Evidence for differences in the sexual transmission efficiency of HIV strains with distinct drug resistance genotypes

Background. The transmission of drug-resistant human immunodeficiency virus type 1 (HIV-1) is a matter of major concern, because it could compromise the response to antiretroviral therapy. Material and methods. From 1997 through 2003, genotypic drug resistance profiles in 89 patients with recent HIV-1 seroconversion were compared in a case-control study with HIV-1 genotypes obtained from 520 subjects identified at Hospital Carlos III in Madrid, Spain, as "potential transmitters" of drug-resistant virus. This group consisted of HIV-infected patients experiencing virologic failure of antiretroviral therapy. Results. Drug resistance mutations were recognized in 15 (16.8%) of 89 patients with recent HIV-1 seroconversion (the seroconverter group), providing resistance to nucleoside reverse-transcriptase inhibitors (NRTIs) in 14.6%, nonnucleoside reverse-transcriptase inhibitors (NNRTIs) in 3.4%, and protease inhibitors (PIs) in 3.4%. Among individuals who were potential transmitters of HIV-1 ( the potential transmitter group), drug resistance mutations were found in 80%, providing resistance to NRTIs in 73.7%, NNRTIs in 36.4%, and PIs in 38.7%. The estimated ratio of individuals with recent HIV-1 seroconversion to potential transmitters for drug-resistance genotypes was 0.23 for resistance to NRTIs, 0.09 for resistance to NNRTIs, and 0.09 for resistance to PIs. For specific resistance mutations, the ratio of individuals with recent HIV-1 seroconversion to potential transmitters was 0.18 for 41L, 0.20 for 215Y/F (including revertants), 0.06 for 184V, 0.04 for 103N, and 0.14 for 181C when considering drug resistance mutations in the reverse transcriptase (RT) gene; the ratio was 0.12 for 46L, 0.06 for 82A/T/S, and 0.08 for 90L, when examining PI resistance mutations. Conclusion. Strains of HIV with some drug resistance genotypes ( 41L, 215Y/F, and 181C in the RT gene and 46L in the protease gene) may be more efficiently transmitted than strains with other drug resistance mutations ( 184V and 103N in the RT gene and 82A/S/T and 90M in the protease gene).