Have the explosive HIV epidemics in sub-Saharan Africa been driven by higher community viral load?

Abu-Raddad, Laith J.a,b,c,*; Barnabas, Ruanne V.c,e,f,*; Janes, Hollyc,g; Weiss, Helen A.i; Kublin, James G.c; Longini, Ira M. Jrj,k; Wasserheit, Judith N.d,e,f,h; the HIV Viral Load Working Group

doi: 10.1097/QAD.0b013e32835cb927
Epidemiology and Social

Objective: The HIV epidemic has carved contrasting trajectories around the world with sub-Saharan Africa (SSA) being most affected. We hypothesized that mean HIV-1 plasma RNA viral loads are higher in SSA than other areas, and that these elevated levels may contribute to the scale of epidemics in this region.

Design and methods: To evaluate this hypothesis, we constructed a database of means of 71 668 viral load measurements from 44 cohorts in seven regions of the world. We used linear regression statistical models to estimate differences in viral load between regions. We also constructed and analyzed a mathematical model to describe the impact of the regional viral load differences on HIV epidemic trajectory.

Results: We found substantial regional viral load heterogeneity. The mean viral load in SSA was 0.58 log10 copies/ml higher than in North America (95% confidence interval 0.45–0.71); this represents about a four-fold increase. The highest mean viral loads were found in Southern and East Africa, whereas in Asia, Europe, North America, and South America, mean viral loads were comparable. Mathematical modeling indicated that conservatively 14% of HIV infections in a representative population in Kenya could be attributed to the enhanced infectiousness of patients with heightened viral load.

Conclusion: We conclude that community viral load appears to be higher in SSA than in other regions and this may be a central driver of the massive HIV epidemics in this region. The elevated viral loads in SSA may reflect, among other factors, the high burden of co-infections or the preponderance of HIV-1 subtype C infection.

Author Information

aInfectious Disease Epidemiology Group, Weill Cornell Medical College – Qatar, Cornell University, Qatar Foundation – Education City, Doha, Qatar

bDepartment of Public Health, Weill Cornell Medical College, Cornell University, New York, New York

cVaccine and Infectious Disease Division

dClinical Research Division, Fred Hutchinson Cancer Research Centre, Seattle, Washington

eDepartment of Global Health

fDepartment of Medicine

gDepartment of Biostatistics

hDepartment of Epidemiology, Schools of Medicine and Public Health, University of Washington, Seattle, Washington, USA

iMRC Tropical Epidemiology Group, Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, UK

jDepartment of Biostatistics

kEmerging Pathogens Institute, Colleges of Public Health and Medicine, University of Florida, Gainesville, Florida, USA.

*These authors contributed equally to this study.

Correspondence to Dr Laith J. Abu-Raddad, Infectious Disease Epidemiology Group, Weill Cornell Medical College – Qatar, Qatar Foundation – Education City, P.O. Box 24144, Doha, Qatar. Tel: +974 4492 8321; fax: +974 4492 8333; e-mail: lja2002@qatar-med.cornell.edu

Received 29 July, 2012

Revised 7 November, 2012

Accepted 16 November, 2012

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website (http://www.AIDSonline.com).

© 2013 Lippincott Williams & Wilkins, Inc.