Fusion resistance and decreased infectability as major host cell determinants of coronavirus persistence.
Mouse hepatitis virus persists in cultures of a subline (designated LM-K) of mouse LM cells but produces a lytic infection in L-2 cells. Persistence in the LM-K cells was not accompanied by production of ts mutants or of soluble anti-MHV factors. Infectious center assay demonstrated an approximately 500-fold lower level of infectibility by MHV of the LM-K cells as compared to L-2 cells. On an infected cell basis, production levels of infectious progeny and viral RNA were comparable between the two cell lines. The extent of virus-induced cell-cell fusion, however, was markedly reduced in the LM-K cells. Cell-mixing experiments showed that both infected L-2 and LM-K cells have the capacity of fusing with neighboring uninfected L-2 cells but not with uninfected LM-K cells. This suggests that the decreased level of fusion observed in the LM-K infection is due not to absence of viral fusion protein at the cell surface, but rather to an inherent resistance of the LM-K cell membrane to MHV-induced fusion. It is believed that such fusion resistance in LM-K cells moderates virus dissemination throughout the culture, thereby contributing to a state of virus persistence.
D000818:Animals; D002459:Cell Fusion; D002460:Cell Line; D003588:Cytopathogenic Effect, Viral; D008561:Membrane Fusion; D051379:Mice; D006517:Murine hepatitis virus / Q000502:physiology*; D012367:RNA, Viral / Q000096:biosynthesis; D014760:Viral Fusion Proteins; D014764:Viral Proteins / Q000502:physiology; D014779:Virus Replication
D012367:RNA, Viral; D014760:Viral Fusion Proteins; D014764:Viral Proteins