Abstract:
:Using isogenic recombinant murine coronaviruses expressing wild-type murine hepatitis virus strain 4 (MHV-4) or MHV-A59 spike glycoproteins or chimeric MHV-4/MHV-A59 spike glycoproteins, we have demonstrated the biological functionality of the N-terminus of the spike, encompassing the receptor binding domain (RBD). We have used two assays, one an in vitro liposome binding assay and the other a tissue culture replication assay. The liposome binding assay shows that interaction of the receptor with spikes on virions at 37 degrees C causes a conformational change that makes the virions hydrophobic so that they bind to liposomes (B. D. Zelus, J. H. Schickli, D. M. Blau, S. R. Weiss, and K. V. Holmes, J. Virol. 77: 830-840, 2003). Recombinant viruses with spikes containing the RBD of either MHV-A59 or MHV-4 readily associated with liposomes at 37 degrees C in the presence of soluble mCEACAM1(a), except for S(4)R, which expresses the entire wild-type MHV-4 spike and associated only inefficiently with liposomes following incubation with soluble mCEACAM1(a). In contrast, soluble mCEACAM1(b) allowed viruses with the MHV-A59 RBD to associate with liposomes more efficiently than did viruses with the MHV-4 RBD. In the second assay, which requires virus entry and replication, all recombinant viruses replicated efficiently in BHK cells expressing mCEACAM1(a). In BHK cells expressing mCEACAM1(b), only viruses expressing chimeric spikes with the MHV-A59 RBD could replicate, while replication of viruses expressing chimeric spikes with the MHV-4 RBD was undetectable. Despite having the MHV-4 RBD, S(4)R replicated in BHK cells expressing mCEACAM1(b); this is most probably due to spread via CEACAM1 receptor-independent cell-to-cell fusion, an activity displayed only by S(4)R among the recombinant viruses studied here. These data suggest that the RBD domain and the rest of the spike must coevolve to optimize function in viral entry and spread.
journal_name
J Viroljournal_title
Journal of virologyauthors
Tsai JC,Zelus BD,Holmes KV,Weiss SRdoi
10.1128/jvi.77.2.841-850.2003subject
Has Abstractpub_date
2003-01-01 00:00:00pages
841-50issue
2eissn
0022-538Xissn
1098-5514journal_volume
77pub_type
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pub_type: 杂志文章
doi:10.1128/JVI.72.7.5717-5727.1998
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.67.12.7705-7710.1993
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/jvi.77.18.10168-10171.2003
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.13.2.411-418.1974
更新日期:1974-02-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.71.9.6509-6516.1997
更新日期:1997-09-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.80.2.671-681.2006
更新日期:2006-01-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.00175-12
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.66.6.3494-3503.1992
更新日期:1992-06-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.45.2.715-726.1983
更新日期:1983-02-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.68.8.5300-5305.1994
更新日期:1994-08-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.52.2.719-721.1984
更新日期:1984-11-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2015-01-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/jvi.76.18.9481-9492.2002
更新日期:2002-09-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2020-01-31 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2014-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2017-03-29 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.60.2.423-430.1986
更新日期:1986-11-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.00819-19
更新日期:2019-10-15 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.65.2.796-804.1991
更新日期:1991-02-01 00:00:00