Impaired Entry of Soluble Receptor-Resistant Mutants of Mouse Hepatitis Virus Into Cells Expressing MHVR2 Receptor

Virology. 2000 Jul 20;273(1):80-9. doi: 10.1006/viro.2000.0409.

Abstract

Mouse hepatitis virus (MHV) JHMV and its soluble receptor-resistant (srr) mutants, srr7, srr11, and srr18, grew and induced syncytia equally well in BHK-R1 cells expressing the MHVR1 receptor derived from MHV-susceptible BALB/c mice. In contrast, srr growth and syncytia formations were drastically reduced relative to wild-type (wt) virus in BHK-R2 cells expressing the MHVR2 receptor from MHV-resistant SJL mice. Infections by these srr mutants in BHK-R2 cells were 0.7 to 1.5 log10 less efficient than those of wt virus. BHK cells expressing both MHVR1 and MHVR2 supported srr replication to the same extent as did BHK-R1 cells, suggesting that inefficient infection by srr mutants in BHK-R2 cells resulted from the absence of the effective receptor MHVR1. Virus-receptor binding tests failed to demonstrate a difference between the abilities of wt and srr18 to bind MHVR2. The binding of srr7 and srr11 to both MHVR1 and MHVR2 was revealed lower by two- to fourfold relative to the wt binding. The fusion activity of srr S proteins as examined by the expression with recombinant vaccinia virus was apparently lower than that of the wt S protein in BHK-R2 cells, while there was not such a remarkable difference in BHK-R1 cells. This suggests that the most likely reason for inefficient infection by mutants in BHK-R2 is impaired virus entry into cells. These observations suggest that inefficient infections in BHK-R2 cells by srr mutants occur in the absence of a functional receptor MHVR1, which plays an important role in srr entry into cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD
  • Carcinoembryonic Antigen
  • Cell Adhesion Molecules
  • Cell Fusion
  • Cell Line
  • Cell Membrane / metabolism
  • Cricetinae
  • Giant Cells / cytology
  • Giant Cells / metabolism
  • Giant Cells / virology
  • Glycoproteins / genetics
  • Glycoproteins / metabolism*
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism
  • Murine hepatitis virus / genetics*
  • Murine hepatitis virus / growth & development
  • Murine hepatitis virus / metabolism
  • Murine hepatitis virus / physiology*
  • Mutation / genetics*
  • Receptors, Virus / genetics
  • Receptors, Virus / metabolism*
  • Solubility
  • Spike Glycoprotein, Coronavirus
  • Transfection
  • Viral Envelope Proteins / genetics
  • Viral Envelope Proteins / metabolism
  • Viral Plaque Assay

Substances

  • Antigens, CD
  • CD66 antigens
  • Carcinoembryonic Antigen
  • Ceacam1 protein, mouse
  • Ceacam2 protein, mouse
  • Cell Adhesion Molecules
  • Glycoproteins
  • MHV surface projection glycoprotein
  • Membrane Glycoproteins
  • Receptors, Virus
  • Spike Glycoprotein, Coronavirus
  • Viral Envelope Proteins
  • spike glycoprotein, SARS-CoV