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Virology. 2000 Jul 20;273(1):80-9.

Impaired entry of soluble receptor-resistant mutants of mouse hepatitis virus into cells expressing MHVR2 receptor.

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National Institute of Neuroscience, NCNP 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502, Japan.


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.

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