Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome
Zachary A Klase1, Svetlana Khakhina1, Adriano De Bernardi Schneider2
1Department of Biological Sciences, University of the Sciences, Philadelphia, Pennsylvania, 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.
Insights
Zika virus causes microcephaly in fetuses and Guillain-Barré syndrome in adults. This review compares Zika neuropathogenesis to TORCH infections, exploring flavivirus replication and cell susceptibility.
Area of Science:
- Virology
- Immunology
- Neuropathology
Background:
- The Zika virus epidemic is linked to severe fetal and adult neurological conditions.
- Understanding Zika's pathogenesis is crucial due to its emerging global health impact.
Purpose of the Study:
- To analyze Zika virus fetal neuropathogenesis using a comparative pathology approach.
- To contextualize Zika's effects by drawing parallels with TORCH infections.
- To summarize flavivirus cell susceptibility and replication mechanisms.
Main Methods:
- Comparative pathology analysis.
- Literature review of Zika virus and TORCH infections.
- Summary of flavivirus cell tropism and replication.
Main Results:
- Parallels between Zika and TORCH infections reveal common neuropathogenic themes.
- Specific cell susceptibilities to Zika and other flaviviruses are identified.
- Key molecular mechanisms of flavivirus replication are highlighted.
Conclusions:
- Comparative analysis provides insights into Zika's fetal neuropathogenesis.
- Understanding flavivirus replication is key to addressing Zika-associated pathology.
- Further research is needed to fully elucidate Zika's mechanisms.
