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.
Conclusions:
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.
Peptides Mimicking the β7/β8 Loop of HIV-1 Reverse Transcriptase p51 as “Hotspot-Targeted” Dimerization Inhibitors
