Vimentin immunoreactivity was examined in brain tissues from non-neurological and various human central nervous system disease cases. In all brain tissues examined, vimentin immunoreactivity was intensely positive in ependymal cells and subpial tissues, and weakly positive in some capillaries and some white matter astrocytes. In affected areas of Alzheimer's disease (AD), Pick's disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and cerebral infarction cases, numerous intensely vimentin-immunopositive astrocytes of both protoplasmic and fibrous morphology were demonstrated. A few such astrocytes were also observed in Parkinson's disease and progressive supranuclear palsy. ALS, MS and infarction brains also had numerous, strongly vimentin-positive, round and fat-laden microglia/macrophages. In AD and ALS, a few reactive microglia with irregularly enlarged shapes were vimentin positive. In AD, they were almost exclusively related to senile plaques.

Rats were infected with herpes simplex virus type I (HSV-1) by corneal scarification. The spread of virus in the brain, the infiltration of leucocytes into infected areas, and the expression of major histocompatibility complex (MHC) glycoproteins by brain cells were assessed as a function of time by immunohistochemistry. Virus moved along neuronal pathways, achieving widespread distribution in the brain by days 8-10 when the illness appeared most severe. Granulocytes, T-lymphocytes, and monocytes infiltrated the tissue matrix at sites of infection. Microglial cells were induced to express MHC class I and class II glycoproteins. Reactive microglia near the sites of infection most vigorously expressed such glycoproteins. At the peak of the infection they were detectable on microglia throughout the brain, including areas apparently separated from active infection. Evidence of viral antigens, as well as microglial MHC expression, had largely disappeared by day 30. Neurons, astrocytes, and oligodendroglial cells failed to express MHC antigens.

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The immediate-early (IE) and early proteins induced by murine cytomegalovirus (Smith strain) in permissively infected 3T3-L1 murine fibroblasts were identified by SDS polyacrylamide gel electrophoresis. Ten proteins were classified as IE by their time of synthesis and by their synthesis in the presence of actinomycin D following reversal of a cycloheximide mediated protein synthesis block. By exclusion, seven proteins were classified as early class. Eleven of these proteins were precipitated by MCMV antiserum. The role of IE and early proteins in the replication of the virus was studied by infection of a murine macrophage cell line (J 774A.1) and human foreskin fibroblast (HFF) cells. The infections were characterized as nonpermissive by several criteria, including lack of production of infectious virus or viral DNA. However, the major IE and early MCMV proteins were detected in the nonpermissively infected cells. The block to virus replication in the macrophage and human fibroblast cells appeared to occur after the switch from IE to early protein synthesis, but before viral DNA replication.

No abstract