scholarly journals Rubella Virus Capsid Protein Modulates Viral Genome Replication and Virus Infectivity

2004 ◽  
Vol 78 (8) ◽  
pp. 4314-4322 ◽  
Author(s):  
Min-Hsin Chen ◽  
Joseph P. Icenogle

ABSTRACT The structural proteins (SP) of the Togaviridae can be deleted in defective interfering RNAs. The dispensability of viral SP has allowed construction of noninfectious viral expression vectors and replicons from viruses of the Alphavirus and Rubivirus genera. Nevertheless, in this study, we found that the SP of rubella virus (RUB) could enhance expression of reporter genes from RUB replicons in trans. SP enhancement required capsid protein (CP) expression and was not due to RNA-RNA recombination. Accumulation of minus- and plus-strand RNAs from replicons was observed in the presence of SP, suggesting that SP specifically affects RNA synthesis. By using replicons containing an antibiotic resistance gene, we found 2- to 50-fold increases in the number of cells surviving selection in the presence of SP. The increases depended significantly on the amount of transfected RNA. Small amounts of RNA or templates that replicated inefficiently showed more enhancement. The infectivity of infectious RNA was increased by at least 10-fold in cells expressing CP. Moreover, virus infectivity was greatly enhanced in such cells. In other cells that expressed higher levels of CP, RNA replication of replicons was inhibited. Thus, depending on conditions, CP can markedly enhance or inhibit RUB RNA replication.

2006 ◽  
Vol 80 (8) ◽  
pp. 3966-3974 ◽  
Author(s):  
Wen-Pin Tzeng ◽  
Jason D. Matthews ◽  
Teryl K. Frey

ABSTRACT The rubella virus capsid protein (C) has been shown to complement a lethal deletion (termed ΔNotI) in P150 replicase protein. To investigate this phenomenon, we generated two lines of Vero cells that stably expressed either C (C-Vero cells) or C lacking the eight N-terminal residues (CΔ8-Vero cells), a construct previously shown to be unable to complement ΔNotI. In C-Vero cells but not Vero or CΔ8-Vero cells, replication of a wild-type (wt) replicon expressing the green fluorescent protein (GFP) reporter gene (RUBrep/GFP) was enhanced, and replication of a replicon with ΔNotI (RUBrep/GFP-ΔNotI) was rescued. Surprisingly, replicons with deleterious mutations in the 5′ and 3′ cis-acting elements were also rescued in C-Vero cells. Interestingly, the CΔ8 construct localized to the nucleus while the C construct localized in the cytoplasm, explaining the lack of enhancement and rescue in CΔ8-Vero cells since rubella virus replication occurs in the cytoplasm. Enhancement and rescue in C-Vero cells were at a basic step in the replication cycle, resulting in a substantial increase in the accumulation of replicon-specific RNAs. There was no difference in translation of the nonstructural proteins in C-Vero and Vero cells transfected with the wt and mutant replicons, demonstrating that enhancement and rescue were not due to an increase in the efficiency of translation of the transfected replicon transcripts. In replicon-transfected C-Vero cells, C and the P150 replicase protein associated by coimmunoprecipitation, suggesting that C might play a role in RNA replication, which could explain the enhancement and rescue phenomena. A unifying model that accounts for enhancement of wt replicon replication and rescue of diverse mutations by the rubella virus C protein is proposed.


Virology ◽  
2000 ◽  
Vol 275 (1) ◽  
pp. 20-29 ◽  
Author(s):  
Robert Duncan ◽  
Ali Esmaili ◽  
Lok Man J. Law ◽  
Sylvie Bertholet ◽  
Chris Hough ◽  
...  

1998 ◽  
Vol 12 (3) ◽  
pp. 323-330 ◽  
Author(s):  
Michel Schmidt ◽  
Nina Tuominen ◽  
Tove Johansson ◽  
Stefan A. Weiss ◽  
Kari Keinänen ◽  
...  

2013 ◽  
Vol 110 (50) ◽  
pp. 20105-20110 ◽  
Author(s):  
V. Mangala Prasad ◽  
S. D. Willows ◽  
A. Fokine ◽  
A. J. Battisti ◽  
S. Sun ◽  
...  

2021 ◽  
Author(s):  
Jipeng Xie ◽  
Tong Jiang ◽  
Zhifang Li ◽  
Xiangdong Li ◽  
Zaifeng Fan ◽  
...  

Abstract Positive-stranded RNA viruses usually remodel host endomembrane system to form virus-induced intracellular vesicles for replication during infections. The genus Potyvirus of Potyviridae represents the largest number of positive single-stranded RNA viruses and causes great damage on crop production worldwide. Though potyviruses have wide host ranges, each potyvirus infects relatively limited host species. Phylogenesis and host range analysis can divide potyviruses into monocot-infecting and dicot-infecting groups, suggesting that some infection mechanism, probably on replication may be distinct for each group. Comprehensive studies on the model dicot-infecting turnip mosaic virus indicated that the 6K2-induced replication vesicles are derived from endoplasmic reticulum (ER) and subsequently target chloroplasts for viral genome replication. However, we have no knowledge on the replication site of monocot-infecting potyviruses. In this study, we firstly show that the precursor 6K2-VPg-Pro polyproteins of dicot-infecting potyviruses and monocot-infecting potyviruses phylogenetically cluster in two separate groups. With a typical gramineae-infecting potyvirus sugarcane mosaic virus (SCMV), we found that SCMV replicative double-stranded RNA (dsRNA) forms aggregates in cytoplasm but does not associate with chloroplasts. SCMV 6K2-VPg-Pro-induced vesicles colocalize with replicative dsRNA. Moreover, SCMV 6K2-VPg-Pro-induced structures target multiple intracellular organelles including ER, Golgi apparatus, mitochondria and peroxisomes, and have no evident association with chloroplasts. In conclusion, SCMV remodels multiple intracellular organelles for its genomic RNA replication.


2010 ◽  
Vol 5 (4) ◽  
pp. 571-584 ◽  
Author(s):  
Carolina S Ilkow ◽  
Steven D Willows ◽  
Tom C Hobman

1988 ◽  
Vol 69 (3) ◽  
pp. 603-612 ◽  
Author(s):  
K. Takkinen ◽  
G. Vidgren ◽  
J. Ekstrand ◽  
U. Hellman ◽  
N. Kalkkinen ◽  
...  

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