Host gene influences sensitivity to interferon action selectively for influenza virus View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1980-02

AUTHORS

O Haller, H Arnheiter, J Lindenmann, I Gresser

ABSTRACT

Several examples of genetically determined resistance to different viruses have been studied in mice1. Inborn resistance due to the allele Mx in A2G mice may be characterised as follows: resistance is specific for members of the orthomyxo family (influenza virus)2; it is expressed in different organs and cells2–6; and it is independent of a functioning immune system3,4,7. The only means of rendering resistant mice fully susceptible to influenza virus has been treatment with potent anti-interf eron serum8, indicating that interf eron is important in resistance. Interf eron is generally thought to inhibit the multiplication of all animal viruses relatively indiscriminately. Therefore, it had seemed unlikely that interferon was involved in this resistance, as A2G mice were selectively resistant to influenza virus albeit as sensitive as control mice to several other viruses4. There are, however, examples in which the genetic control of the production of interferon or the sensitivity to interferon action is expressed selectively for a given virus. Thus, De Maeyer and coworkers have shown that four different If loci control the amount of circulating interferon produced after injection of mice with Newcastle disease virus (NDV)9, mouse mammary tumour virus10, or Sendai virus (personal communication). Hanson et al.11 found that cultures of cells from C3H RV mice, resistant to Arbo B virus infection, were much more susceptible to the inhibitory effect of interferon when tested with Arbo B viruses than cultures taken from susceptible C3H mice. We present here results, showing that cultures of macrophages from mice resistant to orthomyxoviruses (Mx positive) can be protected by much smaller amounts of interferon than are necessary to protect cultures from susceptible mice when these cultures are infected with influenza virus; whereas no difference in sensitivity to interferon is observed when cultures are infected with vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMC). We believe that these results showing a genetic control of sensitivity to interferon action specific for a given virus are related to the in vivo resistance of A2G mice to influenza virus. If applicable to man, these results may also be of importance in understanding individual variations in sensitivity to viral infections. More... »

PAGES

660-662

Journal

TITLE

Nature

ISSUE

5748

VOLUME

283

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/283660a0

    DOI

    http://dx.doi.org/10.1038/283660a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1000466200

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/7354853


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