HIV-1 DNA predicts disease progression and post-treatment virological control
James P Williams,
Jacob Hurst,
Wolfgang Stöhr,
Nicola Robinson,
Helen Brown,
Martin Fisher,
Sabine Kinloch,
David Cooper,
Mauro Schechter,
Giuseppe Tambussi,
Sarah Fidler,
Mary Carrington,
Abdel Babiker,
Jonathan Weber,
Kersten K Koelsch,
Anthony D Kelleher,
Rodney E Phillips,
John Frater,
on behalf of the SPARTAC trial investigators
Affiliations
James P Williams
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom
Jacob Hurst
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom; The Oxford Martin School, Institute for Emerging Infections, Oxford, United Kingdom
Wolfgang Stöhr
Medical Research Council Clinical Trials Unit, Institute of Clinical Trials and Methodology, University College London, London, United Kingdom
Nicola Robinson
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom; The Oxford Martin School, Institute for Emerging Infections, Oxford, United Kingdom; Oxford National Institute of Health Research Biomedical Research Centre, Oxford, United Kingdom
Helen Brown
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom; The Oxford Martin School, Institute for Emerging Infections, Oxford, United Kingdom; Oxford National Institute of Health Research Biomedical Research Centre, Oxford, United Kingdom
Martin Fisher
Department of Sexual Health and HIV, Brighton and Sussex University Hospitals, Brighton, United Kingdom
Sabine Kinloch
Division of Infection and Immunity, School for Life Sciences, University College London, London, United Kingdom
David Cooper
The Kirby Institute of New South Wales, Sydney, Australia
Mauro Schechter
Hospital Escola São Francisco de Assis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
Giuseppe Tambussi
Department of Infectious Diseases, Ospedale San Raffaele, Milan, Italy
Sarah Fidler
Division of Medicine, Wright Fleming Institute, Imperial College, London, United Kingdom
Mary Carrington
Cancer and Inflammation Program, Laboratory of Experimental Immunology, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, United States; Ragon Institute of MGH, MIT and Harvard, Cambridge, United States
Abdel Babiker
Medical Research Council Clinical Trials Unit, Institute of Clinical Trials and Methodology, University College London, London, United Kingdom
Jonathan Weber
Division of Medicine, Wright Fleming Institute, Imperial College, London, United Kingdom
Kersten K Koelsch
The Kirby Institute of New South Wales, Sydney, Australia; St Vincent's Centre for Applied Medical Research, Sydney, Australia
Anthony D Kelleher
The Kirby Institute of New South Wales, Sydney, Australia; St Vincent's Centre for Applied Medical Research, Sydney, Australia
Rodney E Phillips
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom; The Oxford Martin School, Institute for Emerging Infections, Oxford, United Kingdom; Oxford National Institute of Health Research Biomedical Research Centre, Oxford, United Kingdom
John Frater
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom; The Oxford Martin School, Institute for Emerging Infections, Oxford, United Kingdom; Oxford National Institute of Health Research Biomedical Research Centre, Oxford, United Kingdom
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. Clinical trial registration: ISRCTN76742797 and EudraCT2004-000446-20