Semliki Forest virus infection of laboratory mice: a model to study the pathogenesis of viral encephalitis

Fazakerley, John K.

doi:10.1007/978-3-7091-0572-6_16

Cited by 23 publications

(31 citation statements)

References 63 publications

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“…All strains cross the blood-brain barrier, and virulent strains cause lethal encephalomyelitis 5-7 days aer infection. However, avirulent strains induce nonlethal demyelinating disease that generally lasts up to 30 days aer infection [51][52][53] and are lethal for the developing foetus [54].…”

Section: Semliki Forest Virusmentioning

confidence: 99%

The Pathogenesis of Alphaviruses

Atkins

2013

ISRN Virology

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Alphaviruses are enveloped single-stranded positive sense RNA viruses of the family Togaviridae. e genus alphavirus contains nine viruses, which are of medical, theoretical, or economic importance, and which will be considered. Sindbis virus (SINV) and Semliki Forest (SFV), although of some medical importance, have largely been studied as models of viral pathogenicity. In mice, SINV and SFV infect neurons in the central nervous system and virulent strains induce lethal encephalitis, whereas avirulent strains of SFV induce demyelination. SFV infects the developing foetus and can be teratogenic. Venezuelan Equine Encephalitis virus, Eastern Equine Encephalitis virus, and Western Equine Encephalitis virus can induce encephalitis in horses and humans. ey are prevalent in the Americas and are mosquito transmitted. Ross River virus, Chikungunya virus (CHIKV), and O'nyong-nyong virus (ONNV) are prevalent in Australasia, Africa and Asia, and Africa, respectively. ONNV virus is transmitted by Anopheles mosquitoes, while the other alphaviruses are transmitted by culicine mosquitoes. CHIKV has undergone adaptation to a new mosquito host which has increased its host range beyond Africa. Salmonid alphavirus is of economic importance in the farmed salmon and trout industry. It is postulated that future advances in research on alphavirus pathogenicity will come in the �eld of innate immunity.

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Section: Semliki Forest Virusmentioning

confidence: 99%

The Pathogenesis of Alphaviruses

Atkins

2013

ISRN Virology

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“…Alphavirus infections, including Semliki Forest virus (SFV) and Sindbis virus (SINV), have been at the forefront of studies of virus-induced cell death and provide important tractable model systems to study many aspects of virus pathogenesis (2,17,18,31). Alphaviruses enter cells by receptor-mediated endocytosis (33).…”

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confidence: 99%

Semliki Forest Virus-Induced Endoplasmic Reticulum Stress Accelerates Apoptotic Death of Mammalian Cells

Barry

Atkinson

Ferguson

et al. 2010

J Virol

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The alphavirus Semliki Forest virus (SFV) and its derived vectors induce apoptosis in mammalian cells.Here, we show that apoptosis is associated with the loss of mitochondrial membrane potential followed by the activation of caspase-3, caspase-8, and caspase-9. Cell death can be partially suppressed by treatment with the pan-caspase inhibitor zVAD-fmk. To determine the role of SFV structural proteins in cell death, the temporal course of cell death was compared in cells infected with SFV and cells infected with SFV virus replicon particles (VRPs) lacking some or all of the virus structural genes. In the absence of virus structural proteins, cell death was delayed. The endoplasmic reticulum (ER) stress response, as determined by the splicing of X-box binding protein 1 (XBP1) transcripts and the activation of caspase-12, was activated in virus-infected cells but not in VRP (SFV lacking structural genes)-infected cells. The C/EBP-homologous protein (CHOP) was upregulated by both virus and VRP infections. The virus envelope proteins but not the virus capsid protein triggered ER stress. These results demonstrate that in NIH 3T3 cells, SFV envelope glycoproteins trigger the unfolded protein response of the ER and accelerate apoptotic cell death initiated by virus replicase activity.

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“…Infection of mice with the A7(74) strain of Semliki Forest virus (SFV), an alphavirus of the family Togaviridae, has been well characterized as a tractable model of virus encephalitis (Fazakerley, 2004). This system has the advantage over many other models of encephalitis in that SFV is efficiently neuroinvasive allowing the study of central nervous system (CNS) events without direct intracerebral inoculation and consequent disturbance of the blood-brain barrier; it also produces lesions of inflammatory demyelination.…”

mentioning

confidence: 99%

In Semliki Forest virus encephalitis, antibody rapidly clears infectious virus and is required to eliminate viral material from the brain, but is not required to generate lesions of demyelination

Atkinson

Ballany

Boyd

et al. 2008

Journal of General Virology

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Semliki Forest virus (SFV) infection of the laboratory mouse provides a well-characterized tractable system to study the pathogenesis of virus encephalitis and virus induced demyelination. In mMT mice, which have no antibodies, infectious virus persisted in both the serum and the brain for several weeks, indicating that antibodies are required to eliminate infectious virus. In immunocompetent mice, virus infectivity in the brain was undetectable after the first week of infection, but virus RNA levels declined slowly. Following SFV infection, lesions of demyelination were present in the brains of both immunocompetent and mMT mice, indicating that antibodies are not required to generate lesions of demyelination.

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Semliki Forest virus infection of laboratory mice: a model to study the pathogenesis of viral encephalitis

Cited by 23 publications

References 63 publications

The Pathogenesis of Alphaviruses

The Pathogenesis of Alphaviruses

Semliki Forest Virus-Induced Endoplasmic Reticulum Stress Accelerates Apoptotic Death of Mammalian Cells

In Semliki Forest virus encephalitis, antibody rapidly clears infectious virus and is required to eliminate viral material from the brain, but is not required to generate lesions of demyelination

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