Submitted to: Veterinary Pathology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 1/11/2001
Publication Date: N/A
Citation: Interpretive Summary: Marek's disease (MD) is a disease of chickens caused by a herpesvirus. Many tissues are affected, but the progression of the disease in the brain has not been well studied. The brain is important because MD infection can cause temporary nervous symptoms known as transient paralysis. The present study describes the progression of the disease and infection in the brain at different times after infection. Viral antigens and DNA were detected. Two types of lesions were seen, an early inflammatory type and a later proliferative type. Each lesion type was composed of different classes of cells. Cell antigens associated with the major histocompatibility complex (MHC) increased or decreased during infection, depending on the antigen type. These findings provide needed information on the development of MD lesions in the brain and suggest new ways for diagnosis and control of the disease.
Technical Abstract: Marek s disease virus (MDV) infection in the brain was chronologically studied after inoculating 3 week-old chickens of two genetic lines with two strains of serotype 1 MDV representing two pathotypes (v and vv+). Viral replication in the brain was strongly associated with the development of lesions. Three viral antigens (pp38, gB and meq) were detected in the brain of infected birds. Marked differences between v and vv+ pathotypes of MDV were identified for level of virus replication, time course of brain lesions and expression of major histocompatibility complex (Mhc) antigens. Two lesion types (inflammatory and proliferative) occurred in the brain of birds inoculated with vv+MDV but only inflammatory lesions were observed in birds inoculated with vMDV. Inflammatory lesions, mainly composed by macrophages, T cell CD4+ and T cell CD8+, started at 6-10 dpi and were transient. Proliferative lesions, characterized by severe infiltrates of T cells CD4+CD8- (blast), started at 19-26 dpi and persisted. Expression of Mhc antigens in endothelial cells and infiltrating cells within the brain was influenced by MDV infection. Up-regulation of Mhc-II occurred in all treatment groups. Mhc-I was down-regulated only in those groups inoculated with vv+MDV.