2019 Volume 93 Issue 3 Pages 312-318
To evaluate the longitudinal trends of integrase (IN) polymorphisms and integrase strand transfer inhibitor (INSTI)-associated drug resistance mutations in the Tokai area, we analyzed newly diagnosed individuals with HIV-1 subtype B (n=882) that were divided into two periods 2009-2013 and 2014-2017.
Overall, 113 variable residues, 167 positions in the IN region were mutated in >1% of individuals. E138K (1.4% in 2014-2017) was observed as a non-polymorphic accessory resistance mutation. The frequency of E138K was relatively higher in the Tokai area, compared with other reports. Seven of 8 HIV-1 sequences carrying E138K belonged to the same transmission cluster, suggesting that the higher rates of E138K may be partly due to the circulating specific virus. In the polymorphic accessary mutation, the L74M/I and E157 Q showed an increase in the prevalence of HIV-1 in 2009-2013 compared with 2014-2017.
So far, no resistance mutation which confers any severely reduced INSTI susceptibility has been observed in the Tokai area. These data may provide useful information regarding the clinical response to current INSTIs and to the novel mechanism of action of drugs targeting HIV-1 integrase.