The 3A and 2B proteins from rhinovirus inhibit the secretory apparatus of the host cell. Rhinovirus is a major cause of respiratory problems in asthma patients, and the exacerbation of asthma by rhinovirus has been the subject of many clinical studies. Those studies reveal a correlation between the strain of virus used in the study and the conclusion drawn about the role of rhinovirus in asthma. My research will test the hypothesis that those rhinovirus strains which exacerbate asthma also fail to block protein secretion, allowing release of immune messengers and inflammation. I will use molecular genetics to test the 3A and 2B proteins from several rhinovirus strains for secretory inhibition. I will then isolate secretion-permissive alleles of 3A and/or 2B, and test them in the context of the parent viruses using reporter proteins for secretory function as well as functional assays testing cellular transport of immune messengers in rhinovirus-infected cells.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32HL067557-03
Application #
6638786
Study Section
Virology Study Section (VR)
Program Officer
Rothgeb, Ann E
Project Start
2002-06-01
Project End
Budget Start
2003-06-01
Budget End
2004-05-31
Support Year
3
Fiscal Year
2003
Total Cost
$48,148
Indirect Cost
Name
Stanford University
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
009214214
City
Stanford
State
CA
Country
United States
Zip Code
94305
Kuo, Lydia E; Zukowska, Zofia (2007) Stress, NPY and vascular remodeling: Implications for stress-related diseases. Peptides 28:435-40