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Coronaviruses pp 111-116 | Cite as

Effects of Mouse Hepatitis Virus Infection on Host Cell Metabolism

  • Stanley Tahara
  • Cornelia Bergmann
  • Gary Nelson
  • Richard Anthony
  • Therese Dietlin
  • Shigeru Kyuwa
  • Stephen Stohlman
Chapter
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 342)

Abstract

A time dependent decrease in cell surface expression of major histocompatibility complex (MHC) class 1 proteins was found during JHMV infection of the mouse macrophage J774.1 cells line by radioimmunoassay. MHC class I, actin and CSF-1 receptor mRNA levels were also found to decrease during infection. Surprisingly, not all host cell mRNA were similarly affected, suggesting that the apparent MHV-induced translational shut off of host cell protein synthesis during infection was specific for only some host cell mRNAs. Interestingly, two mRNAs found to be refractory to JHMV infection encode monokines, suggesting a role in pathogenesis. To understand the mechanism(s) of this preferential mRNA stability and the apparent shut off of host cell mRNA, translation lysates were prepared from infected and uninfected cells. Translation of host mRNAs in these extracts showed no apparent loss of translational ability in the infected cells vs. the uninfected cells; however, viral mRNAs were preferentially translated in the lysates from the infected cells. Chimeric mRNAs containing the MHV leader upstream of a globin reporter gene showed that preferential translation was a property of the MHV leader RNA. Deletional analysis showed that the sequences responsible for this cis translational augmentation are in a 12 nucleotide (nt) tract at the 3’ end of the leader. The previously reported interaction of the nucleocapsid protein with these nts suggest that it may play a role in translational augmentation of MHV mRNAs.

Keywords

Major Histocompatibility Complex Class Uninfected Cell Viral mRNAs Mouse Hepatitis Virus Receptor mRNA Level 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Schneider, R.I., and T. Shenk. Ann. Rev. Biochem. 56:317–332, (1987).PubMedCrossRefGoogle Scholar
  2. 2.
    Lai, M.M.-C. Ann. Rev. Microbiol. 44:303–333, (1990).CrossRefGoogle Scholar
  3. 3.
    Hilton, A., Mizzen, L., Macintyre, G., Cheley S., and R. Anderson. J. Gen. Virol. 67:923–932, (1986).PubMedCrossRefGoogle Scholar
  4. 4.
    Stohlman, S.A., Brayton, P.R., Fleming, J.O., Weiner, L.P., and M.M.-C. Lai. J. Gen. Virol. 63:265–275, (1982).PubMedCrossRefGoogle Scholar
  5. 5.
    Stohlman, S.A., Kyuwa, S., Cohen, M., Bergmann, C., Polo, J.M., Yeh, J, Anthony, R., and J.G. Keck. Virol. 189:217–224, (1992).CrossRefGoogle Scholar
  6. 6.
    Tahara, S.M., Dietlin, T.A., Dever, T.E., Merrick, W.C. and L.M. Worrilow. J. Biol. Chem. 266:3594–3601, (1991).PubMedGoogle Scholar
  7. 7.
    Williamson, J., Kyuwa, S., Wang, F.-I. and S.A. Stohlman. Adv. Exp. Biol. Med. 276:557–563, (1990).CrossRefGoogle Scholar
  8. 8.
    Stohlman, S.A., Baric, R.S., Nelson, G.W., Soe, L.H., Welter, L.M. and R.J. Deans. J. Virol. 4288–4295, (1988).Google Scholar
  9. 9.
    Stohlman, S.A., and L.P. Weiner. Arch. Virol. 57:53–61, (1978).PubMedCrossRefGoogle Scholar
  10. 10.
    Kyuwa, S. and S.A. Stohlman. Seminar Virol. 1:273–280, (1990).Google Scholar
  11. 11.
    Robbins, D., Shirazi, Y., Drysdale, B., Lieberman, A., Shin, H. and M. Shir. J. Immunol. 139:2593–2597, (1987).PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1994

Authors and Affiliations

  • Stanley Tahara
    • 1
  • Cornelia Bergmann
    • 1
    • 2
  • Gary Nelson
    • 1
    • 2
  • Richard Anthony
    • 1
    • 2
  • Therese Dietlin
    • 1
  • Shigeru Kyuwa
    • 3
  • Stephen Stohlman
    • 1
    • 2
  1. 1.Departments of MicrobiologyUniversity of Southern California School of MedicineLos AngelesUSA
  2. 2.Departments of NeurologyUniversity of Southern California School of MedicineLos AngelesUSA
  3. 3.Department of Animal PathologyUniversity of TokyoJapan

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