EQUINE HERPESVIRUS-1 MUTANTS DEVOID OF GLYCOPROTEIN-B OR GLYCOPROTEIN-M ARE APATHOGENIC FOR MICE BUT INDUCE PROTECTION AGAINST CHALLENGE INFECTION

Equine herpesvirus 1 (EHV-1) mutants devoid of the open reading frames (ORFs) of either glycoprotein (g) B or M were constructed and tested for their immunogenic potential in a murine model of EHV-1 infection. The mutant viruses were engineered using the virulent EHV-I strain Rac L11 or the modified live vaccine strain RacH by inserting the Escheric hia coli LacZ gene into the viral ORFs. RacL11-infected mice showed si gns typical of an EHV-I infection, whereas mice infected with the EHV- 1 gB- or gM-negative mutants or with RacH did not develop disease. No difference in the pathogenic potential of RacL11 gB- and gM-negative v iruses was observed after application of either phenotypically complem ented or negative viruses. However, revertant RacL11 viruses in which the gB or gM gene had been restored caused EHV-l-related symptoms that were indistinguishable from those induced by RacL11. Mice that had be en immunized with phenotypically negative gB- and gM-deficient EHV-I w ere challenged with the RacL11 virus 25 days after immunization. Mock- immunized mice developed EHV-I disease and high virus loads in their l ungs were observed. In contrast, mice immunized with the mutant Viruse s did not exhibit El-IV-l-caused disease. It was concluded (i) that de letion of either gB or gM abolished the virulence of strain RacL11 and (ii) that immunization with gB- or gM-negative EHV-I elicited a prote ctive immunity that was reflected by both virus-neutralizing antibodie s and EHV-1-specific T-cells in spleens of immunized mice, (C) 1997 Ac ademic Press.