Interferon Induction by Lymphocytic Choriomeningitis Viruses Correlates with Maximum Virulence

Jacobson, Steven; Friedman, Robert M.; Pfau, C. J.

doi:10.1099/0022-1317-57-2-275

Cited by 34 publications

(24 citation statements)

References 20 publications

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“…infection with either LCMV Docile or Aggressive, both viral isolates induced similar acid-stable antiviral activities, presumably IFN-cq/~, in 6 to 16 week old individuals of the mouse strains investigated. These results differ from those obtained in young (3 to 4 week old) C3HeB/FeJ and ICR mice (Jacobson et al, 1981) where LCMV Aggressive was found to be a much more potent IFN inducer than LCMV Docile. The kinetics of IFN titres found in our study corresponded however with those measured in newborn BALB/c and C3H mice (Riviere et al, 1980) infected with the Pasteur strain of LCMV (CIPV 76001).…”

Section: Short Communicationcontrasting

confidence: 99%

“…with a lethal dose of LCMV Pasteur (CIPV 76001) survived when treated with anti-IFN serum (Saron et al, 1982). Treatment of LCMV Docile-infected mice with IFN inducers such as poly(I).poly(C), tilorone hydrochloride and Newcastle disease virus provoked the Aggressive pattern of LCM disease (Jacobson et al, 1981). These findings indicated that the antiviral property of IFN might play a fatal role in the outcome of the disease caused by LCMV.…”

Section: Short Communicationmentioning

confidence: 72%

“…These findings indicated that the antiviral property of IFN might play a fatal role in the outcome of the disease caused by LCMV. This notion was supported by experiments showing differences in the IFN-cq/~ serum titres induced by infection with LCMV Docile and Aggressive (Jacobson et al, 1981). In this study we searched for a possible correlation between the outcome of the disease caused by i.c.…”

Section: Short Communicationmentioning

confidence: 95%

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Lack of Correlation between Serum Titres of Interferon ,beta, Natural Killer Cell Activity and Clinical Susceptibility in Mice Infected with Two Isolates of Lymphocytic Choriomeningitis Virus

Leist¹,

Aguet

Hässig

et al. 1987

Journal of General Virology

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SUMMARYIntracerebral infection of adult immunocompetent mice with most strains of lymphocytic choriomeningitis virus (LCMV) caused a systemic infection and led to severe meningoencephalitis and death due to the induced T cell immune response. The susceptibility of congenic mice to the two plaque variants Docile and Aggressive of LCMV strain UBC was shown to be mouse strain-dependent. To investigate the possible correlation between acid-stable interferon (IFN) and natural killer (NK) cell responses and the susceptibility to the two UBC LCMV substrains, serum titres of acidstable antiviral activity, presumably IFN-~,fl and NK cell activities were determined in various mouse strains at different times after intracerebral infection. The two viral isolates induced comparable IFN-c~,fl serum titres and caused similar NK activities in the same mouse strain. Between different mouse strains, marked differences in the kinetics and amount of IFN production were observed, yet there was no correlation with the susceptibility to the two UBC LCMV substrains. Additionally, there was no correlation between the magnitude of the IFN-e,fl serum titres and the NK activities induced in the spleen by the viral inocula. Overall, the findings suggest that levels of circulating IFN-c~,//are only of minor importance for the development of LCM disease. , 1960); locally many isolates of LCMV cause an immunologically T cellmediated, lethal central nervous system disease in most mouse strains (Jacobson & Pfau, 1980, Pfau et al., 1982. The susceptibility of congenic mice to the two plaque variants Docile and Aggressive of LCMV UBC has been shown to be mouse strain-dependent (Zinkernagel et al., 1985). Of the mouse strains investigated in this study, A/J, BALB/c, B10. Br and C57BL/6 mice were susceptible to LCMV Aggressive and resistant to LCMV Docile; B10.AKM, B10.G, DBA/1 and SWR/J were killed by both LCMV isolates; CBA/J mice survived i.c. inoculation of LCMV Aggressive and DBA/2 mice were resistant to both viruses. ICR +/+ outbred mice were susceptible to both viral isolates whereas ICR nu/nu mice survived i.c. inoculation of LCMV Docile and Aggressive. Intracerebral (i.c.) injection of lymphocytic choriomeningitis (LCM) virus (LCMV) into mice causes a systemic infection because most of the inoculum escapes from the brain via blood vessels (MiresInterferons (IFN) play an important role in recovery from acute primary viral infections. The use ofanti-IFN serum to neutralize IFN which is liberated by infected cells leads to uncontrolled spread of virus and rapid evolution of lethal disease in encephalomyocarditis, herpes simplex, t Present address:

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Section: Short Communicationcontrasting

confidence: 99%

Section: Short Communicationmentioning

confidence: 72%

Section: Short Communicationmentioning

confidence: 95%

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Lack of Correlation between Serum Titres of Interferon ,beta, Natural Killer Cell Activity and Clinical Susceptibility in Mice Infected with Two Isolates of Lymphocytic Choriomeningitis Virus

Leist¹,

Aguet

Hässig

et al. 1987

Journal of General Virology

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“…26,32,33,52) and in this study, we showed that a very similar response is induced in the acute phase of LCMV infections that go on to persist. Type 1 IFNs may be induced by several cellular pathways.…”

Section: Discussionsupporting

confidence: 71%

Multiple Mechanisms Contribute to Impairment of Type 1 Interferon Production during Chronic Lymphocytic Choriomeningitis Virus Infection of Mice

Lee

Burke

Montoya

et al. 2009

The Journal of Immunology

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Type 1 IFNs, innate cytokines with important effector and immunomodulatory properties, are rapidly induced in the acute phase of many virus infections; however, this is generally a transient response that is not sustained during virus persistence. To gain insight into mechanisms that can contribute to down-regulation of type 1 IFN production during virus persistence, we analyzed type 1 IFN production during acute and chronic lymphocytic choriomeningitis virus (LCMV) infection. High-level type 1 IFN production was transiently up-regulated in cells including plasmacytoid and conventional dendritic cells (DCs) following LCMV infection of mice, but LCMV persistence was associated with only low-level type 1 IFN production. Nonetheless, chronically infected mice were able to up-regulate type 1 IFN production in response to TLR3, 7, and 9 ligands, albeit less efficiently than uninfected mice. Splenic DC numbers in mice chronically infected with LCMV were decreased, and the remaining cells exhibited a reduced response to TLR stimulation. LCMV-infected cell lines efficiently up-regulated type 1 IFN production following TLR ligation and infection with a DNA virus, but exhibited a defect in type 1 IFN induction following infection with Sendai, an RNA virus. This block in type 1 IFN production by infected cells, together with abnormalities in DC numbers and functions, likely contribute to the low-level type 1 IFN production in mice chronically infected with LCMV. Impairment of type 1 IFN production may both promote virus persistence and impact on host immunocompetence. Understanding the mechanisms involved may assist in development of strategies for control of virus persistence and superinfection.

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“…T cell-produced IFN-3, may locally enhance MHC expression in focal areas of infection, thereby increasing the sensitivity of T cell recognition of virus-infected tissue. Recent findings (15) show that IFN treatment of mice infected intracranially with LCMV leads to increased mortality. Since death in this system has been shown to be caused by virus-specific T celldependent destruction of brain tissue (16), it is possible that IFN may be enhancing H-2 antigen expression on the surface of brain tissue (12), leading to Various concentrations of IFN-/3 and Con A supernatant containing IFN-~' activity were added to LCMV-infected MEF.…”

Section: Resultsmentioning

confidence: 99%

Interferon enhances the susceptibility of virus-infected fibroblasts to cytotoxic T cells.

Bukowski¹,

Welsh²

1985

The Journal of Experimental Medicine

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Interferon (IFN) pretreatment of low-passage mouse embryonic fibroblasts (MEF) infected with lymphocytic choriomeningitis virus or vaccinia virus rendered these cells two to three times more susceptible to lysis by H-2 restricted, virus-specific cytotoxic T lymphocytes (CTL) than control, virus-infected MEF. The increased sensitivity to lysis correlated with increased expression of surface H-2 antigens, but not viral antigens. Continuous cell lines already highly sensitive to CTL-mediated lysis and already expressing high levels of surface H-2 antigens were unaffected by IFN pretreatment. These results suggest that IFN treatment, by increasing surface H-2 levels, may result in increased association of surface H-2 and virus antigens, leading to enhanced recognition and lysis by virus-specific CTL.

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Interferon Induction by Lymphocytic Choriomeningitis Viruses Correlates with Maximum Virulence

Cited by 34 publications

References 20 publications

Lack of Correlation between Serum Titres of Interferon ,beta, Natural Killer Cell Activity and Clinical Susceptibility in Mice Infected with Two Isolates of Lymphocytic Choriomeningitis Virus

Lack of Correlation between Serum Titres of Interferon ,beta, Natural Killer Cell Activity and Clinical Susceptibility in Mice Infected with Two Isolates of Lymphocytic Choriomeningitis Virus

Multiple Mechanisms Contribute to Impairment of Type 1 Interferon Production during Chronic Lymphocytic Choriomeningitis Virus Infection of Mice

Interferon enhances the susceptibility of virus-infected fibroblasts to cytotoxic T cells.

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