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© Research
Publication : Journal of acquired immune deficiency syndromes (1999)

Lack of primary mutations associated with integrase inhibitors among HIV-1 subtypes B, C, and F circulating in Brazil

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of acquired immune deficiency syndromes (1999) - 01 May 2009

Passaes CB, Guimarães ML, Fernandez SL, Lorete Rdos S, Teixeira SL, Fernandez JC, Morgado MG

Link to Pubmed [PMID] – 19262402

J. Acquir. Immune Defic. Syndr. 2009 May;51(1):7-12

BACKGROUND:

Antiretroviral drugs targeting integrase (IN) have recently been approved for use in combined and salvage therapeutic interventions.

OBJECTIVE:

To evaluate the presence of natural polymorphisms and resistance mutations associated with IN inhibitors among HIV-1 subtypes B, C, and F samples obtained from drug-naive individuals and patients failing highly active antiretroviral therapy in Brazil.

METHODS:

Proviral DNA was obtained from blood samples of 105 HIV-1-positive drug-naive patients infected by B, C, or F subtypes and plasma viral RNA from 30 subtype B-infected individuals failing highly active antiretroviral therapy. The IN region was amplified by nested polymerase chain reaction and automatically sequenced for subtype determination. Translated amino acid sequences were inspected for IN mutations associated with antiretroviral resistance.

RESULTS:

Eleven mutations described as conferring in vitro resistance to IN strand transfer inhibitors were detected among the HIV-1 Brazilian samples. V72I and V201I were considered as polymorphisms. Major mutations associated with elvitegravir or raltegravir in vivo resistance (Q148K/H/R, N155H) were not detected.

CONCLUSIONS:

Although some naturally occurring polymorphisms were observed, the absence of major resistance mutations for the current IN inhibitors provides a good rationale for the introduction of these drugs in Brazil. These results highlight the importance of the continuous surveillance of IN genetic diversity.

http://www.ncbi.nlm.nih.gov/pubmed/19262402