HIV-1 drug resistance in primary infections in the UK

BMJ ◽  
2001 ◽  
Vol 323 (7313) ◽  
pp. 632-632 ◽  
Author(s):  
S. Fidler ◽  
J. Frater ◽  
J. Clarke ◽  
J. Weber
Keyword(s):  
Drug Resistance ◽  
The Uk ◽  
Hiv 1

scholarly journals HIV-1 drug resistance mutations emerging on darunavir therapy in PI-naive and -experienced patients in the UK

2016 ◽  
Vol 71 (12) ◽  
pp. 3487-3494 ◽  
Author(s):  
Kate El Bouzidi ◽  
Ellen White ◽  
Jean L. Mbisa ◽  
Caroline A. Sabin ◽  
Andrew N. Phillips ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Resistance Mutations ◽  
Drug Resistance Mutations ◽  
The Uk ◽  
Hiv 1

scholarly journals Enhanced surveillance of HIV-1 drug resistance in recently infected MSM in the UK

2016 ◽  
Vol 72 (1) ◽  
pp. 227-234 ◽  
Author(s):  
Emma Cunningham ◽  
Yuen-Ting Chan ◽  
Adamma Aghaizu ◽  
David F. Bibby ◽  
Gary Murphy ◽  
...  
Keyword(s):  
Drug Resistance ◽  
The Uk ◽  
Hiv 1

Drug resistance among patients with HIV-1

2013 ◽  
Vol 4 (5) ◽  
pp. 317-323
Author(s):  
Miłosz Parczewski
Keyword(s):  
Drug Resistance ◽  
Hiv 1

Genetic Diversity and Drug Resistance of HIV-1 CRF55_01B in Guangdong, China

2020 ◽  
Vol 18 (3) ◽  
pp. 210-218
Author(s):  
Guolong Yu ◽  
Yan Li ◽  
Xuhe Huang ◽  
Pingping Zhou ◽  
Jin Yan ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Drug Resistance ◽  
Reverse Transcriptase ◽  
Phylogenetic Analyses ◽  
Resistance Mutations ◽  
Protease Inhibition ◽  
Subtype B ◽  
Primary Drug Resistance ◽  
Hiv 1 ◽  
Primary Drug

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.

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