The herpes simplex virus type I deamidase enhances propagation but is dispensable for retrograde axonal transport into the nervous system
| Autor: | Gregory A. Smith, Austin Stults |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Nervous system
0303 health sciences Innate immune system 030306 microbiology Effector viruses Viral tegument Biology medicine.disease_cause 3. Good health Cell biology 03 medical and health sciences Herpes simplex virus medicine.anatomical_structure Capsid Axoplasmic transport medicine Free nerve ending 030304 developmental biology |
| DOI: | 10.1101/704338 |
| Popis: | Upon replication in mucosal epithelia and transmission to nerve endings, capsids of herpes simplex virus type I (HSV-1) travel retrograde within axons to peripheral ganglia where life-long latent infections are established. A capsid-bound tegument protein, pUL37, is an essential effector of retrograde axonal transport and also houses a deamidase activity that antagonizes innate immune signaling. In this report, we examined whether the deamidase of HSV-1 pUL37 contributes to the neuroinvasive retrograde axonal transport mechanism. We conclude that neuroinvasion is enhanced by the deamidase, but the critical contribution of pUL37 to retrograde axonal transport functions independently of this activity.IMPORTANCEHerpes simplex virus type 1 invades the nervous system by entering nerve endings and sustaining long-distance retrograde axonal transport to reach neuronal nuclei in ganglia of the peripheral nervous system. The incoming viral particle carries a deamidase activity on its surface that antagonizes antiviral responses. We examined the contribution of the deamidase to the hallmark neuroinvasive property of this virus. |
| Databáze: | OpenAIRE |
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