The isolation of syncytium-producing mutants of herpes simplex virus type 1 (KOS strain), which cause extensive cell fusion during otherwise normal
infections, has been reported previously (S. Person, R. W. Knowles, G. S. Read, S. C. Warner, and V. C. Bond, J. Virol. 17:183-190, 1976). Seven of these mutants, plus two syncytial strains obtained elsewhere, were used to compare the incorporation of labeled
galactose into neutral
glycolipids of mock-infected, wild-type-infected, and syncytially infected human embryonic lung cells. Five predominant cellular
glycolipid species were observed, denoted GL-1 through
GL-5 in order of increasing
oligosaccharide chain length; for example, GL-1 and
GL-2 correspond to
glycolipids that contain mono- and
disaccharide units, respectively. Wild-type
virus infection caused an increase in
galactose incorporation into GL-1 and
GL-2 relative to GL-3 through
GL-5. For a single labeling interval from 4 to 10 h after adsorption, syncytial
infections generally resulted in a relatively greater incorporation into more complex
glycolipids than did wild-type
infections. One mutant, syn 20, was compared with wild-type virus throughout
infection by using a series of shorter labeling pulses and appeared to delay by at least 2 h the alterations observed during wild-type
infections. These alterations are apparently due to defects in synthesis, since prelabeled cellular
glycolipids were not differentially degraded during mock or
virus infection.