Receptor-specificity is a key determaint 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 resisant 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.
CITATION STYLE
Nash, T. C., Gallagher, T. M., & Buchmeier, M. J. (1995). MHVR-independent cell-cell spread of mouse hepatitis virus infection requires neutral pH fusion. In Advances in Experimental Medicine and Biology (Vol. 380, pp. 351–357). Springer New York LLC. https://doi.org/10.1007/978-1-4615-1899-0_57
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