• DOI:10.1007/978-1-4615-1899-0_57
• Corpus ID: 40002518

MHVR-independent cell-cell spread of mouse hepatitis virus infection requires neutral pH fusion.

@article{Nash1995MHVRindependentCS,
  title={MHVR-independent cell-cell spread of mouse hepatitis virus infection requires neutral pH fusion.},
  author={T C Nash and Thomas M. Gallagher and Michael J. Buchmeier},
  journal={Advances in experimental medicine and biology},
  year={1995},
  volume={380},
  pages={
          351-7
        }
}

• T. C. Nash, T. Gallagher, M. Buchmeier
• Published 1995
• Biology
• Advances in experimental medicine and biology

Receptor-specificity is a key determinant of viral tropism. In this report, however, we have demonstrated that cell-associated spread of MHV can bypass the requirement for binding to primary receptors and thereby spread to cells that are resistant to MHV infection. Anti-receptor antibody CC1, which blocks infection by MHV virions, failed to prevent cell-associated spread of MHV to receptor-negative BHK cells or receptor-positive DBT cells. Cell-associated MHV may be utilizing an alternative, low-affinity receptor that is inadequate for functional interaction with MHV virions. Theoretically, dissemination of MHV infection through a receptor-independent, cell-associated mechanism in vivo provides the potential for broader host and tissue range, and for spread of infection despite the presence neutralizing antibodies. Receptor-independent, cell-associated spread of MHV requires neutral pH fusion capability. The low pH-dependent MHV variant OBLV60, which utilizes an endocytic route of entry, does not spread through a receptor-independent mechanism. Additionally, antiviral antibodies that block MHV spike-mediated fusion inhibited cell-associated spread of infection.