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Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2
被引:11
作者:
Boussier, Jeremy
[1
,2
,3
]
Levi, Laura
[4
]
Weger-Lucarelli, James
[4
,5
]
Poirier, Enzo Z.
[4
,6
]
Vignuzzi, Marco
[4
]
Albert, Matthew L.
[1
,7
]
机构:
[1] Inst Pasteur, Immubiol Dendrit Cells Unit, Paris, France
[2] Inst Pasteur, Inserm U1223, Paris, France
[3] Univ Paris Diderot, Ecole Doctorale Frontieres Vivant, Paris, France
[4] Inst Pasteur, Viral Populat & Pathogenesis Unit, Paris, France
[5] Virginia Tech, Dept Biomed Sci & Pathobiol, VA MD Reg Coll Vet Med, Blacksburg, VA USA
[6] Francis Crick Inst, Immunobiol Lab, London, England
[7] Insitro, San Francisco, CA 94080 USA
来源:
关键词:
CELL-SURFACE CD4;
MESSENGER-RNA;
CROSS-PROTECTION;
INFECTION;
INTERFERENCE;
MECHANISMS;
EXPRESSION;
STRAINS;
KINASE;
NEF;
D O I:
10.1371/journal.pone.0241592
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
Superinfection exclusion (SIE) is a process by which a virally infected cell is protected from subsequent infection by the same or a closely related virus. By preventing cell coinfection, SIE favors preservation of genome integrity of a viral strain and limits its recombination potential with other viral genomes, thereby impacting viral evolution. Although described in virtually all viral families, the precise step(s) impacted by SIE during the viral life cycle have not been systematically explored. Here, we describe for the first time SIE triggered by chikungunya virus (CHIKV), an alphavirus of public health importance. Using single-cell technologies, we demonstrate that CHIKV excludes subsequent infection with: CHIKV; Sindbis virus, a related alphavirus; and influenza A, an unrelated RNA virus. We further demonstrate that SIE does not depend on the action of type I interferon, nor does it rely on host cell transcription. Moreover, exclusion is not mediated by the action of a single CHIKV protein; in particular, we observed no role for non-structural protein 2 (nsP2), making CHIKV unique among characterized alphaviruses. By stepping through the viral life cycle, we show that CHIKV exclusion occurs at the level of replication, but does not directly influence virus binding, nor viral structural protein translation. In sum, we characterized co-infection during CHIKV replication, which likely influences the rate of viral diversification and evolution.
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页数:22
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