SWINE TESTIS CELLS CONTAIN FUNCTIONAL HEPARAN-SULFATE BUT ARE DEFECTIVE IN ENTRY OF HERPES-SIMPLEX VIRUS

Herpes simplex virus (HSV) enters and infects mast cultured cells. We have found that swine testis cells (ST) produce yields of infectious H SV-1 up to four orders of magnitude lower than those of human embryoni c lung (HEL) and HEp-2 cells because of a defect in virus entry. For S T cells, virus binding is reduced, DNA from input virus cannot be dete cted, and virus proteins are not synthesized. Polyethylene glycol trea tment of ST cells after exposure to HSV allows viral entry, protein sy nthesis, and productive infection. Transfection of viral genomic DNA t hat bypasses the normal entry process produces similar yields of infec tious virus from ST, HEL, and HEp-2 cells. Therefore, all three cell l ines can support the HSV replicative cycle. Biochemical analyses and i nhibition of sulfation by sodium chlorate treatment show that ST cells contain amounts and types of heparan sulfate (HS) similar to those of highly susceptible cells. HSV infection of sodium chlorate-treated HE L and ST cells indicates the presence of a second, non-HS receptor(s) on susceptible HEp-2 and HEL cells that is missing, or not functional, on poorly susceptible ST cells. We conclude that ST cells are defecti ve in HSV entry, contain functional HS, but lack a functional non-HS r eceptor(s) required for efficient HSV-1 entry. Further, ST cells provi de a novel resource that can be used to identify, isolate, and charact erize an HSV nan-HS receptor(s) and its role in the entry and tropism of this important human pathogen.