The genetic variability and the prevalence of drug resistance-associated mutations (DRAM) of HIV-1 isolates from 50 women and 8 children from Feira de Santana, Bahia, Brazil were investigated. DNA samples were obtained and pol sequences were generated by PCR and direct sequencing. Phylogenetic analysis showed that 39 (67.2%) samples were subtype B, four (6.9%) F, one (1.7%) C, and 14 (24.1%) BF recombinants. Four different BF recombination patterns were detected. Twelve (20.7%) samples shared the same breakpoint within the reverse transcriptase (RT) sequence. Fifty-five (94.8%) isolates showed several resistance-associated mutations in the RT and the protease (PR) genes. Ten (17.2%) isolates presented mutations associated with a high level of resistance: nine (15.5%) to nucleoside RT inhibitors (NRTI), four (6.9%) to nonnucleoside RT inhibitors (NNRTI), and three (5.2%) to PR inhibitors (PIs). Subtype B-infected patients had, on average, 0.5 high-level DRAM per sequence while no mutations were observed in BF recombinants, although the two groups were under ARV for a similar period of time. Our data indicate the predominance of the subtype B, followed by BF recombinants in this population, and the dissemination of a recombinant strain in Bahia, which could be related to adaptive advantages of these variants over the predominant subtype B.

HTLV-1/HIV-1 co-infection is associated with severe clinical manifestations, marked immunodeficiency, and opportunistic pathogenic infections, as well as risk behavior. Salvador, the capital of the State of Bahia, Brazil, has the highest HTLV-1 prevalence (1.74%) found in Brazil. Few studies exist which describe this co-infection found in Salvador and its surrounding areas, much less investigate how these viruses circulate or assess the relationship between them. To describe the epidemiological and molecular features of HTLV in HIV co-infected women. To investigate the prevalence of HTLV/HIV co-infection in surrounding areas, as well as the molecular epidemiology of HTLV, a cross sectional study was carried out involving 107 women infected with HIV-1 from the STD/HIV/AIDS Reference Center located in the neighboring City of Feira de Santana. Patient samples were submitted to ELISA, and HTLV infection was confirmed using Western Blot and Polymerase Chain Reaction (PCR). Phylogenetic analysis using Neighbor-Joining (NJ) and Maximum Likelihood (ML) was performed on HTLV LTR sequences in order to gain further insights about molecular epidemiology and the origins of this virus in Bahia. Four out of five reactive samples were confirmed to be infected with HTLV-1, and one with HTLV-2. The seroprevalence of HTLV among HIV-1 co-infected women was 4.7%. Phylogenetic analysis of the LTR region from four HTLV-1 sequences showed that all isolates were clustered into the main Latin American group within the Transcontinental subgroup of the Cosmopolitan subtype. The HTLV-2 sequence was classified as the HTLV-2c subtype. It was also observed that four HTLV/HIV-1 co-infected women exhibited risk behavior with two having parenteral exposure, while another two were sex workers. This article describes the characteristics of co-infected patients. This co-infection is known to be severe and further studies should be conducted to confirm the suggestion that HTLV-1 is spreading from Salvador to surrounding areas.

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Genetic factors from an HIV-1 host can affect the rate of progression to AIDS and HIV infection. To investigate the frequency of mutations in the CCR5 gene, HIV-1 samples from infected women and uninfected individuals were selected for sequencing of the CCR5 gene regions encoding the N- and C-terminal protein domains. Physicochemical CCR5 modeling and potential protein domain analysis were performed in order to evaluate the impact of the mutations found in the properties and structure of CCR5. The p.L55Q mutation in the N-terminal protein domain was observed only in uninfected individuals, with an allelic frequency of 1.8%. Physicochemical analysis revealed that the p.L55Q mutation magnified the flexibility and accessibility profiles and the modeling of CCR5 structures showed resulting in a small deviation to the right, as well as a hydrophobic to hydrophilic property alteration. The p.L55Q mutation also resulted in a slight modification of the electrostatic load of this region. Additionally, three novel silent mutations were found at the C-terminal coding region among HIV-1-infected women. The results suggest that the p.L55Q mutation might alter CCR5 conformation. Further studies should be conducted to verify the role of this mutation in HIV-1 susceptibility.