Role of Interferon in Replication of Virulent and Attenuated Strains of Measles Virus

Mirchamsy, H.; Rapp, Fred

doi:10.1099/0022-1317-4-4-513

Cited by 34 publications

(14 citation statements)

References 9 publications

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“…Ruiz-Gomez and Isaacs (1963a) studied a number of different viruses and reported that the more virulent ones induced the least amounts of interferon. Similar results were obtained for strains of Semliki Forest, measles and Japanese encephalitis viruses (Finter, 1964;Mirchamsy and Rapp, 1969;Rokutanda, 1969). Vilikk (1964), however, found that the amount of interferon produced in mice infected with Sindbis virus was directly related to virus multiplication and he concluded that interferon formation was more probably a secondary response to, rather than a determining factor in, virus replication.…”

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confidence: 74%

The Relationship Between Interferon and Virus Virulence in Influenza Virus Infections of the Mouse

McLaren

Potter

1973

Journal of Medical Microbiology

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THERE have been many attempts to explain the virulence of viruses on the basis of their sensitivity to interferon or their ability to induce interferon in infected cells. Enders (1962) and De Maeyer and Enders (1965) observed that an attenuated strain of measles virus induced larger amounts of interferon than did a virulent strain, but considered that the poorer growth of the attenuated strain was probably not due to the increased production of interferon. Ruiz-Gomez and Isaacs (1963a) studied a number of different viruses and reported that the more virulent ones induced the least amounts of interferon. Similar results were obtained for strains of Semliki Forest, measles and Japanese encephalitis viruses (Finter, 1964;Mirchamsy and Rapp, 1969;Rokutanda, 1969). Vilikk (1964), however, found that the amount of interferon produced in mice infected with Sindbis virus was directly related to virus multiplication and he concluded that interferon formation was more probably a secondary response to, rather than a determining factor in, virus replication. The results obtained by different workers who have attempted to relate virulence to the sensitivity of the viruses to inhibition by interferon have also been contradictory. RuizGomez and Isaacs (1963b), in studies of arboviruses, myxoviruses and poxviruses, found that, with some exceptions, sensitivity to interferon was inversely related to virulence. Similar results have been reported for strains of foot-and-mouth disease virus (Sellers, 1963) and Semliki Forest virus (Finter, 1964). On the other hand, Campbell and Colter found that three variants of Mengo virus which possessed different degrees of virulence for mice had the same sensitivity to interferon; Rokutanda had similar findings with strains of Japanese encephalitis virus.The present study compares the virulence of influenza viruses for mice with the amount of interferon induced by them in the lungs of infected mice and with their in-vitro sensitivity to inhibition by interferon. The findings do not agree with the theory that virus virulence is determined by the properties of poor induction of interferon and low sensitivity to the inhibitory action of interferon, but indicate rather that the amount of interferon induced is determined by the degree of virus replication. MATERIALS AND METHODS Virus strainsThe Ao/WSN (HON1) parent strain of influenza virus and a number of temperaturesensitive (ts) mutants derived from it by 5-fluorouracil treatment were obtained, as lyophilised

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confidence: 74%

The Relationship Between Interferon and Virus Virulence in Influenza Virus Infections of the Mouse

McLaren

Potter

1973

Journal of Medical Microbiology

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“…Several studies have shown that MV strains differ in their IFN-inducing properties, and it has been suggested that virulent MVs can inhibit the induction of type 1 IFN (see, for instance, Mirchamsy & Rapp, 1969 ;Naniche et al, 2000 ;Volckaert-Vervliet et al, 1978). Naniche et al (2000) recently reported that wild-type isolates, which had been isolated and passaged on lymphoid cells, were much weaker inducers of type 1 IFN than the Edmonston strain and the Edmonston-derived Moraten vaccine strain.…”

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confidence: 99%

Measles virus-induced modulation of host-cell gene expression

Bolt¹,

Berg

Blixenkrone-Møller³

2002

Journal of General Virology

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The influence of measles virus (MV) infection on gene expression by human peripheral blood mononuclear cells (PBMCs) was examined with cDNA microarrays. The mRNA levels of more than 3000 cellular genes were compared between uninfected PBMCs and cells infected with either the Edmonston MV strain or a wild-type MV isolate. The MV-induced upregulation of individual genes identified by microarray analyses was confirmed by RT-PCR. In the present study, a total of 17 genes was found to be upregulated by MV infection. The Edmonston strain grew better in the PBMC cultures than the wild-type MV, and the Edmonston strain was a stronger inducer of the upregulated host cell genes than the wild-type virus. The anti-apoptotic B cell lymphoma 3 (Bcl-3) protein and the transcription factor NF-κB p52 subunit were upregulated in infected PBMCs both at the mRNA and at the protein level. Several genes of the interferon system including that for interferon regulatory factor 7 were upregulated by MV. The genes for a number of chaperones, transcription factors and other proteins of the endoplasmic reticulum stress response were also upregulated. These included the gene for the pro-apoptotic and growth arrest-inducing CHOP/GADD153 protein. Thus, the present study demonstrated the activation by MV of cellular mechanisms and pathways that may play a role in the pathogenesis of measles.

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“…Table I Discussion. The effect of AD on yields of the RNA-containing arboviruses (7, 8), Newcastle disease virus ( 9 ) , and human measles virus (6) has been postulated to be the result of inhibition of induction of interferon. This idea correlates with our present data.…”

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confidence: 99%