Search

We studied drug resistance mutations (DRMs) in 2623 pol sequences. Out of 94,828 amino acid substitutions that were detected, 8749 corresponded to nucleoside reverse transcriptase inhibitor (NRTI), 3765 to nonnucleoside reverse transcriptase inhibitor (NNRTI), and 7141 to protease inhibitor (PI) resistance-associated mutations. The most common DRMs were L10I, I54V, L90M, V82A, A71V, L10V, M46I, M184V, M41L, T215Y, D67N, L210W, K70R, N348I, V118I, K103N, Y181C, G190A, K101E, V108I, L100I, V90I, K101Q, and A98G. As expected, DRMs frequencies depended on viral genotype. The amounts of NRTI and PI resistance mutations among B and BF sequences from children were higher than among sequences from adults. The frequencies of PI and NRTI resistance mutations among B and BF sequences from adult men were higher than among sequences from women. Some of these observations can be explained in light of the available epidemiological information, but some cannot, indicating that further studies are needed to understand the antiretroviral resistance epidemics in Argentina.

HIV-1 epidemics in South America are believed to have originated in part from the subtype B epidemic initiated in the Caribbean/North America region. However, circulation of BF recombinants in similar proportions was extensively reported. Information currently shows that many BF recombinants share a recombination structure similar to that found in the CRF12_BF. In the present study, analyzing a set of 405 HIV sequences, we identified the most likely origin of the BF epidemic in an early event of recombination. We found that the subtype B epidemics in South America analyzed in the present study were initiated by a founder event that occurred in the early 1970s, a few years after the introduction of these strains in the Americas. Regarding the F/BF recombinant epidemics, by analyzing a subtype F genomic segment within the viral gene gag present in the majority of the BF recombinants, we found evidence of a geographic divergence very soon after the introduction of subtype F strains in South America. Moreover, through analysis of a subtype B segment present in all the CRF12_BF-like recombination structure, we estimated the circulation of the subtype B strain that gave rise to that recombinant structure around the same time period estimated for the introduction of subtype F strains. The HIV epidemics in South America were initiated in part through a founder event driven by subtype B strains coming from the previously established epidemic in the north of the continent. A second introduction driven by subtype F strains is likely to have encountered the incipient subtype B epidemic that soon after their arrival recombined with them, originating the BF epidemic in the region. These results may explain why in South America the majority of F sequences are found as BF recombinants.

The South American HIV-1 epidemic is characterized by the co-circulation of subtype B and BF recombinant variants. Together with the B and BF genotypes, HIV-1 subtype C (HIV-1C), F1, and several other recombinants have been reported. The epidemiological significance and immune correlates of these "non-B-non-BF" strains circulating in South America are still uncertain and therefore are increasingly attracting the interest of the scientific community. In this study, the South American HIV-1C epidemic was studied using new technologies for the phylogenetic analysis of large datasets. Our results indicate that there is a major clade encompassing most of the South American HIV-1C strains. These analyses also agreed that some strains do not group inside this major clade, suggesting that there could be HIV-1C sequences of different origins circulating in South America. Others have proposed different hypotheses about the origins of HIV-1C strains from South America. This study shows that an exact single origin cannot be determined, a fact that could be attributed to sampling problems, phylogenetic uncertainty, and the shortage of historical and epidemiological data. Currently, the reported data indicate that HIV-1C strains were introduced in Brazil and afterward spread to other regions of South America. By using character optimization on the obtained phylogenetic trees, we observed that Argentina could also be a point in which the HIV-1C epidemic entered South America.

HTLV-1 Cosmopolitan subtype Transcontinental subgroup A has been described among aboriginal communities from the northwest endemic area of Argentina. Moreover, Transcontinental subgroup A and the Japanese subgroup B were reported among blood donors from the nonendemic central region of the country. We carried out the first HTLV-1 phylogenetic study in individuals residing in Buenos Aires capital city. Phylogenetic analysis performed on the LTR region showed that all 44 new strains clustered within the Cosmopolitan subtype, with 42 (95.4%) belonging to Transcontinental subgroup A. Of them, 20 (45.5%) strains grouped in the large Latin American cluster and 4 (9.1%) in the small Latin American cluster. The majority of them belonged to individuals of nonblack origin, grouped with Amerindian strains. Three (6.8%) were closely related to South African references and two monophyletic clusters including only HIV/HTLV-1 coinfected individuals were observed. Interestingly, two (4.5%) new sequences (divergent strains) branched off from all five known Cosmopolitan subgroups in a well-supported clade. In summary, these findings show that HTLV-1 Cosmopolitan subtype Transcontinental subgroup A is infecting residents of Buenos Aires, a nonendemic area of Argentina, and confirm the introduction of divergent strains in the country.

To perform a diversity surveillance study we characterized viral subtypes among newly diagnosed individuals in Buenos Aires city. Plasma samples were collected from 322 drug-naive newly diagnosed HIV-1 individuals attending two voluntary counseling and testing centers. Sequences of pol and vpu genes were obtained from 283 samples and viral subtype was characterized by Neighbor-joining trees and Bootscanning analysis. BF recombinants were found in 56.9% followed by subtype B strains (39.2%). CRF12_BF structure was found in 27% of BF while another 27% had that structure only in one of both genes analyzed. Unusual non-B-non-BF strains were found in 3.9% (11/283). They were further analyzed by database searching and maximum likelihood trees in order to track their origin. Two subtype C sequences were found to be related to South American isolates while another two subtype C sequences and the subtype C segment of a BC recombinant were found to be related to isolates from Senegal. We also identified the CRF16_A2D previously found in Argentina and the CRF06_cpx commonly prevalent in Africa. The B segment of a BD recombinant was also found to be related to the Argentinean Bs suggesting a recombination between an African and a local strain. We also found a BK and two BA recombinants. In conclusion, CRF16_A2D and a new line of subtype C (of Senegalese origin) seem to be successfully established and are now spreading in Buenos Aires. BF recombinants keep recombining with local strains losing the CRF12_BF structure. Altogether they are changing the diversity of HIV in Argentina.