Maternal and child human leukocyte antigens in congenital cytomegalovirus infection. (April 2018)

• Record Type: Journal Article
• Authors: Rovito, Roberta; Claas, Frans H.J.; Haasnoot, Geert W.; Roelen, Dave L.; Kroes, Aloys C.M.; Vossen, Ann C.T.M.
• Is Part Of: Journal of reproductive immunology. Volume 126(2018)
• Page Start: 39
• Page End: 45
• Publication Date: 2018-04
• Subjects: cCMV congenital cytomegalovirus infection -- LTI long-term impairment -- DBS dried blood spot -- mm mismatches -- NIMAs non-inherited maternal antigens -- Ags antigens; Biomarkers -- cCMV -- Clinical outcome -- DBS -- Mother-child HLA; Reproduction -- Immunological aspects -- Periodicals; Immunology -- Periodicals; Allergy and Immunology -- Periodicals; Reproduction -- Periodicals; Reproduction -- Immunologie -- Périodiques; Immunologie -- Périodiques; Immunology; Reproduction -- Immunological aspects; Periodicals; Electronic journals; Electronic journals; 615.766
• DOI: 10.1016/j.jri.2018.01.002
• Languages: English
• ISSNs: 0165-0378

Abstract

Highlights: Maternal-child HLA during congenital CMV infection. Limitation in the use of maternal-neonatal HLA as prognostic markers for cCMV long-term outcome. HLA-DRB1*04 in the children correlates with a better viral control. HLA-B*51 in the children as a potential correlate for a better viral control. Abstract: Congenital Cytomegalovirus infection (cCMV) is the most common cause of congenital infections worldwide causing permanent long-term impairment (LTI). cCMV immunopathogenesis remains largely unknown due to the complex interplay between viral, maternal, placental and child factors. The aim of this study was to determine the possible role of particular HLA antigens, of the number of HLA mismatches (mm) and non-inherited maternal antigens (NIMAs) in a large retrospective nation-wide cohort of children with cCMV and their mothers. HLA Class I (HLA-A, HLA-B and HLA-C) and HLA Class II (HLA-DR and HLA-DQ) were assessed in 96 mother-child pairs in relation to a control group of 5604 Dutch blood donors, but no significant differences were observed. Next, although these HLA antigens could not be assessed in relation to symptoms at birth, nor to LTI, due to the low number of cases, they could be evaluated in relation to CMV viral load. HLA-DRB1*04, and potentially HLA-B*51, was shown to have a protective role in the children as its frequency was increased in the low viral load group compared to the high viral load group, and this remained significant after correction. The number of HLA mm and of NIMAs were not associated to symptoms at birth nor to LTI or viral load. In conclusion, although none of the HLA alleles could be put forward as prognostic marker for long-term outcome, our findings give useful insights into cCMV pathogenesis, and identify potential HLAs that correlate with a better viral control.