi M, Chiappetta S, Della Torre L, Gasparotto E, DOffizi G, Vlassi C, Corpolongo A, Wood R, Pitt J, Orrell C, Cilliers F, Croxford R, Middelkoop K, Bekker LG, Heiberg C, Aploon J, Killa N, Fielder E, Buhler T, Rees H, Venter F, Palanee T, Stevens W, Ingram C, Majam M, Papathanasopoulos M, Ramjee G, Gappoo S, Moodley J, Premrajh A, Zako L, Grosskurth H, Kamali A, Kaleebu P, Bahemuka U, Mugisha J, Njaj HF, Miro JM, Lopez-Dieguez M, Manzardo C, Arnaiz JA, Pumarola T, Plana M, Tuset M, Ligero MC, Garca MT, Gallart T, Gatell JM, Fisher M, Hobbs K, Perry N, Pao D, Maitland D, Heald L, Mulcahy F, Courtney G, ODea S, Reidy D, Leen C, Scott G, Ellis L, Morris S, Simmonds P, Gazzard B, Hawkins D, Higgs C, Anderson J, Mguni S, Williams I, De Esteban N, Pellegrino P, Arenas-Pinto A, Cornforth D, Turner J, Ainsworth J, Waters A, Johnson M, Kinloch S, Carroll A, Byrne P, Cuthbertson Z, Orkin C, Hand J, De Souza C, Weber J, Fidler S, Hamlyn E, Thomson E, Fox J, Legg K, Mullaney S, Winston A, Wilson S, Ambrose P, Taylor S, Gilleran G, Keeling S, Becker A, Boocock C.

Author information

1
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
2
Medical Research Council Clinical Trials Unit, Institute of Clinical Trials and Methodology, University College London, London, United Kingdom.
3
Department of Sexual Health and HIV, Brighton and Sussex University Hospitals, Brighton, United Kingdom.
4
Division of Infection and Immunity, School for Life Sciences, University College London, London, United Kingdom.
5
The Kirby Institute of New South Wales, Sydney, Australia.
6
Hospital Escola São Francisco de Assis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
7
Department of Infectious Diseases, Ospedale San Raffaele, Milan, Italy.
8
Division of Medicine, Wright Fleming Institute, Imperial College, London, United Kingdom.
9
Cancer and Inflammation Program, Laboratory of Experimental Immunology, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, United States.

Abstract

In HIV-1 infection, a population of latently infected cells facilitates viral persistence despite antiretroviral therapy (ART). With the aim of identifying individuals in whom ART might induce a period of viraemic control on stopping therapy, we hypothesised that quantification of the pool of latently infected cells in primary HIV-1 infection (PHI) would predict clinical progression and viral replication following ART. We measured HIV-1 DNA in a highly characterised randomised population of individuals with PHI. We explored associations between HIV-1 DNA and immunological and virological markers of clinical progression, including viral rebound in those interrupting therapy. In multivariable analyses, HIV-1 DNA was more predictive of disease progression than plasma viral load and, at treatment interruption, predicted time to plasma virus rebound. HIV-1 DNA may help identify individuals who could safely interrupt ART in future HIV-1 eradication trials.

KEYWORDS:

HIV-1; antiretroviral therapy; cure; human; human biology; infectious disease; medicine; microbiology; primary infection; reservoir

PMID:
25217531
PMCID:
PMC4199415
DOI:
10.7554/eLife.03821
[Indexed for MEDLINE]
Free PMC Article

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