Guolong Yu1, Yan Li1, Xuhe Huang2, Pingping Zhou2, Jin Yan1, Xinge Yan1, Xiaobing Fu1, Yang Fang1, Jun Liu1, Jie Li1, Xiang He2, Peng Lin1.
Abstract
BACKGROUND: HIV-1 CRF55_01B was first reported in 2013. At present, no report is available regarding this new clade's polymorphisms in its functionally critical regions protease and reverse transcriptase.
OBJECTIVE: To identify the diversity difference in protease and reverse transcriptase between CRF55_01B and its parental clades CRF01_AE and subtype B; and to investigate CRF55_01B's drug resistance mutations associated with the protease inhibition and reverse transcriptase inhibition.
METHODS: HIV-1 RNA was extracted from plasma derived from a MSM population. The reverse transcription and nested PCR amplification were performed following our in-house PCR procedure. Genotyping and drug resistant-associated mutations and polymorphisms were identified based on polygenetic analyses and the usage of the HIV Drug Resistance Database, respectively.
RESULTS: A total of 9.24 % of the identified CRF55_01B sequences bear the primary drug resistance. CRF55_01B contains polymorphisms I13I/V, G16E and E35D that differ from those in CRF01_AE. Among the 11 polymorphisms in the RT region, seven were statistically different from CRF01_AE's. Another three polymorphisms, R211K (98.3%), F214L (98.3%), and V245A/E (98.3 %.), were identified in the RT region and they all were statistically different with that of the subtype B. The V179E/D mutation, responsible for 100% potential low-level drug resistance, was found in all CRF55_01B sequences. Lastly, the phylogenetic analyses demonstrated 18 distinct clusters that account for 35% of the samples.
CONCLUSION: CRF55_01B's pol has different genetic diversity comparing to its counterpart in CRF55_01B's parental clades. CRF55_01B has a high primary drug resistance presence and the V179E/D mutation may confer more vulnerability to drug resistance. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
BACKGROUND: HIV-1 CRF55_01B was first reported in 2013. At present, no report is available regarding this new clade's polymorphisms in its functionally critical regions protease and reverse transcriptase.
OBJECTIVE: To identify the diversity difference in protease and reverse transcriptase between CRF55_01B and its parental clades CRF01_AE and subtype B; and to investigate CRF55_01B's drug resistance mutations associated with the protease inhibition and reverse transcriptase inhibition.
METHODS: HIV-1 RNA was extracted from plasma derived from a MSM population. The reverse transcription and nested PCR amplification were performed following our in-house PCR procedure. Genotyping and drug resistant-associated mutations and polymorphisms were identified based on polygenetic analyses and the usage of the HIV Drug Resistance Database, respectively.
RESULTS: A total of 9.24 % of the identified CRF55_01B sequences bear the primary drug resistance. CRF55_01B contains polymorphisms I13I/V, G16E and E35D that differ from those in CRF01_AE. Among the 11 polymorphisms in the RT region, seven were statistically different from CRF01_AE's. Another three polymorphisms, R211K (98.3%), F214L (98.3%), and V245A/E (98.3 %.), were identified in the RT region and they all were statistically different with that of the subtype B. The V179E/D mutation, responsible for 100% potential low-level drug resistance, was found in all CRF55_01B sequences. Lastly, the phylogenetic analyses demonstrated 18 distinct clusters that account for 35% of the samples.
CONCLUSION: CRF55_01B's pol has different genetic diversity comparing to its counterpart in CRF55_01B's parental clades. CRF55_01B has a high primary drug resistance presence and the V179E/D mutation may confer more vulnerability to drug resistance. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities:
Keywords:
B subtype; CRF01_AE; CRF55_01B; MSM; drug resistance mutations; genetic diversity.
Mesh：
Substances：
Year: 2020
PMID： 32294040 DOI： 10.2174/1570162X18666200415140652
Source DB: PubMed Journal: Curr HIV Res ISSN： 1570-162X Impact factor: 1.581