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All rights reserved. All trademarks displayed on this web site are the exclusive property of the respective holders. Rotbart HA. Viral meningitis. Semin Neurol. Epidemic central nervous system disease of mixed enterovirus etiology. Analysis of laboratory investigations. Am J Hyg. Nonpolio enterovirus and human parechovirus surveillance United States, Aseptic meningitis in children: analysis of cases.

Epidemiological aspects of a St. Louis encephalitis outbreak in Harris County, Texas, J Infect Dis. Balfour HH, Jr. California arbovirus La Crosse infections. Clinical and laboratory findings in 66 children with meningoencephalitis.

California serogroup viruses in New York State: the role of subtypes in human infections. Am J Trop Med Hyg. Colorado tick fever: clinical, epidemiologic, and laboratory aspects of cases in Colorado in Ann Intern Med. Bang HO, Bang J. Involvement of the Central Nervous System in Mumps. Acta Med Scand. An unusual form of lymphocytic choriomeningitis. Arch Neuro Psychiatr. Herpesvirus infections of the human central nervous system. N Engl J Med. Herpes simplex virus type 1 meningitis. Pediatr Infect Dis J.

Hollander H, Stringari S. Human immunodeficiency virus-associated meningitis. Clinical course and correlations. Am J Med. Infect Dis Clin Prac. Echoviruses are a major cause of aseptic meningitis in infants and young children in Kuwait. Virol J. Romero JR. Pediatric group B coxsackievirus infections. Curr Top Microbiol Immunol.

Choriomeningitis and myocarditis in an adolescent with isolation of coxsackie B-5 virus. Am J Clin Pathol. Evidence for cytotoxic T-lymphocyte-target cell interaction in brains of mice infected intracerebrally with lymphocytic choriomeningitis virus.

Acta Neuropathol Berl ; 61 — Myelomonocytic cell recruitment causes fatal CNS vascular injury during acute viral meningitis. This intravital imaging study provided the first data showing that cytotoxic lymphocytes can promote synchronous extravasaton of myelomonocytic cells that damage meningeal blood vessels, contributing to fatal edema during LCMV meningitis. Migration of cytotoxic lymphocytes in cell cycle permits local MHC I-dependent control of division at sites of viral infection.

J Exp Med. This study provided the first data showing that antiviral cytotoxic lymphocytes can migrate through the blood in active stages of cell cycle and undergo cytokinesis upon arrival in the virally infected meninges. Aseptic meningitis caused by the lymphocytic choriomeningitis virus. Clin Neurol Neurosurg. Emerg Infect Dis. Lymphocytic choriomeningitis virus infection in organ transplant recipients--Massachusetts, Rhode Island, Lymphocytic choriomeningitis infection of the central nervous system.

Front Biosci. Nat Immunol. This study demonstrated that antiviral cytotoxic lymphocytes form immunological synapses with infected targets in the virally infected meninges and can engage up to three targets simultaneously to improve killing efficiency.

Type I interferon programs innate myeloid dynamics and gene expression in the virally infected nervous system. PLoS Pathog. Type I interferon was determined in this paper to be responsible for all innate immune gene expression and immune cell dynamics in the brain following infection with LCMV. Functional role of type I and type II interferons in antiviral defense. This study used genetic knockout mice to demonstrate that type I and type II interferons are both required for antiviral immunity.

J Immunol. Aylward B, Yamada T. The polio endgame. The distribution of inflammation and virus in human enterovirus 71 encephalomyelitis suggests possible viral spread by neural pathways. J Neuropathol Exp Neurol. Neurologic complications in children with enterovirus 71 infection. Acute neurologic illness of unknown etiology in children - colorado, august-september Greenlee JE. The equine encephalitides. Differential localization of neurons susceptible to enterovirus 71 and poliovirus type 1 in the central nervous system of cynomolgus monkeys after intravenous inoculation.

J Gen Virol. Infection with enterovirus 71 or expression of its 2A protease induces apoptotic cell death. Induction of apoptosis by Sindbis virus occurs at cell entry and does not require virus replication. Inflammation is a component of neurodegeneration in response to Venezuelan equine encephalitis virus infection in mice. J Neuroimmunol. Sindbis virus-induced neuronal death is both necrotic and apoptotic and is ameliorated by N-methyl-D-aspartate receptor antagonists.

Using NMDA receptor antagonists, the authors of this study demonstrated that virus-induced death of cortical neurons is mediated by glutamate excitotoxicity. Coxsackievirus targets proliferating neuronal progenitor cells in the neonatal CNS. This study demonstrated how coxsackievirus B3 seeds the neonatal brain by infecting neuroprogenitor cells, which then migrate along the rostral migratory stream.

Pathogenesis of flavivirus encephalitis. Fatal fulminant pan-meningo-polioencephalitis due to West Nile virus. Brain Pathol. Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis.

A preliminary neuropathological study of Japanese encephalitis in humans and a mouse model. Lindquist L. Tick-borne encephalitis. Toll-like receptor 3 has a protective role against West Nile virus infection. Caspase 3-dependent cell death of neurons contributes to the pathogenesis of West Nile virus encephalitis.

The mechanism of cell death during West Nile virus infection is dependent on initial infectious dose. J Neuroinflammation. Interleukin-1 and tumor necrosis factor-alpha synergistically mediate neurotoxicity: involvement of nitric oxide and of N-methyl-D-aspartate receptors.

Brain Behav Immun. Japanese encephalitis virus-infected macrophages induce neuronal death. J Neuroimmune Pharmacol. Nitric oxide and viral infection: NO antiviral activity against a flavivirus in vitro, and evidence for contribution to pathogenesis in experimental infection in vivo.

Mishra MK, Basu A. Minocycline neuroprotects, reduces microglial activation, inhibits caspase 3 induction, and viral replication following Japanese encephalitis.

J Neurochem. Transmission of West Nile virus from an organ donor to four transplant recipients. Central nervous system HIV-1 infection. Early viral brain invasion in iatrogenic human immunodeficiency virus infection. Immunol Rev. Macrophage entry mediated by HIV Envs from brain and lymphoid tissues is determined by the capacity to use low CD4 levels and overall efficiency of fusion.

Intercompartmental recombination of HIV-1 contributes to env intrahost diversity and modulates viral tropism and sensitivity to entry inhibitors. Genetic analyses of HIV-1 from different tissues revealed that intercompartmental recombination leads to viral diversity and phenotypic changes within a single host.

Neuronal loss in the frontal cortex in HIV infection. Bagashev A, Sawaya BE. HIV-1 coat protein neurotoxicity prevented by calcium channel antagonists. This study demonstrated that HIV-1 gp protein induces neurotoxicity by increasing intracellular calcium levels.

Kaul M, Lipton SA. Chemokines and activated macrophages in HIV gpinduced neuronal apoptosis. Pathways to neuronal injury and apoptosis in HIV-associated dementia. Human immunodeficiency virus type 1 RNA Levels in different regions of human brain: quantification using real-time reverse transcriptase-polymerase chain reaction.

Astrocyte infection by HIV mechanisms of restricted virus replication, and role in the pathogenesis of HIVassociated dementia.

Curr HIV Res. Molecular detection of rabies encephalitis and correlation with cytokine expression. Mod Pathol. Murphy FA. Rabies pathogenesis. Arch Virol. Suppression of cell-mediated immunity by street rabies virus.

Differential effects of rabies and borna disease viruses on immediate-early- and late-response gene expression in brain tissues. Tsiang H. Neuronal function impairment in rabies-infected rat brain.



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