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)

Abstract

Cicloxolone sodium (CCX) is a broad spectrum antiviral agent which has a largely non-specific and complex mode of antiviral action. However, the experimental finding that herpes simplex virus type 2 (HSV-2) (strain HG52) is consistently more sensitive to inhibition by CCX than HSV-1 (ll7syn ÷) additionally implies the specific involvement of HSV genes. HSV-1/ HSV-2 intertypic recombinants have been utilized to investigate this genetic difference by comparing their CCX EDso concentrations. No short stretch of HSV-2 DNA was associated with its greater sensitivity to CCX, implying that two or more non-contiguously located HSV genes are involved. Correlating CCX sensitivity with recombinant virus genome structures allowed separate evaluation of the gene regions encoding glycoproteins gB, gC, gD, gE, gG, gH and gI and this suggests that the gene locations encoding gH and gC determine the CCX sensitivity difference. The selective inhibitor of Golgi apparatus glycosylation, monensin, gave results analogous to those obtained with CCX.

Factors influencing the interaction of herpes simplex virus glycoprotein C with the third component of complement

“…The characteristics of the intertypic recombinants BX1 (28-1-19), FX9(5-8), RH6, R-12-3 and R-t2-5 derived from the parental strains 17 syn + (HSV-1) and HG52 (HSV-2) have been described elsewhere [23,29,5]. We are grateful to Prof. Subak-Sharpe, University of Glasgow, U.K., for supplying these recombinants.…”

“…Pretreatment of EAC with anti C3 rabbit anfisera (3). Untreated cells incubated with EAC at room temperature (4) and on ice (5). Incubation in the presence of 100 gg/ml dextran sulfate 5,000 (6), heparin (7), or neomycin (8), respectively…”