ArticlePathogens (Basel, Switzerland)2017
Zika Virus Persistently and Productively Infects Primary Adult Sensory Neurons In Vitro.
Article in Pathogens (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Saxitoxin potentiates human neuronal cell death induced by Zika virus while sparing neural progenitors and astrocytes.Scientific reports · 2024Article
- SARS-CoV-2 Rapidly Infects Peripheral Sensory and Autonomic Neurons, Contributing to Central Nervous System Neuroinvasion before Viremia.International journal of molecular sciences · 2024Article
- Virus as Teratogenic Agents.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Article
- Skeletal Muscle Is an Early Site of Zika Virus Replication and Injury, Which Impairs Myogenesis.Journal of virology · 2021Article
- Molecular mechanisms of zika virus pathogenesis: An update.The Indian journal of medical research · 2021Review
- The journey of Zika to the developing brain.Molecular biology reports · 2020Review
- Iminosugars With Endoplasmic Reticulum α-Glucosidase Inhibitor Activity Inhibit ZIKV Replication and Reverse CytopathogenicityFrontiers in microbiology · 2020Article
- Article
- Zika Virus Replication in Dorsal Root Ganglia Explants from Interferon Receptor1 Knockout Mice Causes Myelin Degeneration.Scientific reports · 2018Article
- Using immunocompromised mice to identify mechanisms of Zika virus transmission and pathogenesis.Immunology · 2018Review
- Autonomic dysfunction: a novel neurological phenotype associated with Zika virus infection?Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2018Article
- Autoimmune Neurological Conditions Associated With Zika Virus Infection.Frontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) has recently surged in human populations, causing an increase in congenital and Guillain-Barré syndromes. While sexual transmission and presence of ZIKV in urine, semen, vaginal secretions, and saliva have been established, the origin of persistent virus shedding into biological secretions is not clear. Using a primary adult murine neuronal culture model, we have determined that ZIKV persistently and productively infects sensory neurons of the trigeminal and dorsal root ganglia, which innervate glands and mucosa of the face and the genitourinary tract, respectively, without apparent injury. Autonomic neurons that innervate these regions are not permissive for infection. However, productive ZIKV infection of satellite glial cells that surround and support sensory and autonomic neurons in peripheral ganglia results in their destruction. Persistent infection of sensory neurons, without affecting their viability, provides a potential reservoir for viral shedding in biological secretions for extended periods of time after infection. Furthermore, viral destruction of satellite glial cells may contribute to the development of Guillain-Barré Syndrome via an alternative mechanism to the established autoimmune response.
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