Role of macrophages in natural resistance to virus infections.

Mogensen, Søren C.

doi:10.1128/mmbr.43.1.1-26.1979

Cited by 181 publications

(85 citation statements)

References 72 publications

(120 reference statements)

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Section: Discussionmentioning

confidence: 99%

“…Cells of the monocyte/macrophage lineage have been implicated as the pivotal cells in natural resistance to a number of viral infections, including two other strains of mouse hepatitis virus (Mogensen, 1979). These studies have relied on either the in vitro growth of virus in macrophages, the ability of macrophages to suppress virus growth in a second susceptible cell type or the in vivo effects of anti-macrophage treatments such as carrageenan or silica particles (Allison, 1974;Mogensen, 1979). Although there are numerous virus infections in which macrophages are believed to play a role in survival from lethal infections, it has recently been shown that mononuclear phagocytes do not play an important role in the clearance of lymphocytic choriomeningitis virus (Lehman-Grube et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

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Delayed-type hypersensitivity response in the central nervous system during JHM virus infection requires viral specificity for protection

Stohlman¹,

Sussman²,

Matsushima³

et al. 1988

Journal of Neuroimmunology

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The JHM strain of mouse hepatitis virus (JHMV) elicits an I-A-restricted delayed-type hypersensitivity (DTH) response mediated by a Thy-1+, Lyt-1+, and CD4+ T cell. Adoptive transfer of these polyclonal CD4+ T cells from immunized mice prevents death in lethally infected recipients without significantly reducing virus titer in the central nervous system (CNS). These observations raise the possibility that the recruitment of mononuclear cells into the CNS may play a critical role in survival from a lethal CNS infection. Transient DTH response to nonviral antigens induced an accumulation of monocytes in the CNS that was maximal at 48 h post-challenge and virtually resolved by 5 days post-challenge. By contrast the induction of prolonged DTH responses resulted in the accumulation of a large number of monocytes that persisted in the CNS for at least 5 days post-challenge. Neither type of DTH reaction suppressed virus replication or prevented death from concomitant lethal JHMV infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Delayed-type hypersensitivity response in the central nervous system during JHM virus infection requires viral specificity for protection

Stohlman¹,

Sussman²,

Matsushima³

et al. 1988

Journal of Neuroimmunology

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“…IFN and macrophages are considered to be important elements in resistance against different viral infections (4,(20)(21)(22). IFN-a/~ is readily induced during the initial phase of infection, well before the generation of an immune response, and IFN-y is rapidly induced following the generation of the immune response directed against the virus.…”

Section: Introductionmentioning

confidence: 99%

A Major Role of Macrophage Activation by Interferon-Gamma During Mouse Hepatitis Virus Type 3 Infection

Lucchiari

Pereira

1990

Immunobiology

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In contrast to adult mice, young A/J mice, developed an acute hepatitis following infection with Mouse Hepatitis virus type 3. 100% of the young animals died 4 to 5 days after the infection and high levels of virus were found in the liver and peritoneal exudate. Very low levels of IFN-gamma were found in the serum and peritoneal exudate of infected young mice. This was in contrast to the levels observed in adult mice. Spleen cells and macrophage cultures from young A/J mice, again in contrast to adult A/J mice, were shown to be unable to synthesize IFN-gamma and IFN-alpha/beta respectively. Macrophages from either young or adult A/J mice were able to be activated with exogenous recombinant IFN-gamma or IFN-alpha/beta, enabling both sets of cells to restrict MHV3 replication. The results indicate that the ability of the immune system to synthesize IFN-gamma and IFN-alpha/beta may play a major role in the age-dependent resistance of A/J mice to MHV3.

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“…These differences are dependent not only on virus strain, but also on host genotype (ii, i4), age (16,28) and the route of inoculation (6). Resistance or susceptibility has, in general, been attributed to the ability or inability of the virus to replicate in macrophages (2,15) for the non-neurotropic strains or in neurons for the neurotropic strains (5,11).…”

Section: Introduetionmentioning

confidence: 99%

The biological relationship of mouse hepatitis virus (MHV) strains and interferon:In vitro induction and sensitivities

Garlinghouse

Smith

Holford

1984

Archives of Virology

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Five prototype strains of mouse hepatitis virus (MHV) -1, -3, -S, -A59 and -JHM were analyzed for their ability to induce interferon (IFN) in seven cell lines of rodent origin. Induction of IFN by all of the prototype MHV strains was infrequent and unpredictable, while IFN was produced consistently by five cell lines treated with known inducers. Priming and/or aging of cells did not enhance IFN induction by the MHV strains except in the case of MHV-A59 which consistently induced moderate levels of IFN on L-cells which were both primed and aged. Kinetic studies of MHV-A59-induced IFN on primed and aged L-cells demonstrated that detectable levels of IFN were not produced until 24 hours post-inoculation (p.i.). Peak levels were attained at 30 hours p.i. with no additional IFN produced through 48 hours p.i. MHV-induced IFN was similar in composition and properties to Newcastle disease virus-induced IFN. The sensitivities of the five MHV strains to eight concentrations of preformed L-cell IFN were also assessed. All strains except MHV-S fit a linear model with MHV-3, MHV-A59 and MHV-JHM having similar slopes. At most concentrations MHV-3 was less sensitive than MHV-1, -A59 or -JHM to IFN. The response curve for MHV-S was non-linear. This strain was more sensitive to the antiviral effects of the pre-formed IFN except at the highest concentrations of IFN used.

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Role of macrophages in natural resistance to virus infections.

Cited by 181 publications

References 72 publications

Delayed-type hypersensitivity response in the central nervous system during JHM virus infection requires viral specificity for protection

Delayed-type hypersensitivity response in the central nervous system during JHM virus infection requires viral specificity for protection

A Major Role of Macrophage Activation by Interferon-Gamma During Mouse Hepatitis Virus Type 3 Infection

The biological relationship of mouse hepatitis virus (MHV) strains and interferon:In vitro induction and sensitivities

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