Abstract
Herpes simplex virus type 1 is photosensitized by treatment with fluorescein isothiocyante (FITC). The inactivation of FITC-treated virions upon subsequent exposure to light is inhibited by the presence of sodium azide, suggesting the involvement of singlet oxygen in the process. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis revealed that treatment with FITC plus light induces crosslinks in viral envelope glycoproteins. Treatment of virions with high concentrations of FITC (50 micrograms/ml) plus light causes a reduction in the adsorption of the virus to monolayers of human embryonic lung cells. For lower concentrations of FITC (10 micrograms/ml) plus light, treated virions adsorb to the host cells, but remain sensitive to light until entry occurs. The loss of light sensitivity coincides with the development of resistance to antibodies. These results are most consistent with a mechanism of entry for herpes simplex virus involving fusion of the viral membrane with the plasma membrane of the host cell.
MeSH Terms
Cell Line
Cell Transformation, Viral/drug effects
Fluorescein-5-isothiocyanate
Fluoresceins/pharmacology
Humans
Kinetics
Light
Lung/embryology
Receptors, Virus/drug effects,metabolism
Simplexvirus/drug effects,metabolism
Thiocyanates/pharmacology
Virion/drug effects,metabolism
Chemicals
Fluoresceins
Receptors, Virus
Thiocyanates
Fluorescein-5-isothiocyanate
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
DeLuca N
Bzik D
Person S
Snipes W
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