Defective interfering particles of respiratory syncytial virus

Treuhaft, Mary W.; Beem, Marc O.

doi:10.1128/iai.37.2.439-444.1982

Cited by 58 publications

(25 citation statements)

References 13 publications

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“…The poor replication in mice of RS virus grown in Vero and MA104 cells may be due to defective interfering particles or to the selection of virus with a low infectivity for mice. It is unlikely that defective interfering particles were produced in Vero or MA104 cells, as all cells were inoculated at low multiplicity of infection (13). Further, dilution of the inoculum failed to increase the infectivity of the virus for mice.…”

Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus infection in mice

Taylor¹,

Stott²,

Hughes³

et al. 1984

Infect Immun

143

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The A2 strain of human respiratory syncytial virus replicated in the nose and lung of BALB/c mice, with virus growing to higher titers in older animals than in younger animals. Virus was recovered from the nose between days 2 and 7 with peak titers on days 3 and 4, and from the lungs between days 2 and 9, with peak titers on days 4 through 6. Serum antibody developed 2 weeks after infection. Viral antigen was demonstrated in the alveolar cells of the lung by immunofluorescence. Histopathological changes included infiltration by mononuclear cells of the peribronchiolar and perivascular tissue, some interstitial thickening, and formation of multinucleated giant cells. Virus could not be recovered from the respiratory tract of mice inoculated with bovine strains of respiratory syncytial virus. Growth of the A2 strain of human respiratory syncytial virus in different cell lines affected its infectivity for mice. Infection of BALB/c mice with respiratory syncytial virus provides a highly reproducible model for the study of the pathogenesis of and mechanisms of immunity to this virus.

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Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus infection in mice

Taylor¹,

Stott²,

Hughes³

et al. 1984

Infect Immun

143

View full text Add to dashboard Cite

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“…RSV antigen was detected in respiratory tract cells and in cells from virus isolation tubes by 107 PFU/ml was diluted 1:100 in the medium indicated and placed in tubes (1 ml per tube); tubes were incubated at either 25 or 4°C (on ice). At 0, 6, and 24 h, the mean surviving virus for each diluent-temperature combination was determined by plaque assay (11) of three replicate tubes in quadruplicate (n = 12). The coefficient of variation for the estimates ranged from 15 to 26%.…”

Section: Methodsmentioning

confidence: 99%

Practical recommendations for the detection of pediatric respiratory syncytial virus infections

Treuhaft¹,

Soukup²,

Sullivan³

1985

J Clin Microbiol

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In our private clinic-hospital setting, respiratory syncytial virus (RSV) was isolated from infants more frequently and sooner from nasal washes (84%; 4.2 days) than from throat swabs (45%; 5.5 days) or nasopharyngeal swabs (39%; 5.7 days). Immunofluorescence of nasal wash cells identified 72% of the infants with virus isolations from nasal washes in less than one day. We therefore recommend the combination of isolation and immunofluorescence on nasal wash specimens for optimal detection of RSV-infected infants. Immunofluorescence of respiratory tract cells was also useful for monitoring the presence of RSV antigen in intubation secretions during ribavirin antiviral therapy. RSV infectivity was maintained in phosphate-buffered saline at room temperature for 6 h. Transport and inoculation of specimens in less than 6 h yielded RSV isolates from 50% of sampled infants during the two RSV seasons examined. For optimal RSV isolation, we recommend inoculation of HEp-2 tubes less than or equal to 4 days old. Replacing medium after 3 days as compared with 7 days did not increase recovery of RSV and provided little practical reduction in time to detection of cytopathology.

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“…DVGs were discovered during the search for factors responsible for reduced infectivity of influenza virus after passages at high titers 2 . DVGs with the ability to interfere with the replication of their parental virus both in vitro and in vivo are found in most positive and negative-sense (ns)RNA viruses 54,[74][75][76][77][78][79][80][81][82] . DVGs accumulate at higher rates than full-length viral genomes in co-infected cells due to their shortened length and, in the case of copy-back species, their highly efficient flanking trailer promoters 83,84 .…”

Section: Roles In Pathogenesismentioning

confidence: 99%

Defective viral genomes are key drivers of the virus–host interaction

2019

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Viruses survive often harsh host environments, yet we know little about the strategies they utilize to adapt and subsist given their limited genomic resources. We are beginning to appreciate the surprising versatility of viral genomes and how replicationcompetent and -defective virus variants can provide means for adaptation, immune escape and virus perpetuation. This Review summarizes current knowledge of the types of defective viral genomes generated during the replication of RNA viruses and the functions that they carry out. We highlight the universality and diversity of defective viral genomes during infections and discuss their predicted role in maintaining a fit virus population, their impact on human and animal health, and their potential to be harnessed as antiviral tools. Review ARticleNATuRe MicRoBiology extinction interfere with replication of a wild-type viral genome 29,30 . Hypermutations and mutations leading to frame shifts also result in defective viruses 31 (Fig. 1a). One example is mutations introduced by the cellular protein APOBEC3G into pro-retroviruses 32 . APOBEC3G deaminates deoxycytidine nucleotides in the viral DNA, leading to hypermutations that interfere with the ability of the viral genome to integrate into the host genome and replicate. Interestingly, in opposition to an interfering activity for these mutated pro-viruses, it has been proposed that defective proviruses enhance fitness and that complementation among them drives viral persistence and pathogenesis 33,34 .Deletions. The genomic viral species most commonly referred to as DVGs are truncated viral genomes resulting from large internal deletions occurring during viral replication. Deletion DVGs tend to bear single large truncations that remove several or all essential genes required for self-propagation while retaining 5′ and 3′ ends as well as other RNA structural elements required for polymerase binding, replication and/or packaging [35][36][37] . Multiple variants also exist, including DVGs that can be described as 'mosaic' in that they appear to be the result of multiple recombination and rearrangement events, including deletions, insertions, duplications and even inversions of parts of the genome [38][39][40] (Fig. 1b). Copy-backs.Copy-back and snap-back DVGs are rearranged genomes in which a sequence is duplicated in reverse complement to create theoretical stem-like structures (panhandle structures for copy-back DVGs or hairpin structures for snap-back DVGs) 41-43 . Copy-back DVGs have been reported in many negative-sense (ns) RNA viruses and are generated from the 5′ end of the genome in a process that produces DVGs with complementary 3′ and 5′ termini 44,45 . If the complementary region of the DVG comprises almost the entire sequence, the DVG can be further characterized as a snap-back DVG 43 (Fig. 1c). Copy-back DVGs are predicted to be generated when the viral RNA-dependent RNA polymerase (RdRP) detaches from the template and reattaches to the nascent strand, copying back the end of the genome 42,46 .

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Defective interfering particles of respiratory syncytial virus

Cited by 58 publications

References 13 publications

Respiratory syncytial virus infection in mice

Respiratory syncytial virus infection in mice

Practical recommendations for the detection of pediatric respiratory syncytial virus infections

Defective viral genomes are key drivers of the virus–host interaction

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