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Journal of Neuroscience, Vol 13, 685-702, Copyright © 1993 by Society for Neuroscience
Spatiotemporal responses of astrocytes, ramified microglia, and brain macrophages to central neuronal infection with pseudorabies virus
L Rinaman, JP Card and LW Enquist
Medical College of Pennsylvania, Department of Anatomy and Neurobiology, Philadelphia 19129.
We examined the responses of astrocytes, ramified microglia, and brain
macrophages to CNS neuronal infection with virulent or attenuated strains
of a swine alpha herpesvirus (pseudorabies virus, PRV). After PRV
inoculation of the rat stomach or pancreas, the temporal course of viral
replication and induced pathology of infected neurons were assessed in the
dorsal motor nucleus of the vagus (DMV) and amygdala using an antiserum
generated against PRV. Specific monoclonal antibodies against glial
fibrillary acidic protein (GFAP), OX42, and ED1 and morphological criteria
were used to classify non-neuronal cells. Both PRV strains infected DMV and
motor neurons and then passed transneuronally to infect brainstem neurons
that innervate the DMV. However, the onset of neuronal infection produced
by the attenuated strain occurred approximately 20 hr later than infection
with the virulent strain. Animals infected with the attenuated strain also
survived longer, permitting transneuronal passage of virus into forebrain
areas of the visceral neuraxis. Neuronal infection with both PRV strains
produced consistent alterations in astrocytes, ramified microglia, and
brain macrophages that correlated spatially and temporally with progressive
stages of viral replication and neuronal pathology. Early stages of
infection were characterized by increases in immunoreactivity for
astrocytic GFAP and microglial OX42 that preceded overt signs of neuronal
pathology. At later stages, GFAP immunoreactivity decreased dramatically in
focal areas of neuronal infection while OX42 immunoreactivity continued to
increase. Subsequently, ED1-immunoreactive brain macrophages infiltrated
these infected areas. Double immunocytochemical labeling demonstrated that
some astrocytes and brain macrophages were immunopositive for viral
antigens but ramified microglia were not. The responses of glia and brain
macrophages are consistent with a proposed role in restricting
extracellular spread of virus by isolating or phagocytosing infected cells.
These phenomena may contribute to the specific transneuronal transport
exhibited by PRV.
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