HIV type 1 pol gene diversity and antiretroviral drug resistance mutations in Santos, Brazil.
HIV-1 antiretroviral drug resistance mutations in subtype B, F, and recombinants B/F in Santos, Brazil were characterized. We studied 83 samples from individuals enrolled at the Brazilian HIV/AIDS programs from Santos. These patients have been treated with multiantiretroviral therapy. Samples were collected in 2006; RNA was extracted from plasma and used as a target to amplify the pol gene of HIV-1. PCR products were sequenced on both strands, phylogenetic analyses were performed by neighbor-joining, and recombination was evaluated by bootscan. pol gene sequencing of the samples revealed that 54 strains belonged to subtype B, 4 were subtype F, 1 was subtype C, and 24 were B/F recombinants. Recombinant break points in 20 samples are the same identified in CRF28_BF and CRF29_BF. Drug resistance mutations identified in common to subtypes B, F, and recombinants B/F were protease inhibitors M46I/L (29%), I54V (24%), A71V (22%), and V82A/F (31%); reverse transcriptase nucleoside resistance mutations M41L (52%), D67N (30%), K70R (26%), M184V (88%), L210W (29%), T215Y/I/F (65%), and K219Q/E/N (28%); and reverse transcriptase nonnucleoside resistance mutation K103N (52%). Our results suggest that, in general, the same amino acids are emerging in both subtypes B, F, and recombinant forms BF due to the selective pressure of antiretrovirals. Recombinant break points in samples are the same as identified in CRF28_BF and CRF29_BF and are recognized as important for the evolution of the local epidemic.
de Sa-Filho
Dercy José
DJ
Laboratório de Biologia Molecular, Centro Universitário Lusíada, Santos/SP, Brazil. dercy@pesquisa.epm.br
Soares
Marta da Silva
Mda S
Candido
Valéria
V
Gagliani
Luiz Henrique
LH
Cavaliere
Elizabeth
E
Diaz
Ricardo Sobhie
RS
Caseiro
Marcos Montani
MM
D000328:Adult; D000595:Amino Acid Sequence; D019943:Amino Acid Substitution / Q000235:genetics; D019380:Anti-HIV Agents / Q000494:pharmacology; D001938:Brazil; D016000:Cluster Analysis; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D010802:Phylogeny; D011110:Polymorphism, Genetic; D012367:RNA, Viral / Q000097:blood / Q000235:genetics / Q000302:isolation & purification; D011995:Recombination, Genetic; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012641:Selection, Genetic; D016415:Sequence Alignment; D017422:Sequence Analysis, DNA; D054302:pol Gene Products, Human Immunodeficiency Virus / Q000737:chemistry / Q000235:genetics*
D019380:Anti-HIV Agents; D012367:RNA, Viral; D054302:pol Gene Products, Human Immunodeficiency Virus; C514824:reverse transcriptase, Human immunodeficiency virus 1; D054303:HIV Reverse Transcriptase; D016333:HIV Protease; C514803:p16 protease, Human immunodeficiency virus 1