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Congenital Zika syndrome: Pitfalls in the placental barrier.
Rev Med Virol. 2018 09; 28(5):e1985.RM

Abstract

Much progress with respect to congenital Zika virus (ZIKV) pathogenesis has been achieved after the 2015 outbreak in Brazil. It is now accepted that ZIKV is vertically transmitted, infects cells of the developing central nervous system and the placenta, yet it is unclear to what extent placental affection contributes to the development of congenital ZIKV. The association between fulminant villitis and severe fetal involvement emerges as a possibility. ZIKV is unique among the Flaviviruses in its ability to be sexually transmitted, possibly responsible for its teratogenicity. Furthermore, there is controversy over the participation of antibody dependent enhancement (ADE) in patients with non-neutralizing anti-Flavivirus antibodies, a phenomenon previously recognized in serious DENV infections. Our aim was to analyze information regarding the contribution of the placental barrier as an actual player in neonatal ZIKV. Therefore, we underwent a systematic review with keywords "Zika virus" and "ZIKV". Articles were screened for relevance concerning the topics of microcephaly, transplacental transmission, sexual transmission, and ADE. We identified variables that affect the severity of congenital Zika syndrome: age of gestation at maternal infection, the extent of placental disruption (villitis), sexual transmission, initial viral replication at the uterine wall, anti-DENV antibodies, and the possibility of antibody-mediated transcytosis of ZIKV through the placenta. These questions may not seem relevant when Zika becomes endemic, and we are no longer witness to the extreme clinical sequelae seen when the virus moves through an immunologically naïve population; however, characterizing the pathogenesis of congenital Zika syndrome will continue to further our understanding.

Authors+Show Affiliations

International Program of Medicine, Universidad Autonoma de Guadalajara, Zapopan, Mexico.Immunology Research Laboratory, International Program of Medicine, Universidad Autónoma de Guadalajara, Zapopan, Mexico.Infectious Diseases Division, Hospital Dr. Angel Leaño, Universidad Autonoma de Guadalajara, Zapopan, Mexico.Immunology Research Laboratory, International Program of Medicine, Universidad Autónoma de Guadalajara, Zapopan, Mexico.

Pub Type(s)

Journal Article
Meta-Analysis
Review
Systematic Review

Language

eng

PubMed ID

29761581

Citation

Robinson, Nia, et al. "Congenital Zika Syndrome: Pitfalls in the Placental Barrier." Reviews in Medical Virology, vol. 28, no. 5, 2018, pp. e1985.
Robinson N, Mayorquin Galvan EE, Zavala Trujillo IG, et al. Congenital Zika syndrome: Pitfalls in the placental barrier. Rev Med Virol. 2018;28(5):e1985.
Robinson, N., Mayorquin Galvan, E. E., Zavala Trujillo, I. G., & Zavala-Cerna, M. G. (2018). Congenital Zika syndrome: Pitfalls in the placental barrier. Reviews in Medical Virology, 28(5), e1985. https://doi.org/10.1002/rmv.1985
Robinson N, et al. Congenital Zika Syndrome: Pitfalls in the Placental Barrier. Rev Med Virol. 2018;28(5):e1985. PubMed PMID: 29761581.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Congenital Zika syndrome: Pitfalls in the placental barrier. AU - Robinson,Nia, AU - Mayorquin Galvan,Evangelina E, AU - Zavala Trujillo,Isidro G, AU - Zavala-Cerna,Maria G, Y1 - 2018/05/15/ PY - 2018/01/30/received PY - 2018/04/11/revised PY - 2018/04/12/accepted PY - 2018/5/16/pubmed PY - 2018/11/28/medline PY - 2018/5/16/entrez KW - ZIKV KW - Zika virus KW - antibody dependent enhancement KW - congenital Zika syndrome KW - microcephaly KW - sexual transmission KW - transplacental transmission SP - e1985 EP - e1985 JF - Reviews in medical virology JO - Rev. Med. Virol. VL - 28 IS - 5 N2 - Much progress with respect to congenital Zika virus (ZIKV) pathogenesis has been achieved after the 2015 outbreak in Brazil. It is now accepted that ZIKV is vertically transmitted, infects cells of the developing central nervous system and the placenta, yet it is unclear to what extent placental affection contributes to the development of congenital ZIKV. The association between fulminant villitis and severe fetal involvement emerges as a possibility. ZIKV is unique among the Flaviviruses in its ability to be sexually transmitted, possibly responsible for its teratogenicity. Furthermore, there is controversy over the participation of antibody dependent enhancement (ADE) in patients with non-neutralizing anti-Flavivirus antibodies, a phenomenon previously recognized in serious DENV infections. Our aim was to analyze information regarding the contribution of the placental barrier as an actual player in neonatal ZIKV. Therefore, we underwent a systematic review with keywords "Zika virus" and "ZIKV". Articles were screened for relevance concerning the topics of microcephaly, transplacental transmission, sexual transmission, and ADE. We identified variables that affect the severity of congenital Zika syndrome: age of gestation at maternal infection, the extent of placental disruption (villitis), sexual transmission, initial viral replication at the uterine wall, anti-DENV antibodies, and the possibility of antibody-mediated transcytosis of ZIKV through the placenta. These questions may not seem relevant when Zika becomes endemic, and we are no longer witness to the extreme clinical sequelae seen when the virus moves through an immunologically naïve population; however, characterizing the pathogenesis of congenital Zika syndrome will continue to further our understanding. SN - 1099-1654 UR - https://www.unboundmedicine.com/medline/citation/29761581/Congenital_Zika_syndrome:_Pitfalls_in_the_placental_barrier_ L2 - https://doi.org/10.1002/rmv.1985 DB - PRIME DP - Unbound Medicine ER -