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Author Notes:

Correspondence to Professor Margaret May, School of Social and Community Medicine, University of Bristol, 39 Whatley Rd, Bristol, BS8 2PS, UK. Tel: +44 117 9287287; fax: +44 117 928 7325; e-mail: m.t.may@bristol.ac.uk

M.J.G. contributed the original idea and to the study design and writing the article.

M.M. performed the statistical analyses and wrote the first draft of the article.

J.S. contributed to study design, supervised the analyses and contributed to the writing of the article.

L.W. contributed to study design.

S.I., S.J. and T.H. contributed to data management.

All authors discussed the study design, results, revised and commented on the article and agreed to it being submitted for publication.

See Publication for full list of authors.

We thank all patients, doctors, and study nurses associated with the participating cohort studies.

The authors declare that they do not have any conflicts of interest.


Research Funding:

This work was supported by the UK Medical Research Council [grant numbers G0700820, MR/J002380/1] and the Department for International Development (DFID).

Jonathan Sterne is funded by National Institute for Health Research Senior Investigator award NF-SI-0611-10168.

Sources of funding of individual cohorts in ART-CC include the Agence Nationale de Recherche sur le SIDA et les hépatites virales (ANRS), the Institut National de la Santé et de la Recherche Médicale (INSERM), the French, German, Italian and Spanish Ministries of Health, the Swiss National Science Foundation (grant 33CS30_134277), the German Centre for infection Research, the Ministry of Science and Innovation and the ‘Spanish Network for AIDS Research (RIS; ISCIII-RETIC RD06/006), the Stichting HIV Monitoring, the European Commission (EuroCoord grant 260694), the British Columbia and Alberta Governments, the Canadian Institutes of Health Research, and unrestricted grants from Abbott, Gilead, Tibotec-Upjohn, ViiV Healthcare, MSD, GlaxoSmithKline, Pfizer, Bristol Myers Squibb, Roche and Boehringer-Ingelheim.

The Montreal Cohort, The McGill University Health Centre Chronic Viral Illness Service Cohort, is supported by les Fonds de Recherches Québec-Santé, (FRQ-S) Réseau SIDA/maladies infectieuses.

Marina Klein is supported by a Chercheur National career award from the FRQ-S.

The UK CHIC Study is funded by the Medical Research Council, UK (Grant numbers G0000199, G0600337, G0900274 and MR/M004236/1).


  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • Infectious Diseases
  • Virology
  • antiretroviral therapy
  • HIV-1 subtype
  • mortality
  • prognosis
  • viral failure

Mortality of treated HIV-1 positive individuals according to viral subtype in Europe and Canada: collaborative cohort analysis

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Journal Title:



Volume 30, Number 3


, Pages 503-513

Type of Work:

Article | Final Publisher PDF


OBJECTIVES: To estimate prognosis by viral subtype in HIV-1-infected individuals from start of antiretroviral therapy (ART) and after viral failure. DESIGN: Collaborative analysis of data from eight European and three Canadian cohorts. METHODS: Adults (N>20 000) who started triple ART between 1996 and 2012 and had data on viral subtype were followed for mortality. We estimated crude and adjusted (for age, sex, regimen, CD4 cell count, and AIDS at baseline, period of starting ART, stratified by cohort, region of origin and risk group) mortality hazard ratios (MHR) by subtype. We estimated MHR subsequent to viral failure defined as two HIV-RNA measurements greater than 500 copies/ml after achieving viral suppression. RESULTS: The most prevalent subtypes were B (15 419; 74%), C (2091; 10%), CRF02AG (1057; 5%), A (873; 4%), CRF01AE (506; 2.4%), G (359; 1.7%), and D (232; 1.1%). Subtypes were strongly patterned by region of origin and risk group. During 104 649 person-years of observation, 1172/20 784 patients died. Compared with subtype B, mortality was higher for subtype A, but similar for all other subtypes. MHR for A versus B were 1.13 (95% confidence interval 0.85,1.50) when stratified by cohort, increased to 1.78 (1.27,2.51) on stratification by region and risk, and attenuated to 1.59 (1.14,2.23) on adjustment for covariates. MHR for A versus B was 2.65 (1.64,4.28) and 0.95 (0.57,1.57) for patients who started ART with CD4 cell count below, or more than, 100 cells/μl, respectively. There was no difference in mortality between subtypes A, B and C after viral failure. CONCLUSION: Patients with subtype A had worse prognosis, an observation which may be confounded by socio-demographic factors.

Copyright information:

Q 2016 Wolters Kluwer Health, Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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