The Role of the Interferon System in Respiratory Syncytial Virus Infections

Moehring, Joan M.; Forsyth, Ben R.

doi:10.3181/00379727-138-36039

Cited by 16 publications

(10 citation statements)

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“…As seen in the present study of BRSV, these differences may be related to the strain of virus (32,34) and/or the origin of the cells. Although there was some variation in the IFN response induced by different WT strains of BRSV and in the IFN response of BAM from different cattle, rBRSVs lacking the NS2 gene consistently induced significantly higher levels of IFN than any of the WT BRSVs.…”

Section: Discussionmentioning

confidence: 62%

Role of Alpha/Beta Interferons in the Attenuation and Immunogenicity of Recombinant Bovine Respiratory Syncytial Viruses Lacking NS Proteins

Valarcher

Furze

Wyld

et al. 2003

J Virol

140

133

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Bovine respiratory syncytial virus (BRSV) is an enveloped, nonsegmented, negative-stranded RNA virus and is a major cause of respiratory disease in young calves (44). BRSV is closely related to human RSV (HRSV), which is a major cause of respiratory disease in young children (10), and the epidemiology and pathogenesis of infection with these viruses are similar (44). These features make BRSV infection in calves a good model for the study of HRSV. HRSV and BRSV belong to the Pneumovirus genus within the Paramyxoviridae family. One of the major differences between this genus and all the other Paramyxoviridae is the presence of two nonstructural (NS) genes called NS1 and NS2. These genes code for two proteins, which are abundantly transcribed in virus-infected cells. Comparison of the sequence of the NS proteins of BRSV with that of HRSV subgroup A and B reveals amino acid identities of 69 and 68% for the NS1 protein and 84 and 83% for the NS2 protein, respectively (8, 39).The role(s) of the NS proteins is not fully defined. They are not essential for virus replication in vitro, although the growth of recombinant HRSV and BRSV lacking these proteins is attenuated in cell culture (8,25,42,51). There is evidence that the HRSV NS1 protein coprecipitates with the M protein (19), and in experiments using HRSV minigenomes, the NS1 protein appears to be a strong inhibitor of viral RNA transcription and replication (1). The NS2 protein also appears to be a transcriptional inhibitor but at a lower level than is the NS1 protein (1). The NS2 protein colocalizes with the P and N proteins in infected cells (60) but does not coprecipitate with any viral protein (19). In addition, the NS1 and NS2 proteins of BRSV and HRSV mediate resistance to the antiviral action of alpha/beta inferferons (IFN-␣/␤) (3, 42).Anti-IFN activity has been described for accessory proteins for a number of other negative-stranded RNA viruses. Of those characterized to date, some block the IFN response by hindering the late-stage activation of antiviral genes. For example, the C protein of Sendai virus inhibits STAT1 activation by hampering phosphorylation and by increasing instability (21, 64) and the V protein of simian virus 5 inhibits the activation of IFN-responsive genes by targeting STAT1 for proteasome-mediated degradation (13). Other viral accessory proteins, such as influenza A virus NS1 protein and Bunyamwera virus NSs protein, inhibit the production of IFN-␣/␤ (58, 61).

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Section: Discussionmentioning

confidence: 62%

Role of Alpha/Beta Interferons in the Attenuation and Immunogenicity of Recombinant Bovine Respiratory Syncytial Viruses Lacking NS Proteins

Valarcher

Furze

Wyld

et al. 2003

J Virol

140

133

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“…All 52 infants recovered from their respiratory syncytial virus infection. The duration of hospital stay ranged from four to 12 days with a mean of [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] (173) days. The duration of hospital stay was not further compared in the two groups as uniform discharge criteria were not applied during the study period.…”

Section: Resultsmentioning

confidence: 99%

Treatment of respiratory syncytial virus infection with recombinant interferon alfa-2a.

Sung

Yin

Oppenheimer

et al. 1993

Archives of Disease in Childhood

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however, had a significantly higher overall score for severity of illness at the start of treatment. More rapid drop of the clinical score was observed in the INF-a-2a group after treatment in the first three days and the two groups had similar clinical severity by day 3. There was no significant difference of the duration ofviral shedding in the two groups. In conclusion, the overall clinical improvement was greater in the treatment group over the first three days, but the duration of viral shedding was not altered.

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“…IL-6 is expressed by RSV-infected lung epithelial cells [8] and monocytes [3,5,18], and its lack of expression in cotton rat secondary infection appears to be linked to the abortive cycle of viral replication. The induction of IFN-a expression by RSV has been controversial, with low or undetectable levels of IFN-a in nasal washes [19][20][21] or in peripheral blood monocytes and macrophages [22,23]. The absence of IFN-a in some human specimens during primary infection may be due to its relatively brief expression, since most patients would not be examined until > 3 days after infection.…”

Section: Discussionmentioning

confidence: 99%

Cytokine and Chemokine Gene Expression after Primary and Secondary Respiratory Syncytial Virus Infection in Cotton Rats

Blanco¹,

Richardson

Darnell

et al. 2002

J INFECT DIS

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The induction of pro- and anti-inflammatory cytokines and chemokines was studied in the lungs of cotton rats after primary or secondary infection with respiratory syncytial virus (RSV). Increases in messenger RNA (mRNA) levels of all genes analyzed were observed during the course of primary infection. In general, mRNA expression peaked between postinfection days 1 and 4 and returned to near-normal levels by day 10. During secondary infection, the expression of some genes (i.e., interferon [IFN]-gamma and interleukin [IL]-10) began earlier, some (i.e., IL-1beta and macrophage inflammatory protein-1beta) began later, and some (i.e., IL-1beta, IL-10, growth-regulated protein, and tumor necrosis factor-alpha) showed prolonged expression, whereas 2 genes (i.e., IFN-alpha and IL-6) were not expressed. This study presents evidence of different kinetics of expression of inflammatory mediators during primary and secondary infection that likely coincide with innate and adaptive immune response and complement previous observations that emphasize the role of inflammation in the pathogenesis of RSV disease.

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The Role of the Interferon System in Respiratory Syncytial Virus Infections

Cited by 16 publications

References 0 publications

Role of Alpha/Beta Interferons in the Attenuation and Immunogenicity of Recombinant Bovine Respiratory Syncytial Viruses Lacking NS Proteins

Role of Alpha/Beta Interferons in the Attenuation and Immunogenicity of Recombinant Bovine Respiratory Syncytial Viruses Lacking NS Proteins

Treatment of respiratory syncytial virus infection with recombinant interferon alfa-2a.

Cytokine and Chemokine Gene Expression after Primary and Secondary Respiratory Syncytial Virus Infection in Cotton Rats

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