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Complement receptor 3 promotes severe ross river virus-induced disease.

Thomas E Morrison¹, Jason D Simmons, Mark T Heise

¹The Carolina Vaccine Institute, University of North Carolina at Chapel Hill, 9024 Burnett Womack, CB #7292, Manning Drive, Chapel Hill, NC 27599. heisem@med.unc.edu.

Journal of Virology

|September 13, 2008

Summary

Complement receptor 3 (CR3) deficiency reduces tissue damage in alphavirus infections like Ross River virus (RRV). This suggests CR3 signaling exacerbates inflammatory arthritis and myositis severity.

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Published on: September 13, 2018

Area of Science:

Immunology
Virology
Molecular Biology

Background:

Alphaviruses, such as Ross River virus (RRV), cause widespread inflammatory arthritis and myositis.
Complement component 3 (C3) is implicated in the destructive phase of RRV-induced disease.
Complement receptor 3 (CR3) is a signaling receptor activated by C3 fragments.

Purpose of the Study:

To investigate the role of CR3 in the pathogenesis of RRV-induced inflammatory disease.
To determine if CR3 deficiency impacts viral replication, cellular infiltration, or disease severity.

Main Methods:

Utilized a mouse model of RRV infection.
Compared disease signs, tissue destruction, viral replication, and cellular infiltrates in wild-type and CR3-deficient (CD11b(-/-)) mice.
Assessed the expression of inflammatory mediators in inflamed tissues.

Main Results:

CR3-deficient mice exhibited less severe disease signs and reduced tissue destruction compared to wild-type mice.
CR3 deficiency did not affect viral replication or the recruitment of immune cells to inflamed sites.
Genetic absence of CR3 led to diminished expression of proinflammatory and cytotoxic effectors, including S100A9/S100A8 and interleukin-6.

Conclusions:

CR3 signaling at inflammatory sites contributes to tissue damage and disease severity in RRV infection.
Targeting CR3-dependent pathways may offer therapeutic strategies for alphavirus-induced inflammatory conditions.