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Association of IL10, IL4, IFNG and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus.

Association of IL10, IL4, IFNG and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus.
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Rodrigues RO, Rabenhorst SH, de Carvalho PG, Sasahara GL, Vasconcelos LM, de Arruda ÉA, da Silva SF, Ribeiro IF, Nagao-Dias EA,


Rodrigues RO, Rabenhorst SH, de Carvalho PG, Sasahara GL, Vasconcelos LM, de Arruda ÉA, da Silva SF, Ribeiro IF, Nagao-Dias EA, (click to view)

Rodrigues RO, Rabenhorst SH, de Carvalho PG, Sasahara GL, Vasconcelos LM, de Arruda ÉA, da Silva SF, Ribeiro IF, Nagao-Dias EA,

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Japanese journal of infectious diseases 2017 02 28() doi 10.7883/yoken.JJID.2016.075

Abstract

We evaluated IL-10 -592 C/A, IL-4 -589 C/T, IFN-γ +874 A/T, CTLA-4 +49 A/G gene polymorphisms in efavirenz hypersensitivity reaction. A total of 63 HIV-positive patients under treatment at a public hospital were included in the study, of which 21 presented efavirenz hypersensitivity. Patients who presented efavirenz hypersensitivity reaction showed a higher frequency of the IL-10 -592A allele than the controls (p = 0.028). The allele A was associated with increased risk to efavirenz hypersensitivity (OR = 2.40). In the case of IL-4, there was no significant difference in the frequency of the IL-4 -589 (C/T) polymorphism between patients and controls. A significant inverse correlation was observed when comparing the CTLA-4 + 49A/G and IL-4 -589 C/T polymorphisms (r = -0.650, p = 0.001); that is, the CTLA-4 +49GG genotype, involved with the lowest capacity of inhibition, was inversely correlated to increased production of the IL-4 -589TT genotype, which induces high production of IL-4. In respect to the CTLA4 +49A/G and IFN-γ +874T/A gene polymorphisms, there were no significant differences in allele and genotype frequencies between the groups. In conclusion, our data suggest that polymorphisms in regulatory regions of cytokine could modulate an individual’s susceptibility to efavirenz hypersensitivity reaction.

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