Herpes simplex virus (HSV) enters and infects most cultured cells. We have found that swine testis cells (ST) produce yields of infectious HSV-1 up to four orders of magnitude lower than those of human embryonic lung (HEL) and HEp-2 cells because of a defect in virus entry. For ST cells, virus binding is reduced, DNA from input virus cannot be detected, and virus proteins are not synthesized. Polyethylene glycol treatment of ST cells after exposure to HSV allows viral entry, protein synthesis, and productive infection. Transfection of viral genomic DNA that bypasses the normal entry process produces similar yields of infectious virus from ST, HEL, and HEp-2 cells. Therefore, all three cell lines can support the HSV replicative cycle. Biochemical analyses and inhibition 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 HEL 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 defective in HSV entry, contain functional HS, but lack a functional non-HS receptor(s) required for efficient HSV-1 entry. Further, ST cells provide a novel resource that can be used to identify, isolate, and characterize an HSV non-HS receptor(s) and its role in the entry and tropism of this important human pathogen
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