scholarly journals Neutralization of reovirus: the gene responsible for the neutralization antigen.

1977 ◽  
Vol 146 (5) ◽  
pp. 1305-1310 ◽  
Author(s):  
H L Weiner ◽  
B N Fields
Keyword(s):  
Gene Segment ◽  
Genome Segment ◽  
Biologic Property ◽  
A Minor ◽  
Outer Capsid

The S1 genome segment of reovirus is linked to type specificity as determined by neutralization antibody. This gene segment codes for a minor outer capsid polypeptide (sigma1). Therefore, sigma1 is the peptide responsible for induction of neutralization antibody and confers type specificity. This biologic property of reovirus was defined using hybrid recombinants clones between reovirus types 1 and 3 and 2 and 3.

scholarly journals Molecular basis of reovirus virulence. Role of the M2 gene.

1980 ◽  
Vol 152 (4) ◽  
pp. 853-868 ◽  
Author(s):  
D H Rubin ◽  
B N Fields
Keyword(s):  
Virulence Gene ◽  
Systemic Infection ◽  
Genome Segment ◽  
Dsrna Segment ◽  
Newborn Mice ◽  
Serotype 1 ◽  
Dsrna Genome ◽  
Outer Capsid

The mammalian reoviruses (serotype 1, strain Lang and serotype 3, strain Dearing) differ in their sensitivity to digestion by chymotrypsin. We have found that the M2 double-stranded RNA (dsRNA) genome segment (encoding the micro1C outer capsid polypeptide) is responsible for this property. In addition to determining response to protease treatement in vitro, we have found that the M2 genome segment also determines the ability of these two viruses successfully to initiate local and systemic infection in newborn mice after peroral inoculation. Thus the M2 dsRNA segment defines a new virulence gene of the mammalian reoviruses.

scholarly journals Generation of simian rotavirus reassortants with diverse VP4 genes using reverse genetics

2019 ◽  
Vol 100 (12) ◽  
pp. 1595-1604 ◽  
Author(s):  
Alexander Falkenhagen ◽  
Corinna Patzina-Mehling ◽  
Antje Rückner ◽  
Thomas W. Vahlenkamp ◽  
Reimar Johne
Keyword(s):  
Viral Entry ◽  
Reverse Genetics ◽  
Genome Segment ◽  
Cell Tropism ◽  
Outer Capsid Protein ◽  
High Genetic Diversity ◽  
Cytopathic Effects ◽  
Reassortant Viruses ◽  
Outer Capsid ◽  
Virus Strains

Species A rotaviruses (RVAs) are a major cause of gastroenteritis in animals and humans. Their genome consists of 11 segments of dsRNA, and reassortment events between animal and human strains can contribute to the high genetic diversity of RVAs. We used a plasmid-based reverse genetics system to investigate the reassortment potential of the genome segment encoding the viral outer capsid protein VP4, which is a major antigenic determinant, mediates viral entry and plays an important role in host cell tropism. We rescued reassortant viruses containing VP4 from porcine, bovine, bat, pheasant or chicken RVA strains in the backbone of simian strain SA11. The VP4 reassortants could be stably passaged in MA-104 cells and induced cytopathic effects. However, analysis of growth kinetics revealed marked differences in replication efficiency. Our results show that the VP4-encoding genome segment has a high reassortment potential, even between virus strains from highly divergent species. This can result in replication-competent reassortants with new genomic, growth and antigenic features.

A minor outer capsid protein, P9, of Rice dwarf virus

2003 ◽  
Vol 148 (11) ◽  
pp. 2275-2280 ◽  
Author(s):  
B. Zhong ◽  
A. Kikuchi ◽  
Y. Moriyasu ◽  
T. Higashi ◽  
K. Hagiwara ◽  
...  
Keyword(s):  
Capsid Protein ◽  
Dwarf Virus ◽  
Rice Dwarf Virus ◽  
Outer Capsid Protein ◽  
A Minor ◽  
Outer Capsid

scholarly journals The Outer Capsid Protein of Rice Dwarf Virus Is Encoded by Genome Segment S8

1989 ◽  
Vol 70 (10) ◽  
pp. 2759-2764 ◽  
Author(s):  
T. Omura ◽  
K. Ishikawa ◽  
H. Hirano ◽  
M. Ugaki ◽  
Y. Minobe ◽  
...  
Keyword(s):  
Capsid Protein ◽  
Genome Segment ◽  
Dwarf Virus ◽  
Rice Dwarf Virus ◽  
Outer Capsid Protein ◽  
Outer Capsid

scholarly journals Avian Reovirus Major μ-Class Outer Capsid Protein Influences Efficiency of Productive Macrophage Infection in a Virus Strain-Specific Manner

2001 ◽  
Vol 75 (11) ◽  
pp. 5027-5035 ◽  
Author(s):  
David O'Hara ◽  
Megan Patrick ◽  
Denisa Cepica ◽  
Kevin M. Coombs ◽  
Roy Duncan
Keyword(s):  
Capsid Protein ◽  
Genome Segment ◽  
Replication Cycle ◽  
Productive Infection ◽  
Avian Reovirus ◽  
Outer Capsid Protein ◽  
Macrophage Infection ◽  
Highly Pathogenic ◽  
Virus Replication Cycle ◽  
Outer Capsid

ABSTRACT We determined that the highly pathogenic avian reovirus strain 176 (ARV-176) possesses an enhanced ability to establish productive infections in HD-11 avian macrophages compared to avian fibroblasts. Conversely, the weakly pathogenic strain ARV-138 shows no such macrophagotropic tendency. The macrophage infection capability of the two viruses did not reflect differences in the ability to either induce or inhibit nitric oxide production. Moderate increases in the ARV-138 multiplicity of infection resulted in a concomitant increase in macrophage infection, and under such conditions the kinetics and extent of the ARV-138 replication cycle were equivalent to those of the highly infectious ARV-176 strain. These results indicated that both viruses are apparently equally capable of replicating in an infected macrophage, but they differ in the ability to establish productive infections in these cells. Using a genetic reassortant approach, we determined that the macrophagotropic property of ARV-176 reflects a post-receptor-binding step in the virus replication cycle and that the ARV-176 M2 genome segment is required for efficient infection of HD-11 cells. The M2 genome segment encodes the major μ-class outer capsid protein (μB) of the virus, which is involved in virus entry and transcriptase activation, suggesting that a host-specific influence on ARV entry and/or uncoating may affect the likelihood of the virus establishing a productive infection in a macrophage cell.

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