DIFFERENCES IN RESISTANCE TO HERPES-SIMPLEX VIRUS TYPE-1 (HSV-1) AMONG OLIGODENDROGLIA DERIVED FROM DIFFERENT STRAINS OF MICE ARE DETERMINED AFTER VIRAL ADSORPTION BUT PRIOR TO THE EXPRESSION OF IMMEDIATE-EARLY (IE) GENES

Citation
Ee. Thomas et al., DIFFERENCES IN RESISTANCE TO HERPES-SIMPLEX VIRUS TYPE-1 (HSV-1) AMONG OLIGODENDROGLIA DERIVED FROM DIFFERENT STRAINS OF MICE ARE DETERMINED AFTER VIRAL ADSORPTION BUT PRIOR TO THE EXPRESSION OF IMMEDIATE-EARLY (IE) GENES, Journal of neurovirology, 3(3), 1997, pp. 197-205
Citations number
35
Categorie Soggetti
Neurosciences,Virology
Journal title
ISSN journal
13550284
Volume
3
Issue
3
Year of publication
1997
Pages
197 - 205
Database
ISI
SICI code
1355-0284(1997)3:3<197:DIRTHV>2.0.ZU;2-7
Abstract
The nature of an innate cellular resistance to HSV-1 of cultured murin e oligodendrocytes (OLs) in three strains of mice (C57BL/6J, Balb/cByJ and A/J) was investigated. The expression of immediate early (ICP4), early (ICP8) and late (gC) antigens in primary OL cultures was studied using an indirect immunofluorescence (IF) technique. HSV-1 infected O Ls from C57BL/6J mice showed no viral antigens at 24 h post infection (p.i.) but rather a marked delay in antigen expression beginning at 60 h p.i. In contrast all three proteins were expressed in A/J OLs at 24 h p.i. while Balb/cByT OLs showed an intermediate protein expression pattern. These results suggest that the innate cellular resistance to HSV-1 is determined prior to the expression of immediate early viral a ntigens, To further study these differences, the adsorption capacity b etween the three mouse strains was compared using dextran purified, [H -3]thymidine labelled virus. No differences in HSV-1 adsorption were i dentified. Results from viral penetration studies approached statistic al significance suggesting that penetration may be impaired in C57BL/6 J and Balb/cByT OLs when compared to A/J OLs and is likely fusion inde pendent. The selective differences in HSV-1 resistance mediated by OLs , reflect differences in virus host cell interactions, that likely con tribute to differences in mortality, viral spread, and the ability of virus to induce central nervous system (CNS) demyelination.