Central nervous system alterations as sequelae of Venezuelan equine encephalitis virus infection in the rat
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Abstract:
Alterations of the Central Nervous System (CNS) in rats surviving acute infection with a virulent strain of Venezuelan Equine Encephalitis (VEE) virus were studied by light and electron microscopy. Cavitary necrosis of the cerebral cortex, macrophage activity and degenerative axonal changes were considered to be sequelae of the lesions induced during the acute phase of the infection. Mononuclear cell infiltrates of the neuropil, 3 mth after inoculation, were related to the immune response of the host. Focal lesions and mononuclear cell activity in the brain are thought to be the equivalent of the lesions induced in the CNS of humans during VEE virus infection. The findings are discussed in the light of recent reports of cerebral dysfunction occurring as a sequel of VEE virus infection in children.Keywords:
Neuropil
Summary Neuropil is a fundamental form of tissue organization within brains 1 . In neuropils, densely packed neurons synaptically interconnect into precise circuit architecture 2,3 , yet the structural and developmental principles governing nanoscale precision in bundled neuropil assembly remain largely unknown 4–6 . Here we use diffusion condensation, a coarse-graining clustering algorithm 7 , to identify nested circuit structures within the C. elegans cerebral neuropil (called the nerve ring). We determine that the nerve ring neuropil is organized into four tightly bundled strata composed of related behavioral circuits. We demonstrate that the stratified architecture of the neuropil is a geometrical representation of the functional segregation of sensory information and motor outputs, with specific sensory organs and muscle quadrants mapping onto particular neuropil strata. We identify groups of neurons with unique morphologies that integrate information across strata and that create a sophisticated honeycomb-shaped scaffold that encases the strata within the nerve ring. We resolve the developmental sequence leading to stratified neuropil organization through the integration of lineaging and cell tracking algorithms with high resolution light-sheet microscopy, and reveal principles of cell position, migration and hierarchical outgrowth that guide neuropil organization. Our results uncover conserved design principles underlying nerve ring neuropil architecture and function, and a pioneer neuron-based, temporal progression of outgrowth that guides the hierarchical development of the layered neuropil. Our findings provide a blueprint for using structural and developmental approaches to systematically understand neuropil organization within brains.
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Cyclophosphamide altered not only the pathological picture of virus encephalitis, but also enhanced the invasiveness of viruses and produced fatal forms of disease to which monkeys were otherwise resistant. Normal patas monkeys infected either i.c. or intranasally (i.n.) with louping ill developed clinical encephalitis from which they recovered, but when cyclophosphamide was administered the disease proved fatal. Normal rhesus monkeys inoculated i.n. with virulent western equine encephalitis virus developed neither clinical disease nor CNS lesions, but after treatment with cyclophosphamide they developed fatal encephalitis. The viruses of louping ill, Venezuelan equine encephalitis and Western equine encephalitis when given without an immunosuppressant usually gave rise to acute inflammatory CNS pathology, but when the monkeys were given cyclophosphamide, the inflammatory reaction was replaced by a degenerative process causing both neuronal necrosis and spongy degeneration.
Immunosuppression
Encephalitis Viruses
Viral encephalitis
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Abstract : The clinical observations of four human cases of infection with the Venezuelan equine encephalitis virus are described. The infections occurred in the laboratory. Venezuelan equine encephalitis virus was isolated from all four patients.
Encephalitis Viruses
Veterinary virology
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Alterations of the Central Nervous System (CNS) in rats surviving acute infection with a virulent strain of Venezuelan Equine Encephalitis (VEE) virus were studied by light and electron microscopy. Cavitary necrosis of the cerebral cortex, macrophage activity and degenerative axonal changes were considered to be sequelae of the lesions induced during the acute phase of the infection. Mononuclear cell infiltrates of the neuropil, 3 mth after inoculation, were related to the immune response of the host. Focal lesions and mononuclear cell activity in the brain are thought to be the equivalent of the lesions induced in the CNS of humans during VEE virus infection. The findings are discussed in the light of recent reports of cerebral dysfunction occurring as a sequel of VEE virus infection in children.
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The arthropod-borne encephalitides are an important cause of equine and human morbidity in the Americas. Between 1975 and 1978, 6970 human cases of arboviral encephalitis were reported in the United States of America; however, this represents only a fraction of the true incidence. St Louis encephalitis (4824 cases), California encephalitis (1035 cases), and western equine encephalitis (WEE, 947 cases) accounted for 98.5% of all reported infections. Approximately 1000-4000 cases of equine encephalitis occur annually in the United States, the majority due to WEE. In tropical America, important outbreaks of Venezuelan, eastern, and western equine encephalitis, and of Rocio encephalitis have occurred.In this article, epidemiological aspects of arboviral encephalitis outbreaks occurring within the past 5 years are reviewed. In addition, summaries of current research activities on the ecology and epidemiology of St Louis, western equine, Venezuelan equine, Rocio, and California encephalitis viruses are presented, and the problem of control of these infections is discussed.
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Early and sustained treatment with interleukin-12 (IL-12) ameliorated disease in a mouse model of infection with the encephalitogenic flavivirus, St. Louis encephalitis virus (SLEV, Japanese encephalitis serogroup). However, this effect was not reproduced in murine infections with either the flavivirus tick-bore encephalitis virus (TBEV) or the alphavirus Venezuelan equine encephalitis virus (VEEV). IL-12 exacerbated TBEV disease when used in conjunction with monoclonal antibody (mAb), suggesting an enhancement of immunopathology, and was without clinical effects in VEEV infection. These data confirm the need to fully understand the pathogenesis of viral infection before cytokine intervention may be employed as a broad-spectrum antiviral therapy.
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Tick-borne encephalitis
Togaviridae
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Clinical findings on Venezuelan Equine Encephalitis virus infection and the teratogenic effects of several Togaviruses are described. Similarities between the intrauterine alterations induced by Venezuelan Equine Encephalitis virus and rubella virus are pointed out. Findings described by Wenger in 1967 were those of massive cerebral necrosis in fetuses of women presumably suffering of encephalitis and they are commented along with the development of an animal experimental model at the end of 1970-1980. Pathogenesis of the intrauterine infection seemed to be related to changes in the placental vessels, vascular changes in the central nervous system were also described in rats surviving Venezuelan Equine Encephalitis experimental infection; similar changes were described in the brain of children with post rubella syndrome. The need for multidisciplinary studies in the endemic areas of Venezuelan Equine Encephalitis in order to detect sequelae of the viral effects in utero is emphasized. Finally, some experimental animal models are proposed to examine diverse aspects on intrauterine effect of Venezuelan Equine Encephalitis virus.
Pathogenesis
Viral encephalitis
Encephalitis Viruses
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Eastern equine encephalitis (EEE) and Venezuelan equine encephalitis (VEE) are associated with severe morbidity and mortality in equines and humans. In the U.S., EEE is both the least frequent and the most lethal of the principal arbovirus encephalitides.
To examine features of an outbreak of encephalitis in humans and horses in Darien, an eastern province of Panama, researchers identified 19 patients with encephalitis admitted to …
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Viral encephalitis
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Seventeen young boars were exposed to spontaneous infection with Japanese encephalitis virus (JEV). They manifested scrotal edema, which disappeared about 10 days later, a rise in HI antibody against JEV, two-peak pyrexia, and anorexia. Histopathological examination revealed subacute orchitis, epididymitis, funiculitis, and nonpurulent encephalitis.These changes were marked 1-5 days after the appearance of scrotal edema. Organization of the testis, low and insufficient spermatogenesis, and nonpurulent encephalitis were noticed over a period from 7 to 41 days after the appearance of scrotal edema.
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