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Query: UMLS:C0014070 (
encephalomyelitis
)
13,017
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
If rabbits were given total body irradiation and infected wih vaccinia virus (strain Elstree) a severe disease developed with a
viraemia
lasting up to 12 days. The clearance of the virus from the peripheral blood was severely impaired by x-ray doses above 800 R. The attenuated vaccinia virus strain MV did not turn virulent, if it was injected to irradiated rabbits. With caution it can be assumed that live vaccines, containing attenuated viruses, may be given to immunosuppressed persons. Rats are not susceptible to ectromelia-virus (mouse-poxvirus); overt clinical sympatoms, however, with a mortality of 30 per cent developed in irradiated rats. This proofs that specific poxviruses can be transferred to another species. As the experimental conditions are unnatural, this may occur only rarely in immunosuppressed persons. After intracerebral infection of Balb-C-mice with low doses of vaccinia virus two types of infection were seen: 1. a severe cytocidal infection of leptomeninges, chorioid plexus and vessels; 2. a noncytocidal, latent infection of glial cells and neurons. Several animals developed a picture resembling experimental allergic
encephalomyelitis
. It seems that irradiation altered the antigenic conditions of the cytoplasmic membranes in non-cytocidally infected cells. The model might explain some processes in the pathogenesis of demylinating diseases.
...
PMID:Studies on poxvirus infections in irradiated animals. 625 May 14
Invasion sites of avian
encephalomyelitis
virus in the internal organs of orally infected chicks were determined by the immunofluorescent method. The invasion began when the epithelium tunica mucosae of the duodenum (together with the proventriculus, jejunum, or cecum in certain birds killed at postinoculation day 1) became test-positive.
Viremia
persisted for more than 5 days in the early stage of infection, then the pancreas was rapidly infected, followed by the liver, kidney, and spleen. Subsequently, the virus spread to the CNS. Rapid infection of the duodenum and pancreas was clearly observable.
...
PMID:Invasion of avian encephalomyelitis virus from the gastrointestinal tract to the central nervous system in young chickens. 630 18
Akabane virus, an arthropod-borne Bunyavirus, is the major cause of epizootics of congenital malformations in ruminants in Australia, Japan, Korea, and Israel, and is suspected to be a cause of sporadic outbreaks elsewhere. Blood-sucking insects, such as biting midges, transmit the virus horizontally to vertebrates. Climatic factors influence the seasonal activity and geographic range of the vector population and, therefore, occurrence of related disease. Inoculated ruminants seroconvert rapidly after a short subclinical
viremia
. Infection is of consequence only if ruminants are pregnant and not protected by adequate specific neutralizing antibodies. In naive pregnant animals, virus may spread hematogenously to replicate and persist in trophoblastic cells of placental cotyledons and subsequently invade the fetus. A distinct tropism for immature rapidly dividing cells of the fetal central nervous system and skeletal muscle results in direct virus-induced necrotizing
encephalomyelitis
and polymyositis. If fetuses survive, such injury may manifest as arthrogryposis, hydranencephaly, porencephaly, microencephaly, hydrocephalus, or
encephalomyelitis
at term. The earlier in gestation that fetal infection occurs, the more severe the lesions, reflecting the large population of vulnerable cells and lack of fetal immunocompetency at earlier stages of pregnancy. Injury during the period of critical cell migration and differentiation in organogenesis may substantially disrupt structural development in target organs. Late gestational infections cause nonsuppurative inflammation in the brain and spinal cord, premature birth, or fetal death with stillbirth or abortion. Affected neonates are nonviable. Control is by vaccination but is not always justified economically. Akabane viral infections must be differentiated from infections with other teratogenic viruses (including related Bunyaviruses), inherited conditions, and maternal intoxications. Diagnosis is made by serology and viral isolation.
...
PMID:Akabane virus. 772 35
Pools of adult female chicken mites, Dermanyssus gallinae (De Geer), were allowed to feed on chicks that had been inoculated with eastern equine
encephalomyelitis
(
EEE
) virus and that had a
viremia
level of 10(6.2)-10(6.6) plaque-forming units per milliliter of blood. Virus remained detectable by plaque assay in samples of these mites for 30 d after the infectious blood meal. Virus was not recovered from any of 151 progeny of virus-exposed female mites. Mites that had fed on viremic chicks were allowed to feed on naive chicks 3, 7, 11, 15, or 30 d later.
EEE
virus was transmitted to chicks by these mites on days 3 (one transmission in four trials) and 7 (one transmission in four trials). Both transmissions were confirmed by the presence of virus in chick blood 24-72 h after mites had fed, and by plaque-reduction neutralization assays of 21-d convalescent chick sera against the original viral strain.
...
PMID:Laboratory transmission of eastern equine encephalomyelitis virus to chickens by chicken mites (Acari: Dermanyssidae). 843 39
The effect of salt concentration in larval rearing water on the susceptibility of adult Aedes taeniorhynchus (Wiedemann) and Aedes sollicitans (Skuse) to infection with eastern equine
encephalomyelitis
(
EEE
) virus was tested in the laboratory. Ae. sollicitans was more susceptible to infection (79%, n = 82) and viral dissemination (16%) with
EEE
virus than was Ae. taeniorhynchus (42%, n = 184) and (5%), respectively, when fed on a chick with a
viremia
of 10(7) +/- 0.1 plaque-forming units/ml; however, infection rates in adults were not affected by rearing in salt concentrations ranging from fresh water to brackish water containing 2.4% sea salts (1 part fresh water and 2 parts seawater). When fed on the same viremic 6-d-old chicken, all 48 Aedes albopictus (Skuse), reared in fresh water, became infected. Similarly, Venezuelan equine encephalitis viral infection or dissemination rates did not vary among Ae. taeniorhynchus adults that were reared in water containing 0, 1, or 2% sea salts.
...
PMID:Effect of salt concentration in larval rearing water on susceptibility of Aedes Mosquitoes (Diptera: Culicidae) to eastern equine and Venezuelan equine encephalitis viruses. 977 90
Intracerebral inoculation of field-isolates as well as established strains of equine herpesvirus-1 (EHV-1) in suckling mice results in viral replication in neurons and glial cells and induces encephalitis. By intraperitoneal (i.p.) inoculation, no histological lesion was observed in the central nervous system (CNS) in suckling mice with the EHV-1 HH1 strain (HH1), whereas a neuroadapted variant (NHH1) produced by serial passage of HH1 in the mouse brain caused severe
encephalomyelitis
after i.p. inoculation. The purpose of this study was to determine the route of neuroinvasion after i.p. inoculation of NHH1 and to clarify the effects of the brain passage on viral neuroinvasion. NHH1, but not HH1, targeted splenic and pulmonary macrophages and omental fat cells on days 1 and 2 post-inoculation (p.i.). From days 1 to 3 p.i., cell-associated
viremia
was occurred in NHH1-infected mice, but not in HH1-infected mice. On day 4 p.i., viral antigen was detected in a few endothelial cells, perivascular glial cells and neurons in the CNS in NHH1-infected mice. The number of viral antigen-positive cells increased markedly after day 5 p.i. In contrast, no viral antigen-positive cell was detected in the CNS in HH1-infected mice, except for a few nerve cells in the thoracic cord on day 4 p.i. These results suggest that NHH1 neuroinvasion is hematogenous and is correlated with enhanced extraneural virus growth.
...
PMID:Passage of equine herpesvirus-1 in suckling mouse brain enhances extraneural virus growth and subsequent hematogenous neuroinvasion. 1241 67
A new agent, DA, has been isolated from a spontaneously paralyzed mouse. Its biological properties and the pathology of lesions in experimental infection indicate close relationship with the Theiler group of
encephalomyelitis
viruses. Serological studies were inconclusive. The intracerebral neutralization test failed to reveal measurable antibody and other routes of inoculation were unsuitable because of low invasiveness of the agent. Repeated vaccination of females did not render their offspring resistant to homologous intracerebral challenge. The occurrence of early
viremia
is reported following intracerebral inoculation of the DA strain and also the known Theiler strains, 4727, FA, and GD-VII. The pathology of mice experimentally infected with DA and with known members of the Theiler group is described. Attention is called to the demyelinating lesion of the cord in mice surviving for several months and to the persistence of virus in the CNS of such animals. Another characteristic feature of the pathology was the degeneration of ventral nerve roots and in some mice of the peripheral nerves. Similar changes were not seen with strains of Theiler virus other than DA. Spheroidal bodies of undetermined significance were found in the lesions. Finally the occurrence of myositis after intracerebral inoculation, not only mice infected with the DA virus, but also with the 4727 and FA strains, is described and discussed.
...
PMID:Observations on encephalomyelitis of mice (DA strain). 1302 47
Two virus strains were isolated from the central nervous systems of two fatal human cases during an epidemic of
encephalomyelitis
in Austria. Monkeys, mice, and chick embryos proved susceptible; rabbits and guinea-pigs were refractory. The experimental disease in monkeys was characterized by acute meningo-
encephalomyelitis
, which was localized particularly in the grey matter of the brain stem, the cerebellum, the medulla, and the anterior horns of the spinal cord. The virus produced discrete lesions on the chorioallantoic membrane of the chick embryo. In monkeys,
viraemia
was demonstrated for a period of at least 6-8 days before the development of the clinical illness.The virus was shown to be closely related to that of Russian spring-summer encephalitis. Neutralizing and complement-fixing antibodies could be demonstrated in patients' sera.
...
PMID:Virus meningo-encephalitis in Austria. III. Pathogenic and immunological properties of the virus. 1437 99
Efficacy of the Recombitek Equine West Nile Virus (WNV) vaccine was evaluated against a WNV intrathecal challenge model that results in WNV-induced clinical disease. Ten vaccinated (twice at days 0 and 35) and 10 control horses were challenged 2 weeks after administration of the second vaccine with a virulent WNV by intrathecal administration. After the challenge, eight of 10 controls developed clinical signs of
encephalomyelitis
whereas one vaccinate exhibited muscle fasciculation only once. Nine controls and one vaccinate developed a fever. Histopathology revealed mild to moderate nonsuppurative encephalitis in eight controls and one vaccinate. None of the vaccinates and all of the controls developed WNV
viremia
after challenge. All vaccinated horses developed antibodies to WNV after vaccination. These and results of previous studies demonstrate efficacy of the Recombitek WNV vaccine against WNV-induced clinical disease and natural challenge with WNV-infected mosquitoes.
...
PMID:Evaluation of the efficacy provided by a Recombinant Canarypox-Vectored Equine West Nile Virus vaccine against an experimental West Nile Virus intrathecal challenge in horses. 1703 48
Host species have evolved mechanisms that can inhibit pathogen replication even after a cell has been successfully invaded. Here we show that tripartite-motif protein 21 (TRIM21), a ubiquitously expressed E3 ubiquitin ligase that targets viruses inside the cytosol, protects mice against fatal viral infection. Upon infection with mouse adenovirus-1, naive mice lacking TRIM21 succumb to
encephalomyelitis
within 7 d. In contrast, wild-type mice rapidly up-regulate TRIM21 and control
viremia
. Trim21 heterozygous mice have a haploinsufficiency phenotype in which reduced TRIM21 expression leads to a viral load that is higher than wild types but lower than knockouts. TRIM21 is a high-affinity antibody receptor that allows antibodies to operate inside an infected cell. In passive transfer experiments at high viral dose, antisera that fully protects wild-type mice fails to protect most Trim21 knockout animals. These results demonstrate that TRIM21 provides potent antiviral protection and forms an important part of the humoral immune response.
...
PMID:Intracellular antibody receptor TRIM21 prevents fatal viral infection. 2384 60
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