TREM-1 Interacts with Rotavirus Proteins and Drives Inflammatory Responses: A Combined Experimental and Computational...

Area of Science:

• Virology
• Immunology
• Cell Biology

Background:

• Rotavirus (RV) is a major cause of diarrheal diseases (DDs) and mortality.
• The precise mechanisms of RV pathophysiology and host-virus interactions require further investigation.
• TREM-1 (triggering receptor expressed on myeloid cells 1) amplifies inflammatory responses in various diseases.

Purpose of the Study:

• To investigate the potential association between TREM-1 and rotavirus (RV) infection.
• To explore TREM-1's role in RV-induced inflammation and cellular effects.

Main Methods:

• Analysis of public transcriptomic data for TREM-1 expression in RV-infected subjects.
• In vitro infection of monocytes and MA104 cells with RV, with and without TREM-1 inhibitors.
• Measurement of IL-1β production and assessment of cytopathic effects.
• In silico simulations to predict interactions between TREM-1 and RV proteins.

Main Results:

• TREM-1 and associated genes were upregulated in RV-infected mice and children.
• TREM-1 inhibition significantly decreased IL-1β production in infected monocytes.
• TREM-1 inhibition reduced cytopathic effects in RV-infected MA104 cells.
• In silico analysis suggested interactions between TREM-1 and RV proteins VP5* and NSP4.

Conclusions:

• TREM-1 is implicated in rotavirus (RV) infection.
• TREM-1 acts as a mediator of inflammatory responses during RV infection.
• TREM-1 is involved in the host-virus relationship, potentially interacting with viral proteins.