HIV-1 subtypes and drug-resistance mutation sites in HIV/AIDS patients with antiretroviral-therapy failure

Objective To analyze the characteristics of HIV-1 subtypes and drug-resistance mutation sites among HIV-infected patients who received high-efficiency antiretroviral therapy but failed.

Methods A total of 130 plasma samples were collected from the patients who received antiviral treatment for 6 months in Taizhou City of Zhejiang Province in 2021 but failed the treatment and the viral load was ≥1 000 copies·mL^-1. Nucleic acid in the samples was extracted， and the pol gene was amplified by nested reverse transcription PCR. After next-generation sequencing， online tools were used to compare and analyze the subtypes and drug-resistant mutation sites.

Results A total of 110 samples were successfully sequenced. The main HIV-1 subtype was CRF01_AE， accounting for 42.72% （47 cases）， followed by CRF07_BC， 35.45% （39 cases）； CRF08_BC， 10.00% （11 cases）； CRF85_BC， 8.18% （9）； and a small number of B subtype， 1.81% （2 cases） and C subtype， 1.81% （2 cases）. The online tool comparison showed that there were 67 cases with mutations of drug-resistance sites and 61 cases with drug-resistance. The mutation sites were mainly M184V， K103N， K65R and V181C， and the mutation rates were 20.00% （22 cases）， 10.91% （12 cases）， 8.18% （9 cases） and 8.18% （9 cases）， respectively. These mutation sites caused different degrees of resistance to nucleoside reverse transcriptase inhibitors （NRTI）， non- nucleoside reverse transcriptase inhibitors （NNRTI） and protease inhibitors （PI）， including 45 cases of NRTI， 61 cases of NNRTI and 2 cases of PI resistance.

Conclusion The HIV infected people who fail the treatment in Taizhou are mainly with the subtypes CRF01_AE and CRF07_BC. The rate of drug-resistance mutation is at a moderate level， mainly due to the mutation of NRTI and NNRTI drug-resistance sites， and a small number of PI drug-resistance sites. Therefore， the antiviral treatment plan for HIV infected people should be reasonably adjusted， and the detection of drug-resistance mutation sites should be strengthened to avoid the generation of transmissible drug-resistance strains.