Lack of detectable interaction between HSV-1 and integrins or tachykinins

Several viruses are known to utilize cellular integrin molecules to gain en try into cells. Because of the ability of herpes simplex virus type 1 (HSV- 1) to disrupt cellular adhesion, as seen particularly in ocular infections, we examined the ability of several peptides, containing known integrin rec ognition sequences, to interfere with plaque formation of HSV-1 in epitheli al cells. We also examined the possible involvement of tachykinins in virus entry. We did not detect any decrease in plaque formation by HSV-1 in the presence of Arg-Gly-Asp, Asp-Gly-Glu-Ala, or EILDV peptides or in the prese nce of monoclonal antibodies to the human beta 1 or beta 4 integrin subunit . Substance P or inhibitors of the NK1 or NK2 tachykinin receptors also had no inhibitory effects on HSV-1 plaque formation.