Whole-exome sequencing reveals insights into genetic susceptibility to Congenital Zika Syndrome.
Víctor BordaRonaldo S FranciscoJoseane B CarvalhoGuilherme L MoraisAtila Duque RossiPaula PezzutoGirlene S AzevedoBruno L Schamber-ReisElyzabeth Avvad PortariAdriana Suely de Oliveira MeloMaria Elisabeth Lopes MoreiraLetícia Cunha GuidaDaniela P CunhaLeonardo Henrique Ferreira GomesZilton Farias Meira de VasconcelosFabio Rueda FauczAmilcar TanuriConstantine A StratakisRenato Santana de AguiarCynthia Chester CardosoAna Tereza Ribeiro de VasconcelosPublished in: PLoS neglected tropical diseases (2021)
Congenital Zika Syndrome (CZS) is a critical illness with a wide range of severity caused by Zika virus (ZIKV) infection during pregnancy. Life-threatening neurodevelopmental dysfunctions are among the most common phenotypes observed in affected newborns. Risk factors that contribute to susceptibility and response to ZIKV infection may be related to the virus itself, the environment, and maternal genetic background. Nevertheless, the newborn's genetic contribution to the critical illness is still not elucidated. Here, we aimed to identify possible genetic variants as well as relevant biological pathways that might be associated with CZS phenotypes. For this purpose, we performed a whole-exome sequencing in 40 children born to women with confirmed exposure to ZIKV during pregnancy. We investigated the occurrence of rare harmful single-nucleotide variants (SNVs) possibly associated with inborn errors in genes ontologically related to CZS phenotypes. Moreover, an exome-wide association analysis was also performed using a case-control design (29 CZS cases and 11 controls), for both common and rare variants. Five out of the 29 CZS patients harbored known pathogenic variants likely to contribute to mild to severe manifestations observed. Approximately, 30% of affected individuals carried at least one pathogenic or likely pathogenic SNV in genes candidates to play a role in CZS. Our common variant association analysis detected a suggestive protective effect of the rs2076469 in DISP3 gene (p-value: 1.39 x 10-5). The IL12RB2 gene (p-value: 2.18x10-11) also showed an unusual distribution of nonsynonymous rare SNVs in control samples. Finally, genes harboring harmful variants are involved in processes related to CZS phenotypes such as neurological development and immunity. Therefore, both rare and common variations may be likely to contribute as the underlying genetic cause of CZS susceptibility. The variations and pathways identified in this study may also have implications for the development of therapeutic strategies in the future.
Keyphrases
- zika virus
- copy number
- genome wide
- dengue virus
- dna methylation
- aedes aegypti
- risk factors
- genome wide identification
- case control
- end stage renal disease
- pregnant women
- gestational age
- ejection fraction
- risk assessment
- genome wide analysis
- newly diagnosed
- bioinformatics analysis
- early onset
- case report
- young adults
- patient reported outcomes
- birth weight
- single molecule
- current status
- high resolution
- transcription factor
- peritoneal dialysis
- preterm birth
- blood brain barrier
- congenital heart disease