Presenter(s)

Malabika Bhowmik, Tooba Shafeeque Ahmed Momin

Comments

Presentation: 1:15-2:30, Kennedy Union Ballroom

Download

Download Project (858 KB)

Description

Title: ZFP36L1 suppresses Rotavirus and Norovirus replication, moderates the virus-induced hyperinflammation and suppresses host cell damage.Malabika Bhowmik, Tooba MominPrimary Advisor: Mrigendra RajputDepartment of Biology, University of Dayton, Dayton, Ohio, USA 45469 Most acute viral infections cause damage in the host body either directly when the virus hijacks the host cell machinery, changes cell physiology, causes cell death by viral proteins, or indirectly by hyperinflammation. Zinc finger proteins (ZFP) are one of the highly abundant proteins in eukaryotes. Due to their distinctive structure, ZFPs bind with different cellular components such as DNA, RNA, lipids, or other proteins. A specific type of ZFP, ZFP36L1, belongs to the CCCH-type ZFP, which has been identified as a regulator of RNA metabolism. It is known to control the overall turnover of cellular mRNA including mRNA of cytokine mediators and cytokines by breaking it down through poly A tail using the deadenylation mechanism. The current study was designed to investigate the role of ZFP36L1 on virus replication and moderating virus-induced inflammation. Our results showed that stable overexpression of ZFP36L1 through lentivirus transduction significantly reduces Rotavirus and Norovirus titre as well as it moderated virus-induced proinflammatory cytokines like IFN-α and TNF-α with reduced virus-induced cytopathic effect in cells. While knockdown of ZFP36L1 significantly enhanced viral titre, virus-induced cytokines with more cytopathic effect. Our results also showed that ZFP36L1 overexpression does not affect macrophage (RAW 264.7) migration as compared to control while knockdown of ZFP36L1 significantly enhanced the macrophage migration in trans-wells. Overall, our study showed that overexpression of ZFP36L1 suppresses the virus (Rotavirus and Norovirus) replication and moderates the virus-induced hyperinflammation and thus mitigates virus-induced damage in the host.

Publication Date

4-17-2024

Project Designation

Graduate Research

Primary Advisor

Mrigendra Rajput

Primary Advisor's Department

Biology

Keywords

Stander Symposium, College of Arts and Sciences

Institutional Learning Goals

Scholarship

ZFP36L1 suppresses Rotavirus and Norovirus replication, moderates the virus-induced hyperinflammation and suppresses host cell damage.

Share

COinS