Epidemiological Changes of Respiratory Syncytial Virus (RSV) Infections in Israel

Hirsh, Shira; Hindiyeh, Musa; Kolet, Liat; Regev, Liora; Sherbany, Hilda; Yaary, Karnit; Mendelson, Ella; Mandelboim, Michal

doi:10.1371/journal.pone.0090515

Cited by 40 publications

(50 citation statements)

References 44 publications

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“…This phenomenon has been shown experimentally in animal models (1)(2)(3), as well as in humans given the live-attenuated IAV vaccine in clinical studies (4)(5)(6)(7), and has been postulated as a major factor in determining the rate of IAV antigenic drift (8). This temporary immunity has also been observed epidemically when the respiratory syncytial virus season was delayed as a result of the 2009 pandemic IAV outbreak occurring earlier than is normally seen with seasonal strains (9)(10)(11). Although observations of influenza-induced temporary immunity are well documented, how this protection is established is unknown.…”

mentioning

confidence: 84%

Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity

Hamilton

Sachs

Lim

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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A brief window of antigen-nonspecific protection has been observed after influenza A virus (IAV) infection. Although this temporary immunity has been assumed to be the result of residual nonspecific inflammation, this period of induced immunity has not been fully studied. Because IAV has long been characterized as a cytopathic virus (based on its ability to rapidly lyse most cell types in culture), it has been a forgone conclusion that directly infected cells could not be contributing to this effect. Using a Cre recombinase-expressing IAV, we have previously shown that club cells can survive direct viral infection. We show here not only that these cells can eliminate all traces of the virus and survive but also that they acquire a heightened antiviral response phenotype after surviving. Moreover, we experimentally demonstrate temporary nonspecific viral immunity after IAV infection and show that surviving cells are required for this phenotype. This work characterizes a virally induced modulation of the innate immune response that may represent a new mechanism to prevent viral diseases.influenza virus | RNA sequencing | alternative cell fate | antiviral immunity T here have been reports of a short period after influenza A virus (IAV) infection during which subsequent respiratory viral infection is restricted. This phenomenon has been shown experimentally in animal models (1-3), as well as in humans given the live-attenuated IAV vaccine in clinical studies (4-7), and has been postulated as a major factor in determining the rate of IAV antigenic drift (8). This temporary immunity has also been observed epidemically when the respiratory syncytial virus season was delayed as a result of the 2009 pandemic IAV outbreak occurring earlier than is normally seen with seasonal strains (9-11). Although observations of influenza-induced temporary immunity are well documented, how this protection is established is unknown.We have previously shown that respiratory epithelial cells (principally club cells) are infected by IAV and are capable of clearing infection and surviving for long periods in vivo (12). These surviving cells, characterized by an inflammatory transcriptional profile, contributed to bronchiolar epithelium damage. However, it was unclear why these cells would prolong an inflammatory state beyond the resolution of infection.In this report, we test the hypothesis that cells surviving IAV infection are involved in protecting the host from subsequent viral respiratory infections. We reasoned that the turnover of "survivor cells" could explain the temporary nature of IAVinduced antiviral immunity. We show that the cells that survive direct IAV infection are reprogrammed and exhibit an increased antiviral response to secondary infection and type I IFN. We also show that the overall immune response to secondary infection is different from the response to the primary infection. Finally, we demonstrate temporary, antigen-nonspecific viral immunity in the mouse model and show that surviving cells are required for this pr...

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mentioning

confidence: 84%

Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity

Hamilton

Sachs

Lim

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Genotypes GA2 and BA are also the most common RSV genotypes worldwide [30,32,34]. Recent data from Israel indicated that the majority of RSV-A viruses detected during 2008-2012 was GA2 [32]. These data also suggest that GA2 has been the predominant RSV-A genotype circulating in the Middle East between 2006 and 2012 [32].…”

Section: Geographical Differences In Rsv Genotypesmentioning

confidence: 95%

“…Monitoring circulating RSV strains in different geographical regions is essential, particularly in the western, eastern, northwestern, and southeastern parts of Iran, where available data is lacking. The continuous circulation of genotype GA2 emphasizes the stability of this subtype; it has become an epidemic in Europe, Asia and Africa [30,32,33]. Genotypes GA2 and BA are also the most common RSV genotypes worldwide [30,32,34].…”

Section: Geographical Differences In Rsv Genotypesmentioning

confidence: 99%

“…The continuous circulation of genotype GA2 emphasizes the stability of this subtype; it has become an epidemic in Europe, Asia and Africa [30,32,33]. Genotypes GA2 and BA are also the most common RSV genotypes worldwide [30,32,34]. Recent data from Israel indicated that the majority of RSV-A viruses detected during 2008-2012 was GA2 [32].…”

Section: Geographical Differences In Rsv Genotypesmentioning

confidence: 99%

“…Recent data from Israel indicated that the majority of RSV-A viruses detected during 2008-2012 was GA2 [32]. These data also suggest that GA2 has been the predominant RSV-A genotype circulating in the Middle East between 2006 and 2012 [32]. However conflicting data exist on whether RSV evolution is temporally or geographically related [30,32].…”

Section: Geographical Differences In Rsv Genotypesmentioning

confidence: 99%

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Prevalence of human respiratory syncytial virus circulating in Iran

Salimi

Tavakoli-Yaraki

Yavarian

et al. 2016

Journal of Infection and Public Health

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Respiratory syncytial virus (RSV) is a leading cause of acute respiratory infection during early childhood and is associated with a great burden on patients, parents, and society. While no treatment is yet available, results from recent phase 2 clinical trials of cell-entry inhibitors and RSV vaccines are promising. To prepare for introduction of these novel therapeutics, good understanding of its molecular epidemiology and continuous RSV surveillance data are necessary. This paper provides an overview of RSV prevalence and genotype distribution in Iran from 1996 to 2013. This meta-analysis includes 21 published studies. In total, 775 (18.7%) of 4140 respiratory specimens were positive for RSV infection. The male-female ratio of RSV-positive patients was 1.5:1. Significant peaks of RSV infection were detected during the cold season (November-March). RSV infection was mainly observed in patients <2 years of age. Phylogenetic studies showed that genotypes GA1, GA2, GA5, and BA co-circulated in Iran in 2007-2013. This review highlights the necessity of introducing standard molecular surveillance programs to inform the epidemiological, clinical, and pathological characteristics of various RSV genotypes. Improved understanding of the molecular epidemiology will be useful for development of novel RSV therapeutics.

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Epidemiological characteristics and immune status of children with Respiratory Syncytial Virus

Shao

Shang

et al. 2014

Journal of Medical Virology

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Respiratory Syncytial Virus (RSV) infections are the dominant cause of pneumonia in children. In order to determine the epidemiological characteristics and immune status of children with Respiratory Syncytial Virus, a prospective study was performed among patients with RSV infection. Comparisons between RSV pneumonia group and normal control group, RSV pneumonia group had lower IL-2 (median levels, pg/ml: 3.8 vs. 5.1, P < 0.01), and higher IL-4 (median levels, pg/ml: 3.2 vs. 2.4, P < 0.01), IL-10 (median levels, pg/ml: 12.2 vs. 2.3, P < 0.01), and IFN-γ (median levels, pg/ml: 13.4 vs. 4.6, P < 0.01). The level of IgE among pneumonia patients caused by RSV increased sharply (median levels, mg/L: 48.1 vs. 8.8, P < 0.01). Another amazing finding is that after birth, the degree of IgE of the children infected by RSV increases gradually with age. This effect is at its peak in 0.6 years old. The IgE and eosinophil levels were higher when patients suffered from RSV pneumonia with wheeze (IgE median levels, IU/ml: with wheeze: 72.74 vs. without wheeze: 11.5, P < 0.05; eosinophil median levels, ×10(9) /l: with wheeze: 0.21 vs. without wheeze: 0.05, P < 0.05). The main morbidity crowd is the children under the age of 1 year old. The downregulation of IL2 and the upregulation of IL-4, IL-10, IFN-γ, and IgE happen after RSV infection.

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Epidemiological Changes of Respiratory Syncytial Virus (RSV) Infections in Israel

Cited by 40 publications

References 44 publications

Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity

Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity

Prevalence of human respiratory syncytial virus circulating in Iran

Epidemiological characteristics and immune status of children with Respiratory Syncytial Virus

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