Use of N‐acetylethyleneimine [AEI] for the inactivation of semliki forest virus in vitro

Amor, Sandra; Webb, H. E.

doi:10.1002/jmv.1890190409

Cited by 3 publications

(1 citation statement)

References 7 publications

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“…In mice with severe combined immunodeficiency (SCID) or athymic nu/nu mice, SFV A7(74) establishes a persistent infection of the brain; athymic nu/nu mice survive this infection longer than SCID mice (Amor & Webb, 1986;Fazakerley & Webb, 1987). To determine whether the brain IFN response remained activated during persistent infection, CB17 nu/nu mice were inoculated intraperitoneally with 5000 p.f.u.…”

Section: Ifn Gene Transcription In the Brain Continues During Persistmentioning

confidence: 99%

The type I interferon system protects mice from Semliki Forest virus by preventing widespread virus dissemination in extraneural tissues, but does not mediate the restricted replication of avirulent virus in central nervous system neurons

Atkinson

Breakwell

McKimmie

et al. 2007

Journal of General Virology

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Semliki Forest virus (SFV) infection of the mouse provides a powerful model to study the pathogenesis of virus encephalitis. SFV and other alphavirus-based vector systems are increasingly used in biotechnology and medicine. This study analysed the strong susceptibility of this virus to type I interferon (IFN) responses. Following intraperitoneal infection of adult mice, SFV strain A7(74) was efficiently (100 %) neuroinvasive. In contrast, SFV4 was poorly (21 %) neuroinvasive. Upon entry into the brain, both viruses activated type I IFN responses. As determined by quantitative RT-PCR, activation of the IFN-a gene was proportional to virus RNA load. An intact type I IFN system was required for protection against both strains of SFV. IFN strongly curtailed virus spread in many cell types and in many tissues. In mice with an intact type I IFN system, infected cells were rarely observed and tissue tropism was difficult to determine. In the absence of a functional type I IFN system, the tropism and the potential for rapid and widespread infection of this virus was revealed. Virus infection was readily observed in the myocardium, endocardium, exocrine pancreas, adipose tissue, smooth muscle cells and in the brain in meningeal cells, ependymal cells and oligodendrocytes. In the brains of mice with and without type I IFN responses, virus infection of neurons remained rare and focal, indicating that the previously described restricted replication of SFV A7(74) in neurons is not mediated by type I IFN responses. INTRODUCTIONSemliki Forest virus (SFV) is a mosquito-borne virus that naturally circulates in sub-Saharan Africa. The virus is an alphavirus of the family Togaviridae. Natural human and equine infections have been described (Mathiot et al., 1990). The virus is closely related to Chikungunya virus, responsible recently for an outbreak of severe arthralgia in the islands of the Indian Ocean (Schuffenecker et al., 2006). Other alphaviruses include Sindbis virus in North Africa and Europe; Eastern, Western and Venezuelan equine encephalitis viruses in the Americas and Ross River virus in Australia. SFV infection of laboratory mice provides a tractable model system for the study of virus pathogenesis and in particular virus encephalitis (Fazakerley, 2004). Virulence in mice has been characterized for several natural isolates and their laboratory-passaged strains (Bradish et al., 1971). The most commonly studied strains include A7 and A7(74), which are avirulent in adult mice, and L10 and the prototype, which are virulent in adult mice. All strains of SFV are virulent in neonatal or young suckling mice (Bradish et al., 1971;Pusztai et al., 1971;Seamer et al., 1967).The most characterized avirulent strain of SFV, A7(74), is virulent in mice infected at the age of 11 days or less, but is avirulent in older mice; virus dissemination in the central nervous system (CNS) is increasingly restricted with age (Oliver et al., 1997). In 4-5-week-old mice, intraperitoneal inoculation of SFV A7(74) results in a high-titre plasma vira...

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Section: Ifn Gene Transcription In the Brain Continues During Persistmentioning

confidence: 99%

The type I interferon system protects mice from Semliki Forest virus by preventing widespread virus dissemination in extraneural tissues, but does not mediate the restricted replication of avirulent virus in central nervous system neurons

Atkinson

Breakwell

McKimmie

et al. 2007

Journal of General Virology

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

Fazakerley

2004

Emergence and Control of Zoonotic Viral Encephalitides

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Immunoelectron microscopical labelling of a glycolipid in the envelopes of brain cell-derived budding viruses, Semliki Forest, influenza and measles, using a monoclonal antibody directed chiefly against galactocerebroside resulting from Semliki Forest virus infection

Pathak

Illavia

Khalili-Shirazi

et al. 1990

Journal of the Neurological Sciences

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Use of N‐acetylethyleneimine [AEI] for the inactivation of semliki forest virus in vitro

Cited by 3 publications

References 7 publications

The type I interferon system protects mice from Semliki Forest virus by preventing widespread virus dissemination in extraneural tissues, but does not mediate the restricted replication of avirulent virus in central nervous system neurons

The type I interferon system protects mice from Semliki Forest virus by preventing widespread virus dissemination in extraneural tissues, but does not mediate the restricted replication of avirulent virus in central nervous system neurons

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

Immunoelectron microscopical labelling of a glycolipid in the envelopes of brain cell-derived budding viruses, Semliki Forest, influenza and measles, using a monoclonal antibody directed chiefly against galactocerebroside resulting from Semliki Forest virus infection

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