Viral Immunology: Tripp Laboratory
- Home
- Who We Are
- Lab Overview
- Research Projects
- Facilities
- Publications
- Opportunities
- Tripp Lab in the News
- Links
- Lab Protocols
- Contact Us
Christine Oshansky
Office: (706) 583-8920
Lab: (706) 542-9862
Research Interests
Respiratory syncytial virus (RSV) is the most common cause of serious lower respiratory tract disease in infants and young children worldwide. Because RSV infection does not induce long-term immunity, reinfection occurs throughout life.
Our long term goal is to understand the mechanisms by which RSV evades the immune response to aid replication and/or establish persistent infection. The noticeable effects of RSV proteins on cytokine and chemokine expression during the immune response to infection suggest that RSV may modulate the host suppressor of cytokine signaling (SOCS) family of proteins. SOCS proteins are a class of proteins that include eight members SOCS1 to SOCS7 and CIS. SOCS proteins can bind to cytoplasmic portions of receptors and occupy docking sites for STATs and other proteins as well as target other substrates for proteasomal degradation. Because the RSV fusion (F) surface protein has been shown to interact with Toll-like receptor (TLR)-4 on the cell surface, the specific hypothesis of my research is that RSV mediates TLR induction of the host SOCS pathway to inhibit the antiviral type I interferon response to facilitate RSV replication.
Publications
- Tripp RA, Oshansky C, and Alvarez R. Cytokines and respiratory syncytial virus infection. Proc Am Thorac Soc. 2005;2(2):147-9. Review.
This page last updated March 10, 2010 .
