MHVR-Independent Cell-Cell Spread of Mouse Hepatitis Virus Infection Requires Neutral pH Fusion

  • Therese C. Nash
  • Thomas M. Gallagher
  • Michael J. Buchmeier
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 380)


Mouse hepatitis virus (MHV) attaches to susceptible cells through the interaction of MHV spike glycoprotein (S) with cellular receptors of the murine carcinoembryonic antigen (CEA) gene family1,2. Cells that lack murine CEA, including cells that are not of murine origin, are resistant to infection3; binding to MHV receptors appears to be a necessary step in the infection of cells by virions. The presence of murine CEA, however, is not required for cell-cell spread of MHV infection4. Cells that lack a functional MHV receptor can become productively infected through incorporation into MHV-induced syncytia. Syncytium formation is a consequence of spike-mediated cell-cell fusion. In this report, we investigated the role of spike-mediated fusion in receptor-independent, cell-associated spread of MHV infection.


Syncytium Formation Mouse Hepatitis Virus Spike Glycoprotein Lysosomotropic Agent Heptad Repeat Region 
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.


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Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • Therese C. Nash
    • 1
  • Thomas M. Gallagher
    • 2
  • Michael J. Buchmeier
    • 1
  1. 1.Department of NeuropharmacologyThe Scripps Research InstituteLa JollaUSA
  2. 2.Department of Microbiology and ImmunologyLoyola University Medical CenterMaywoodUSA

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