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CUL5 and APOBEC3G polymorphisms are partially implicated in HIV-1 infection and antiretroviral therapy in a Brazilian population.

CUL5 and APOBEC3G polymorphisms are partially implicated in HIV-1 infection and antiretroviral therapy in a Brazilian population.
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da Silva RC, Coelho AV, Moura RR, Arraes LC, Brandão LA, Guimarães RL, Crovella S,


da Silva RC, Coelho AV, Moura RR, Arraes LC, Brandão LA, Guimarães RL, Crovella S, (click to view)

da Silva RC, Coelho AV, Moura RR, Arraes LC, Brandão LA, Guimarães RL, Crovella S,

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Current HIV research 2017 03 15() doi 10.2174/1570162X15666170315114900

Abstract
BACKGROUND
Host restriction factors are cellular proteins able to diminish or block viral replication in a cell-specific way. Objetive and Method: We evaluated the distribution of selected SNPs in APOBEC3G (rs3736685, rs2294367) and CUL5 (rs7117111, rs7103534, rs11212495) genes, among 264 HIV-1 infected (HIV-1+) and 259 unexposed uninfected individuals from Northeast Brazil, looking for a possible association with susceptibility to HIV-1 infection, viral load, CD4+ T cell count and success of antiretroviral therapy.

RESULTS
We observed that the rs11212495 CUL5 G allele and the CUL5 rs7103534-rs7117111 CG haplotype were more frequent among unexposed uninfected individuals than in HIV-1 infected individuals, suggesting an association with a lower susceptibility to HIV-1 infection. Moreover, the APOBEC3G rs2294367 C/G genotype correlated with delayed viral load suppression. Being aware that our findings showed some differences with those reported in the literature, confirming the heterogeneity of the associations described, possibly depending upon the different ethnicities analyzed and the low number of individuals enrolled in all studies, and also considering that our HIV-infection susceptibility control group was constituted by unexposed uninfected individuals instead of exposed uninfected individuals (individuals quite rare and difficult to be enrolled).

CONCLUSION
Our findings report novel genetic variants, different from the ones exhaustively described, associated with susceptibility to HIV-1 (CUL5 rs7103534, rs7117111) and partial viral load control (APOBEC3G rs2294367). Replica studies performed on higher number of subjects and subsequent validation of the functional role of CUL5 and APOBEC3G genetic variants associated with HIV-1 infection and viral replication are envisaged to confirm our and the literature findings.

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