Encephalomyocarditis virus infection and pig disease in Queensland

Hill, B. D.; Ketterer, P. J.; Rodwell, B.J.; Eaves, F. W.; Webster, W. R.

doi:10.1111/j.1751-0813.1985.tb14138.x

Cited by 19 publications

(13 citation statements)

References 4 publications

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“…Mummified and dead piglets following natural or experimental infec-stillborn swine fetuses were submitted by attending veteritions with EMCV. 1,4,11,15 Transplacental EMCV infec-narians or were collected by the authors during herd visits. tion has been demonstrated in pregnant sows, 15,17 and…”

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confidence: 99%

Outbreaks in Quebec Pig Farms of Respiratory and Reproductive Problems Associated with Encephalomyocarditis Virus

et al. 1991

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Abstract. Encephalomyocarditis virus (EMCV) was isolated from tissues of aborted fetuses and weaned and suckling piglets from 4 different pig farms in Quebec. The farms were experiencing reproductive failure in sows of different parities concomitant to respiratory problems in suckling and postweaning piglets. At necropsy, gross lesions were confined to the lung and consisted of pulmonary congestion and edema of various degrees. Lesions of multifocal interstitial to proliferative pneumonia were found in the lungs of these piglets.

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confidence: 99%

Outbreaks in Quebec Pig Farms of Respiratory and Reproductive Problems Associated with Encephalomyocarditis Virus

et al. 1991

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“…This virus was first isolated from non-human primates in 1945 [11]. Small rodents, especially rats, have been suspected to be reservoir hosts or carriers for the virus [12]. EMCV has a wide host range among domestic and wild animals, and it has a worldwide distribution [13,14].…”

Section: Encephalomycarditis Virusmentioning

confidence: 99%

Role of Microglia in Oxidative Toxicity Associated with Encephalomycarditis Virus Infection in the Central Nervous System

Ano

Sakudo

Onodera

2012

IJMS

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The single-stranded RNA encephalomyocarditis virus (EMCV) can replicate in the central nervous system (CNS) and lead to prominent brain lesions in the stratum pyramidale hippocampus and the stratum granulosum cerebelli. Activated microglia cells infected by EMCV produce a massive burst of reactive oxygen species (ROS) via NADPH oxidase 2 (NOX2) activation, leading to neuronal death. Balancing this effect is mechanisms by which ROS are eliminated from the CNS. Cellular prion protein (PrPC) plays an important antioxidant role and contributes to cellular defense against EMCV infection. This review introduces recent knowledge on brain injury induced by EMCV infection via ROS generation as well as the involvement of various mediators and regulators in the pathogenesis.

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“…1975 ). Small rodents, especially rats, have been considered to be reservoir hosts or carriers of the virus ( Hill et al . 1985 ; Acland & Littlejohns 1986).…”

mentioning

confidence: 99%

“…It causes lethal acute myocarditis in piglets and fetal death or abortion in pregnant sows (Kim et al 1989), and additionally myelitis or encephalitis in small animals such as mice and hamsters (Oren et al 1975). Small rodents, especially rats, have been considered to be reservoir hosts or carriers of the virus (Hill et al 1985;Acland & Littlejohns 1986). Matsuzaki et al (1989a) reported that adult rats showed no susceptibility to EMC virus, though many other species of laboratory rodents were susceptible to EMC virus (Matsuzaki et al 1989b;Hirasawa et al 1991;Petruccelli et al 1991;Doi et al 1995;Takeda et al 1995;Ueno et al 1996).…”

mentioning

confidence: 99%

Age‐related changes in susceptibility of rat brain slice cultures including hippocampus to encephalomyocarditis virus

Ueno-Yamanouchi

Uetsuka

et al. 1999

Int J Experimental Path

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Replication of the D variant of encephalomyocarditis virus (EMC-D) and its cytopathic effects were studied in the brain slice cultures including hippocampus (hippocampal slice) obtained from postnatal 1-, 4-, 7-, 14-, 28-and 56-day-old Fischer 344 rats. At 0, 12, 24, 36 and 48 h after infection, virus titres of the slices and culture media were assayed. Viral replication was observed in cultures from 1-to 28-day-old rats, and the highest titre was recorded in the slice and culture medium from the youngest rat. The peak of virus titre decreased with age and no distinct viral replication was observed in the cultures from 56-day-old rats. Light microscopy revealed that degenerative and necrotic changes appeared in the infected hippocampal slices from 1- to 28-day-old rats, and the changes became less prominent with age. In situ hybridization and indirect immunofluorescence staining showed that positive signals of viral RNA and antigen were prominent in younger rats and decreased with age. These results suggest that an age-related decrease in the susceptibility of rat brain to EMC-D is less related to the maturation of the immune system but possibly to that of the neurone.

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Encephalomyocarditis virus infection and pig disease in Queensland

Cited by 19 publications

References 4 publications

Outbreaks in Quebec Pig Farms of Respiratory and Reproductive Problems Associated with Encephalomyocarditis Virus

Outbreaks in Quebec Pig Farms of Respiratory and Reproductive Problems Associated with Encephalomyocarditis Virus

Role of Microglia in Oxidative Toxicity Associated with Encephalomycarditis Virus Infection in the Central Nervous System

Age‐related changes in susceptibility of rat brain slice cultures including hippocampus to encephalomyocarditis virus

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