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PLoS Negl Trop Dis. 2016 Aug 25;10(8):e0004877. doi: 10.1371/journal.pntd.0004877. eCollection 2016 Aug.

Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome.

Author information

1
Department of Biological Sciences, University of the Sciences, Philadelphia, Pennsylvania, United States of America.
2
Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte, North Carolina, United States of America.
3
Department of Medicine, Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America.
4
Zika Foundation, College Station, Texas, United States of America.
5
Atheric Pharmaceutical, Scottsville, Virginia, United States of America.
6
Global Clinical Scholars Research Training Program, Harvard Medical School, Boston, Massachusetts, United States of America.

Abstract

The ongoing Zika virus epidemic in the Americas and the observed association with both fetal abnormalities (primary microcephaly) and adult autoimmune pathology (Guillain-Barré syndrome) has brought attention to this neglected pathogen. While initial case studies generated significant interest in the Zika virus outbreak, larger prospective epidemiology and basic virology studies examining the mechanisms of Zika viral infection and associated pathophysiology are only now starting to be published. In this review, we analyze Zika fetal neuropathogenesis from a comparative pathology perspective, using the historic metaphor of "TORCH" viral pathogenesis to provide context. By drawing parallels to other viral infections of the fetus, we identify common themes and mechanisms that may illuminate the observed pathology. The existing data on the susceptibility of various cells to both Zika and other flavivirus infections are summarized. Finally, we highlight relevant aspects of the known molecular mechanisms of flavivirus replication.

PMID:
27560129
PMCID:
PMC4999274
DOI:
10.1371/journal.pntd.0004877
[Indexed for MEDLINE]
Free PMC Article

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