ISGylation during Human Parainfluenza Virus Type 3 Infection

---

Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B582
Abstract ID: 5207

Presenting Author:
Lindsay G Miller , Graduate Student at Washington State Univ.

Abstract:

Human parainfluenza virus type 3 (HPIV3) causes lower respiratory illnesses such as pneumonia or bronchiolitis in infants, young children, and the immunocompromised. HPIV3 associated airway inflammatory diseases manifest as a result of host mediated exaggerated inflammatory response, though limited knowledge exists regarding HPIV3-host interactions. ISGylation is a ubiquitin- like modification that plays a role in controlling various aspects of virus infections and is the process by which Interferon stimulated gene 15 (ISG15) is conjugated to target proteins by ubiquitin-like conjugating enzymes. Several respiratory viruses induce ISGylation, and this event has been shown to modulate virus-host interaction, typically leading to a restriction in viral replication. Because of its antiviral property, some viruses possess proteins which restrict ISGylation. So far, the role of ISGylation during HPIV3 infection has not been established, and as such, no HPIV3 viral protein has been identified in regulating ISGylation. We show that HPIV3 can induce ISGylation in both myeloid immune (macrophages) and non-myeloid stromal (epithelial cells) cells. Our studies also show HPIV3 encoded non-structural C protein inducing ISGylation in cells expressing the C protein.  The role of ISGylation during HPIV3 infection and the mechanism by which viral C protein induces ISGylation will be discussed.