Journal
PLOS PATHOGENS
Volume 14, Issue 7, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1007167
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Categories
Funding
- Wellcome Trust
- Royal Society [107652/Z/15/Z]
- Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health
- Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc. [W81XWH-07-20067]
- U.S. Department of Defense (DOD) [W81XWH-07-20067]
- Bridging the Evolution and Epidemiology of HIV in Europe (BEEHIVE) study via a European Research Council Advanced Grant [PBDR-339251]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001040, ZIAAI000361, K01AI125086, ZICAI001052] Funding Source: NIH RePORTER
- MRC [MR/R015600/1] Funding Source: UKRI
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HIV-1 undergoes multiple rounds of error-prone replication between transmission events, resulting in diverse viral populations within and among individuals. In addition, the virus experiences different selective pressures at multiple levels: during the course of infection, at transmission, and among individuals. Disentangling how these evolutionary forces shape the evolution of the virus at the population scale is important for understanding pathogenesis, how drug-and immune-escape variants are likely to spread in populations, and the development of preventive vaccines. To address this, we deep-sequenced two regions of the HIV-1 genome (p24 and gp41) from 34 longitudinally-sampled untreated individuals from Rakai District in Uganda, infected with subtypes A, D, and inter-subtype recombinants. This dataset substantially increases the availability of HIV-1 sequence data that spans multiple years of untreated infection, in particular for different geographical regions and viral subtypes. In line with previous studies, we estimated an approximately five-fold faster rate of evolution at the within-host compared to the population scale for both synonymous and nonsynonymous substitutions, and for all subtypes. We determined the extent to which this mismatch in evolutionary rates can be explained by the evolution of the virus towards population-level consensus, or the transmission of viruses similar to those that establish infection within individuals. Our findings indicate that both processes are likely to be important.
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