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Phylodynamics of HIV-1 Circulating Recombinant Forms 12_BF and 38_BF in Argentina and Uruguay

Gonzalo Bello1*, Paula C Aulicino2, Dora Ruchansky3, Monick L Guimarães1, Cecilio Lopez-Galindez4, Concha Casado4, Hector Chiparelli3, Carlos Rocco2, Andrea Mangano2, Luisa Sen2 and Mariza G Morgado1

Author Affiliations

1 Laboratório de AIDS & Imunologia Molecular, Instituto Oswaldo Cruz - FIOCRUZ, Rio de Janeiro, Brazil

2 Laboratorio de Biología Celular y Retrovirus-CONICET, Hospital de Pediatría J P Garrahan, Buenos Aires, Argentina

3 Laboratorio Nacional de Referencia VIH-SIDA, Servicio Nacional de Laboratorios de Salud Publica - MSP, Montevideo, Uruguay

4 Servicio de Virología Molecular, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain

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Retrovirology 2010, 7:22  doi:10.1186/1742-4690-7-22

Published: 22 March 2010



Although HIV-1 CRF12_BF and CRF38_BF are two epidemiologically important recombinant lineages circulating in Argentina and Uruguay, little is known about their population dynamics.


A total of 120 "CRF12_BF-like" and 20 "CRF38_BF-like" pol recombinant sequences collected in Argentina and Uruguay from 1997 to 2009 were subjected to phylogenetic and Bayesian coalescent-based analyses to estimate evolutionary and demographic parameters.


Phylogenetic analyses revealed that CRF12_BF viruses from Argentina and Uruguay constitute a single epidemic with multiple genetic exchanges among countries; whereas circulation of the CRF38_BF seems to be confined to Uruguay. The mean estimated substitution rate of CRF12_BF at pol gene (2.5 × 10-3 substitutions/site/year) was similar to that previously described for subtype B. According to our estimates, CRF12_BF and CRF38_BF originated at 1983 (1978-1988) and 1986 (1981-1990), respectively. After their emergence, the CRF12_BF and CRF38_BF epidemics seem to have experienced a period of rapid expansion with initial growth rates of around 1.2 year-1 and 0.9 year-1, respectively. Later, the rate of spread of these CRFs_BF seems to have slowed down since the mid-1990s.


Our results suggest that CRF12_BF and CRF38_BF viruses were generated during the 1980s, shortly after the estimated introduction of subtype F1 in South America (~1975-1980). After an initial phase of fast exponential expansion, the rate of spread of both CRFs_BF epidemics seems to have slowed down, thereby following a demographic pattern that resembles those previously reported for the HIV-1 epidemics in Brazil, USA, and Western Europe.