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A METHOD FOR TREATING HCMV IN VASCULAR DISEASE

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R43AI051066-01
Agency Tracking Number: AI051066
Amount: $96,105.00
Phase: Phase I
Program: SBIR
Solicitation Topic Code: N/A
Solicitation Number: N/A
Timeline
Solicitation Year: N/A
Award Year: 2002
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
VIROGENOMICS, INC. 9020 SW WASHINGTON SQUARE RD, STE 140
TIGARD, OR 97223
United States
DUNS: N/A
HUBZone Owned: No
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 JAMES HICKS
 (503) 626-1144
 JIM.HICKS@VIROGENOMICS.COM
Business Contact
 JAMES KORFHAGE
Phone: (503) 626-1144
Email: JWKORFHAGE@AOL.COM
Research Institution
N/A
Abstract

Cardiovascular disease remains the most common cause of death in the United States. While atherosclerosis accounts for the majority of these deaths, other vasculopathies such as restenosis after
coronary angioplasty, and transplant vascular sclerosis (TVS), the hallmark
lesion of chronic solid organ graft rejection, cause significant morbidity and
mortality. Clinical studies have directly associated human cytomegalovirus
(HCMV) with the acceleration of TVS and vascular restenosis foliowing
angioplasty and there is anecdotal evidence for an association with
atherosclerosis. Recent work by Virogenomics' founding scientists has shown
that HCMV infection of arterial, but not venous, smooth muscle cells (SMC)
results in significant cellular migration in vitro. Migration was found to be
dependent on expression of one of the four HCMV encoded chemokine receptors,
US28, and the presence of the chemokines RANTES or MCP-1. Virogenomics is
testing the hypothesis that blocking the expression or function of US28 can
relieve the negative effects of HCMV on vascular disease. In this Phase I
application we propose to test the effect of antisense molecules on the
expression of US28 and its mouse cognate, m33, and furthermore, to test whether
antisense treatment can block SMC migration in vitro. The Phase II goals will
extend this antisense strategy into animal models and eventually to initiate a
drug discovery program to identify small molecules blocking US28 function, with
the ultimate goal of developing human therapeutics for the viral component of
vascular disease.

* Information listed above is at the time of submission. *

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