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Post-transcriptional regulatory elements associated with transcript degradation or transcript instability have been described at the 3’ untranslated region (3’UTR) of the  HLA-G  gene. Considering that HPV infection and aneuploidy, which causes gene instability, are associated with cervical cell malignancy, as well as the fact that HIV infection and HLA-G may modulate the immune response, the present study aimed to compare the frequencies of  HLA-G  3′UTR polymorphic sites (14-base pair  insertion/deletion , + 3142C/G , and + 3187A/G ) between 226 HIV +  women co-infected (n = 82) or not with HPV (n = 144) and 138 healthy women. We also evaluated the relationship between those  HLA-G  3’UTR variants and aneuploidy in cervical cells. HPV types and HLA-G polymorphisms were determined by PCR and sequencing of cervical samples DNA. Aneuploidy in cervical cell was measured by flow cytometry. The  HLA-G  3’UTR 14-bp  ins/del  was not associated with either HIV nor HIV/HPV co-infection. The  +3142G  allele ( p  = 0.049) and  +3142GG  genotype ( p  = 0.047) were overrepresented in all HIV-infected women. On the other hand, the  +3187G  allele ( p  = 0.028) and the  +3187GG  genotype ( p  = 0.026) predominated among healthy women. The + 3142G  ( p  = 0.023) and  +3187A  ( p  = 0.003) alleles were associated with predisposition to HIV infection, irrespective of the presence or not of HIV/HPV co-infection. The diplotype formed by the combination of the +3 142CX  ( CC  or  CG ) and +3 187AA  genotype conferred the highest risk for aneuploidy in cervical cell induced by HPV. The  HLA-G  3’UTR + 3142  and + 3187  variants conferred distinct susceptibility to HIV infection and aneuploidy.

Variation sites at the HLA-G 3’ untranslated region confer differential susceptibility to HIV/HPV co-infection and aneuploidy in cervical cell