Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After intranasal inoculation, mouse hepatitis virus (MHV) gains entry into the central nervous system (CNS) via the olfactory and trigeminal nerves. Under the appropriate conditions, some mice develop clinically apparent demyelinating encephalomyelitis several weeks later, with virus always present in the spinal cord. To determine the pathway by which virus reaches the cord, brains and spinal cords of infected, asymptomatic mice were analyzed by in situ hybridization. Viral RNA was always detected in the anterior part of the upper spinal cord. A similar analysis of mice with the recent onset of hindlimb weakness showed that viral RNA was detected in the same location. The results suggest that MHV is transported to the spinal cord via well-defined neuroanatomic pathways and that viral amplification with resultant clinical disease occurs from this site of persistence in the anterior spinal cord. This process of viral amplification may involve the generation of viral variants as has been described for MHV-infected rats. No major changes in viral RNA or protein could be detected when MHV isolated from mice with hindlimb paralysis was analyzed. The data suggest that the generation of viral variants is not important in the pathogenesis of the late onset of neurological disease induced by MHV in mice.
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PMID:Identification of the spinal cord as a major site of persistence during chronic infection with a murine coronavirus. 215 80

An ozonization method was used to inactivate the viral pathogens of laboratory animals. Ozone at a concentration of over 100 ppm with high humidity was highly virucidal against 4 RNA viruses: HVJ, Theiler's murine encephalomyelitis virus (TMEV), Reo type 3 virus (RV) and murine hepatitis virus (MHV). For the ozone tests, 0.1 ml of a virus suspension in deionized water or saline and was placed in 35-mm dishes. The titer of 10(6) plaque-forming units of TMEV in a liquid-phase, which was highly stable against physical treatments, was reduced within 1 hr to a level of 0 by 300 ppm of ozone at 80% humidity and 22-25 degrees C. HVJ and MHV were more susceptible than TMEV to the ozone treatment. RV was the most resistant of the 4 viruses. The ozonization method may be a good way to disinfect not only for the laboratory animal RNA-viruses (both of enveloped and unenveloped viruses) but also animal rooms, clean rooms and even safety cabinets.
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PMID:Virucidal effect of ozone treatment of laboratory animal viruses. 216 30

Sixteen wild Peromyscus leucopus, trapped for the establishment of a breeding colony, developed signs of neurological damage (trembling, incoordination, circling, head tilt, and lameness of the rear legs) 2-47 days after capture in southern Wisconsin. Spirochetes were cultured from the brain of 5/11 mice, and Borrelia burgdorferi was cultured from 1 brain. A spirochete was isolated from the bladder of 1 mouse. The spirochete was identified by fluorescent antibody staining with the monoclonal antibody specific for B. burgdorferi, H5332. Serum antibodies to the spirochete were found in 14/15 mice. Negative results were obtained in all tests for viruses and bacteria, including Listeria (2/2), Mycoplasma (2/2), mouse hepatitis virus (10/10), Theilers's encephalomyelitis virus (GD VII) (8/8), REO 3 virus (2/2), and lymphocytic choriomeningitis virus (4/4). There was no bacterial growth from brains cultured on eosin methylene blue or blood agar (3/3). Histologic lesions included nonsuppurative cellular infiltrates in the brain, kidney, liver, and lung. Three outbred Swiss-Webster mice were inoculated orally with a suspension of the brain in BSKII medium, and 3 were inoculated with unpassed B. burgdorferi cultured from the brain of a P. leucopus with motor dysfunction. Five of the inoculated mice developed antibody titers of 1:128; one mouse was positive at 1:256. Motor signs of neurologic damage developed in 3/6 mice 2-24 weeks post-inoculation, and B. burgdorferi was detected in the brains of 2 mice by isolation and by fluorescent antibody.
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PMID:Systemic disease in Peromyscus leucopus associated with Borrelia burgdorferi infection. 231 94

The route of entry into the central nervous system (CNS) of most neurtropic viruses has not been established. The coronavirus, mouse hepatitis virus strain JHM (MHV-JHM), causes acute encephalomyelitis and acute and chronic demyelinating diseases and is an important model system for virus-induced neurological disease. Suckling C57BL/6 mice infected intranasally with MHV-JHM develop either the acute encephalomyelitis or a late onset, symptomatic demyelinating encephalomyelitis, depending on whether they are nursed by unimmunized or immunized dams. Analysis by in situ hybridization was used to determine the route of entry of MHV-JHM into the CNS in these mice. At early times, viral RNA was detected only in the trigeminal and olfactory nerves and in their immediate connections in all mice. A few days later, MHV-JHM RNA was found throughout the brain in mice dying of the acute encephalomyelitis, but remained confined to the entry sites in mice which did not develop acute disease. These results suggest that MHV-JHM enters the CNS via an interneuronal route in all mice, but that the presence of maternal antibody prevents the dissemination of virus via extracellular fluid. In addition, MHV-JHM may establish low-level persistence in the trigeminal or olfactory nerve or in one of its connections in mice that do not develop acute encephalomyelitis.
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PMID:Spread of a neurotropic murine coronavirus into the CNS via the trigeminal and olfactory nerves. 254 29

In the present report we provide the strain distribution patterns of susceptibility to acute mouse hepatitis virus type-4 (MHV-4) encephalomyelitis, acute experimental allergic encephalomyelitis (EAE) and vasoactive amine sensitivity (VAAS) for 9 (CXJ) recombinant-inbred strains between BALB/cKe (C) and SJL/J(J) mice. We confirm that susceptibility to MHV-4 is not linked to the H-2 complex, and that all strains susceptible to acute EAE have both a responder H-2 haplotype (H-2s or H-2d) and induced (B. pertussis) VAAS. In addition, we provide evidence that susceptibility to acute EAE induction is controlled by an additional presently unmapped locus and that an EAE-like histopathological disease does not usually follow MHV-4 infection intracerebrally in animals susceptible to MHV-4, acute EAE and induced VAAS.
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PMID:Host genetic regulation of acute MHV-4 viral encephalomyelitis and acute experimental autoimmune encephalomyelitis in (BALB/cKe x SJL/J) recombinant-inbred mice. 257 95

PL/J mice developed chronic relapsing experimental allergic encephalomyelitis (EAE) after receiving syngeneic guinea pig basic protein (GPBP)-immune lymph node cells or spleen cells which were cultured in the presence of GPBP or the encephalitogenic N-terminal peptide of GPBP. The presence of L3T4+ cells and in vitro proliferation in response to GPBP are required for the successful transfer. Pathologically, passively transferred EAE in the virus-free PL/J strain was characterized by an infiltration in the central nervous system by small lymphocytes, followed by the appearance of macrophages, and subsequently by primary demyelination. These findings were similar to those previously observed in chronic relapsing EAE in SJL/J mice. However, in some experiments pathologic examination of the spinal cord showed large demyelinating lesions which were necrotic and infiltrated with eosinophilic polymorphonuclear leukocytes. Sera from mice with this pathology contained antibodies to murine hepatitis virus and extensive search identified a few areas of coronavirus replication. The pathology of autoimmune mediated demyelination may be altered in the presence of coronavirus infection but the clinical pattern of EAE expression did not differ between virus-free and coronavirus-infected mice.
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PMID:Adoptively transferred acute and chronic relapsing autoimmune encephalomyelitis in the PL/J mouse and observations on altered pathology by intercurrent virus infection. 282 23

The JHM strain of murine hepatitis coronavirus is neurotropic in rats, causing either fatal acute encephalomyelitis or subacute demyelinating encephalomyelitis. We have examined the growth properties of three JHM virus isolates in primary rat glial cultures and found a correlation with their ability to cause disease. Wild type JHM virus has the propensity to cause lytic infections in glial cultures, and a temperature-sensitive mutant designated JHM-ts43 invariably produces persistent infections with reduced cytopathic effects (CPE) as compared to the wild type. Moreover, a non-neurotropic isolate, designated JHM-Pi virus, produces either non-productive persistent infections at low multiplicity of infection (m.o.i.) or productive persistent infections at high m.o.i., with, however, no CPE. The phenotypic expression of persistence is glial cell-dependent, since all three viruses produce similarly lytic infections when grown on various susceptible cell lines. The genetic basis of JHM virus persistence can be explained at the level of direct virus-glial cell interactions.
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PMID:Growth pattern of various JHM coronavirus isolates in primary rat glial cell cultures correlates with differing neurotropism in vivo. 283 45

Suckling C57BL/6 mice infected with mouse hepatitis virus strain JHM (MHV-JHM) develop either a fatal acute encephalomyelitis or a late onset demyelinating disease, depending on whether they are nursed by unimmunized or immunized dams. To determine the localization of virus-specific RNA, serial sections of brains from infected and uninfected mice were annealed with a 35S-labeled antisense RNA probe and analyzed by film autoradiography. In the mice with acute encephalomyelitis, viral RNA was present in the mesencephalon, hypothalamus, hippocampus, basal ganglia, subcortical white matter, and thalamus. Viral RNA was detected in the spinal cords of all mice with the late onset, demyelinating encephalomyelitis, but was distributed into three different patterns in the brains of these mice, even though all had the same clinical disease. In the first group, viral RNA was detected only in the brainstem. In the second group, viral RNA was detected in the brainstem, thalamus, and cerebral grey matter. This distribution was consistent with viral spread along well-defined tracts connecting these parts of the brain. In the third group, viral RNA could be detected both in the brainstem and in several white matter tracts within close physical proximity to the optic chiasm. This distribution was consistent with viral spread by an extracellular route from one white matter tract to other tracts which were physically close, but which were not part of the same pathways. These results suggest that MHV-JHM spreads through the central nervous system both along well-defined neuronal pathways and by spread from contiguous structures, but also suggest that viral replicates preferentially in a limited number of areas of the brain. The technique of in situ hybridization with film autoradiography should be generally useful for analyzing macroscopic movements of virus within infected organs.
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PMID:Regional localization of virus in the central nervous system of mice persistently infected with murine coronavirus JHM. 284 47

The presence of maternal antibodies protected suckling C57BL/6 mice from the clinical manifestations of the acute encephalomyelitis caused by mouse hepatitis virus, strain JHM (MHV-JHM), a coronavirus, even though histological evidence of encephalomyelitis was found at early times after inoculation. 100% of infected suckling mice developed a fatal disease in the absence of maternal antibody. By 14 days after inoculation, the brains of all antibody-protected mice examined were nearly normal on histological examination. At 3-8 weeks post-inoculation, approximately 40% of the antibody-protected mice developed a neurological disease characterized by hindlimb paralysis and wasting. Evidence of inflammation and demyelination was apparent in the spinal cord and brainstem. The mice that remained asymptomatic at this time showed few signs of inflammation and none developed clinical disease over the following 9 months. Viral antigen could be detected in most of the mice examined at all times after inoculation, whether symptomatic or not, and was particularly evident in the animals with hindlimb paralysis. MHV-JHM could be consistently cultured from the mice with hindlimb paralysis. These results show that maternal immune factors can completely protect susceptible mice from the acute, fatal, clinical encephalomyelitis caused by MHV-JHM, but cannot prevent the establishment of a latent state and subsequent development of virus-induced, clinically evident, demyelinating disease. This model will be useful for studying the virus and host factors important for the development of MHV-JHM latency and subsequent virus-induced demyelination.
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PMID:Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody. 285 74

Strains of the murine coronavirus mouse hepatitis virus type 4 (MHV-4) which contained a mutation in the E2 peplomer glycoprotein were obtained by selection for resistance to neutralization by monoclonal antibodies. Characterization of six variants representing two independent epitopes on E2, E2B and E2C, by in vitro neutralization and antibody-binding assays demonstrated that selection for an alteration in epitope E2B also resulted in changes in epitope E2C and vice versa. We observed a mutation frequency of approximately 10(-4.3) to 10(-4.6), which is consistent with the expected occurrence of single point mutations. The variant virus strains were attenuated with respect to neurovirulence when compared with wild-type MHV-4. Mice normally develop encephalomyelitis and die after wild-type MHV-4 infection. Mice receiving 2- to 3-log-higher doses of the variant strains survived and developed demyelinating disease. As the disease progressed, evidence of remyelination and ongoing demyelination was observed up to 65 days after infection. Virus reisolated 15 days after infection retained the variant phenotype. The data indicate that the E2 glycoprotein plays a central role in determining the cellular tropism and virulence of MHV-4 in the mouse.
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PMID:Site-specific alteration of murine hepatitis virus type 4 peplomer glycoprotein E2 results in reduced neurovirulence. 301 6


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