Infection of a restrictive cell line (XC cells) by intratypic recombinants of HSV-1: Relationship between penetration of the virus and relative amounts of glycoprotein C

Expression of Immediate-Early Genes in Herpes Simplex Virus Type 1-infected XC Cells: Lack of ICP22 (68K) Polypeptide

“…Thus, it is possible that this type of penetration does not allow IE gene expression and that only the fraction of virus that enters the cells by fusion with cell membranes gives rise to the synthesis of virus RNA. This hypothesis is supported by the observation that promoting virus penetration by fusion with XC cell membranes, employing polyethylene glycol as a fusogen, greatly enhances the expression of HSV-1 in these cells (Epstein et al, 1984). On the other hand, different observations indicate that expression of IE genes is activated by a factor that is a virion component Hertz & Roizman, 1983).…”

“…Using this cell line, we have previously shown that variants of HSV-1 can be divided into two classes according to their penetration capacity (Epstein et al, 1984). When the virus penetrates, virus polypeptides are seen and are regulated in a cascade fashion as in permissive cells.…”

The difference in sensitivity to cicloxolone sodium between herpes simplex virus types 1 and 2 maps to the locations of genes UL22 (gH) and UL44 (gC)

“…Assuming that the sensitivity difference operates through the functioning of either the gC or gH equivalent HSV-2 locus, it is difficult to identify how the sensitivity determination operates in the light of what we know about the functioning of either glycoprotein, gC, which is a virion component, is dispensable and has been shown to be involved in several different functions, gC-I and gC-2 bind the C3b component of complement (McNearney et al, 1987;Seidel-Dugan et al, 1990) and thus may have a role in protecting virus from macrophage attack and/or in protecting infected cells from complement-mediated lysis, gC seems to have a role in modulating both HSV adsorption to cell surfaces and in virus penetration into cells; recent data from Langeland et al (1990) show that although gC is not strictly required for adsorption to the cell receptor(s), the gC-mutant gC-39 exhibits slower kinetics of adsorption compared to wild-type virus, implying that gC has a facilitating role in adsorption. De Luca et al (1982) and Epstein et al (1984) have shown that viruses having a low gC : gB ratio, or which lack gC entirely, have a faster rate of penetration, which suggests that gC has a modulating role in the penetration process.…”

Susceptibility to Herpes Simplex Virus Type 1 Infection of Non-permissive Rat XC(HPRT-) x Permissive Mouse L(TK-) Hybrid Cells

“…Cultures of these cells that have been infected with HSV-1 do not undergo massive cell lysis but continue to grow without producing infectious particles (Garfinkle & McAustan, 1973;Epstein & Jacquemont, 1983). It has recently been shown that penetration of HSV-1 into XC cells is abnormal, most particles entering the cells by pinocytosis instead of by fusion with plasma membranes (Epstein et al, 1980); however, penetration by fusion with host cell membranes may be enhanced by several means, including infection by particular HSV-1 strains and especially those having little or no glycoprotein C in their envelopes (Epstein & Jacquemont, 1983;Epstein et al, 1984), by producing stock virus in particular cell lines (Becker et al, 1974), or simply by promotion of fusion between the virus envelope and the plasma membrane of XC cells with polyethylene glycol (PEG) .…”