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Killer‐cell immunoglobulin‐like receptors and cytomegalovirus reactivation during late pregnancy
Author(s) -
AlvaradoHernández D. L.,
BenítezSánchez A.,
RodríguezCuevas J. S.,
RosalesSaavedra T.,
GuerraPalomares S. E.,
ComasGarcía A.,
Noyola D. E.,
GarcíaSepúlveda C. A.
Publication year - 2016
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12271
Subject(s) - cytomegalovirus , immunology , human cytomegalovirus , population , biology , pregnancy , haplotype , antibody , immune system , virus , genotype , medicine , virology , gene , viral disease , herpesviridae , genetics , environmental health
Summary Human cytomegalovirus ( CMV ) represents an important public health concern as it is associated with severe morbidity and mortality in transplant recipients, HIV ‐infected individuals and pregnant women given the risk of congenital infection. Congenital CMV is a leading cause of neurological sequelae, developmental delay and birth defects worldwide. Cytomegalovirus can be transmitted to the foetus following maternal infection or reactivation. NK cells expressing killer‐cell immunoglobulin‐like receptors ( KIR ) are part of the innate immune system and the first line of defence against viral incursions. Previous reports have shown that KIR genes are associated with CMV infections in the post‐transplant setting. In this study, we set out to determine whether a protective effect of KIR genes over CMV infection is seen in Mexican pregnant women. Cytomegalovirus infection was assessed through nucleic acid testing in 200 pregnant women and 600 healthy blood donors comprising the Mexican mestizo reference population. Killer‐cell immunoglobulin‐like receptors and HLA ‐C genotypes were obtained from 200 pregnant women and 300 reference samples using a comprehensive PCR ‐ SSP approach. We observed statistically lower carrier frequencies of cB 03| tA 01 gene‐content haplotype, of cB 03 haplotype motif, of the KIR 2 DL 5 + 2 DS 3/2 DS 5 gene pair and of KIR 2 DL 5 amongst CMV ‐positive pregnant women in comparison with those CMV negative. None of these were associated with CMV status in the reference population. Logistic regression analysis revealed that the most important factor determining CMV status during third‐trimester pregnancies was the KIR 2 DL 5 + 2 DS 3/2 DS 5 gene pair ( OR 0.376 (95% CI 0.174, 0.811, P = 0.013). Our results indicate that CMV ‐protective KIR gene associations described in Caucasoid populations are also present in the genetically distinct Mexican mestizo population. Our results suggest that certain KIR gene combinations provide protection against CMV infections occurring during late‐term pregnancies, a finding of utmost epidemiological importance given its implication with congenital CMV infections.