- Title Information
- Title
- Gut Pathogen Replication in the Absence of NINJ and Gasdermin-Mediated Plasma Membrane Rupture
- Type of Resource (primo)
- dissertations
- Name:
Personal
- Name Part
- Zhou, Bingyue
- Role
- Role Term:
Text
- creator
- Name:
Personal
- Name Part
- Beura, Lalit
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Crego, Adam
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Lee, Sanghyun
- Role
- Role Term:
Text
- Advisor
- Name:
Corporate
- Name Part
- Brown University. Biology and Medicine: Biotechnology
- Role
- Role Term:
Text
- sponsor
- Origin Information
- Copyright Date
- 2026
- Physical Description
- Extent
- , None p.
- digitalOrigin
- born digital
- Note:
thesis
- Thesis (Sc. M.)--Brown University, 2026
- Genre (aat)
- theses
- Abstract
- This thesis investigates the in vivo role of plasma membrane rupture effectors including NINJ1, NINJ2, GSDMD, and GSDME in regulating enteric viral infection using genetically engineered mouse models with tissue-specific and systemic knockouts. While prior studies have implicated these proteins in lytic cell death and host–pathogen interactions, their functional significance during gut infection remained unclear. To address this question, knockout and control mice were orally infected with rotavirus, murine astrovirus, or murine norovirus, and viral replication was measured through fecal viral shedding using qRT-PCR. Across all three viral models, loss of these plasma membrane rupture effectors did not significantly alter viral burden, replication kinetics, or persistence compared to wild-type controls, regardless of whether gene deletion was restricted to intestinal epithelial cells or occurred systemically. These findings demonstrate that the ninjurin and gasdermin families are largely dispensable for productive enteric viral infection under the conditions examined. Overall, this study provides new insight into the complexity of host–virus interactions in vivo and suggests that plasma membrane rupture machinery may play more nuanced or context-dependent roles in infection, potentially influencing inflammatory responses rather than directly controlling viral replication.
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00968006")
- Topic
- Immunology
- Language
- Language Term (ISO639-2B)
- English
- Record Information
- Record Content Source (marcorg)
- RPB
- Record Creation Date
(encoding="iso8601")
- 20260516