Infection with herps simplex type 1 induces expression of receptors for C3b on mammalian cells previously devoid of such receptors. We have shown that the isolated glycoprotein responsible for this activity (gC) is a potent modulator of complement-mediated cytolysis in vitro, acting by at least two mechanisms. We have also aided in the demonstration of relative complement resistance by cells infected with wild type HSV-1, as opposed to cells infected with gC-defective mutant strains. Future plans include direct binding studies of purified C3 fragments to HSV-1 gC and defined fragments thereof, as well as cells infected with other human herpesviruses. The role of gC as a blocker of infected cell interactions with cytotoxic lymphocytes will also be studied.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Intramural Research (Z01)
Project #
1Z01AI000469-01
Application #
3960633
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1986
Total Cost
Indirect Cost
Name
Niaid Extramural Activities
Department
Type
DUNS #
City
State
Country
United States
Zip Code