A simple procedure for the analysis of the structural proteins of influenza and parainfluenza viruses involving adsorption to erythrocytes

Cowley, Jeff A.; Tannock, G. A.; Barry, Richard D.

doi:10.1016/0166-0934(84)90036-3

Cited by 5 publications

(2 citation statements)

References 20 publications

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“…HPIV-2 and HPIV-4 have a phosphoprotein with a molecular weight (MW) of 49,000 to 53,000 versus 83,000 to 90,000 for HPIV-1 and HPIV-3 (59,70,203,313,339,343,376,396). The largest HPIV protein is the "large" (L) nucleocapsid protein (polymerase, MW 175,000 to 251,000), followed by P (HPIV-1 and HPIV-3).…”

Section: Structural Organizationmentioning

confidence: 99%

Parainfluenza Viruses

2003

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Human parainfluenza viruses (HPIV) were first discovered in the late 1950s. Over the last decade, considerable knowledge about their molecular structure and function has been accumulated. This has led to significant changes in both the nomenclature and taxonomic relationships of these viruses. HPIV is genetically and antigenically divided into types 1 to 4. Further major subtypes of HPIV-4 (A and B) and subgroups/genotypes of HPIV-1 and HPIV-3 have been described. HPIV-1 to HPIV-3 are major causes of lower respiratory infections in infants, young children, the immunocompromised, the chronically ill, and the elderly. Each subtype can cause somewhat unique clinical diseases in different hosts. HPIV are enveloped and of medium size (150 to 250 nm), and their RNA genome is in the negative sense. These viruses belong to the Paramyxoviridae family, one of the largest and most rapidly growing groups of viruses causing significant human and veterinary disease. HPIV are closely related to recently discovered megamyxoviruses (Hendra and Nipah viruses) and metapneumovirus

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Section: Structural Organizationmentioning

confidence: 99%

Parainfluenza Viruses

2003

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“…After electrophoresis the gel was processed for fluorography as described previously (3). Analysis of virions released from MuV-infected cells was performed according to Cowley's method (4). In brief, Vero cells were infected with MuV and after incubation at 37 C for 12 hr [355]-methionine was added and the cells were further cultured for 24 hr.…”

Section: Y Ito Et Almentioning

confidence: 99%

Persistence of Mumps Virus in Mouse L929 Cells

Ito

Tsurudome

Hishiyama

1985

Microbiology and Immunology

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The characteristics of a persistent infection of L929 cells with mumps virus (MuV) is presented.The persistent infection (L-MuV cells) was regulated by interferon (IFN) produced endogenously and almost all the properties showed that the carrier culture was maintained by horizontal transmission of the virus. Small-plaque mutants, but not temperature-sensitive variants, were selected during the persistent infection.MuV released from L-MuV cells (MuV-pi) replicated efficiently in L929 cells, while infection of L929 cells with the original MuV-o resulted in an abortive infection. The efficient replication of MuV-pi in L929 cells can be explained by the findings that MuV-pi induced IFN more slowly and had lower susceptibility to IFN in L929 cells than MuV-o did. M protein was synthesized to a considerable degree in MuV-pi-infected cells, while it could not be detected in MuV-o-infected cells. By contrast, MuV-pi formed small plaques in Vero cell monolayers and the yield of MuV-pi in Vero cells was lower than that of MuV-o.M protein-induced by MuV-pi decayed easily in Vero cells. M protein was considered to be a limiting factor for MuV replication in both cell lines.

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Persistent infections with Sendai virus and Newcastle disease viruses

Lawton

Karimi

Mancinelli

et al. 1986

Archives of Virology

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Persistent infections (Pi) were established in two host-cell systems [Madin-Darby bovine kidney (MDBK) and Madin-Darby canine kidney (MDCK)] with Sendai virus and three strains of NDV, to test the influence of different viruses and host-cell systems. Virus was recovered from the persistently infected cells. An RNA- ts mutant was recovered from a Pi of MDBK cells, but no Pi could be established in MDCK cells with the three strains of NDV. Additionally, the Pi was established exclusively by a virulent strain, NDV-Milano. On the other hand, Sendai virus could establish Pi in MDBK and MDCK cell-systems. Several ts mutants were recovered from "late" passages of Pi, and from an accidental infection, a ts mutant with an altered P polypeptide. Ten other ts mutants were tested, however, the specific ts lesion could not be identified. From three Pi in MDCK cells, host range mutants (ts-f1, ts-f2, and ts-f3) were recovered. One of the mutants (ts-f1) has an altered M (matrix) protein. The host range mutants undergo a productive infection in MDBK and MDCK cells, which are nonpermissive for wild type Sendai virus. The possible significance of the results are discussed.

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A simple procedure for the analysis of the structural proteins of influenza and parainfluenza viruses involving adsorption to erythrocytes

Cited by 5 publications

References 20 publications

Parainfluenza Viruses

Parainfluenza Viruses

Persistence of Mumps Virus in Mouse L929 Cells

Persistent infections with Sendai virus and Newcastle disease viruses

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