Role of T-cells, virus neutralising antibodies and complement-mediated antibody lysis in the immune response against equine herpesvirus type-1 (EHV-1) infection of C3H (H-2k) and BALB/c (H-2d) mice.
The suitability of C3H (H-2k) and BALB/c (H-2d) mice for use as small animal models to study immunity to EHV-1 was assessed. An in vitro T cell response mediated by both CD4+ and CD8+ T cells was detected both during the acute phase of infection and after challenge with a second dose of EHV-1 at two months in lymphocyte populations taken from the spleens of both types of mouse. The responses were apparent until at least 61 days after the primary inoculation. After challenge, T cells from mice previously infected with EHV-1 responded by as early as day 3 after infection and higher levels of T cell proliferation were reached than in mice undergoing a primary infection. Immunological cross-reactivity with the closely related virus, EHV-4 was detected and some activity against herpes simplex virus type-1 (HSV-1) was observed during the acute phase of infection. T cell responses were detected in the draining cervical lymph nodes but not in the inguinal lymph nodes of the mice and these were the primary sites of T cell activation. Complement-dependent virus neutralising antibodies were present by day 8 after infection. These antibodies were also able to lyse EHV-1 infected target cells in vitro. Complement-independent virus neutralising antibodies were found before challenge only in C3H mice. The clinical signs and duration of virus shedding were reduced after challenge. The time course of the appearance of the different immune effector mechanisms is discussed in relation to the clearance of virus from the infected mice. The results suggest that C3H mice provide a better model in which to study potential vaccine candidates against EHV-1 infections of the horse than BALB/c mice.
Alber
D G
DG
Department of Microbiology, University of Leeds.
Greensill
J
J
Killington
R A
RA
Stokes
A
A
D000818:Animals; D000914:Antibodies, Viral / Q000276:immunology*; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D003165:Complement System Proteins / Q000276:immunology; D004195:Disease Models, Animal; D006566:Herpesviridae Infections / Q000276:immunology / Q000517:prevention & control / Q000662:veterinary*; D004861:Herpesvirus 1, Equid / Q000276:immunology*; D006734:Horse Diseases / Q000276:immunology* / Q000517:prevention & control; D006736:Horses; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D018139:Simplexvirus / Q000276:immunology; D013154:Spleen / Q000166:cytology / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors
D000914:Antibodies, Viral; D015704:CD4 Antigens; D016827:CD8 Antigens; D003165:Complement System Proteins