The impact of pandemic influenza A (H1N1) 2009 on the circulation of respiratory viruses 2009–2011

Mak, Gannon C.K.; Wong, April S. Y.; Ho, Winnie Y. Y.; Lim, Wilina

doi:10.1111/j.1750-2659.2011.00323.x

Cited by 68 publications

(78 citation statements)

References 8 publications

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“…This downward trend in 2009 may have been associated with the extensive circulation of H1N1 in this period. A similar phenomenon was reported by Mak and co-workers in Hong Kong and is most likely explained by virus interference 11 . Regarding the severity of respiratory infections, using ICU admission as a surrogate measure, we observed higher rates of ICU admission for RSV and ADV infection in 2007 and 2010, whereas in 2008 and 2009, the highest rates of ICU admission were attributable to H1N1 and ADV ( Table 1).…”

Section: Number Suspicious/confirmed Casessupporting

confidence: 55%

Viral epidemiology of respiratory infections among children at a tertiary hospital in Southern Brazil

de‐Paris

Beck

Pires

et al. 2014

Rev. Soc. Bras. Med. Trop.

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Section: Number Suspicious/confirmed Casessupporting

confidence: 55%

Viral epidemiology of respiratory infections among children at a tertiary hospital in Southern Brazil

de‐Paris

Beck

Pires

et al. 2014

Rev. Soc. Bras. Med. Trop.

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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: 87%

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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“…The putative mechanism that would create dependence or interference among waves of different co-circulating respiratory viruses would be post-infection raised antibody or cytokine concentrations [53][54][55] generated by one viral epidemic preventing an epidemic of a different virus from taking off immediately thereafter. Epidemiological interference among respiratory viruses has been observed in long-term time series in temperate 56,57 and tropical 58 regions, but the strength and duration of this effect is not well understood. In our community study, additional molecular confirmations for a range of respiratory pathogens are now underway to further describe this phenomenon.…”

Section: Discussionmentioning

confidence: 99%

Non-annual seasonality of influenza-like illness in a tropical urban setting

Lam

Wesolowski

Hung

et al. 2017

Preprint

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In temperate countries, influenza and other viral respiratory diseases often have distinct seasonal peaks occurring during colder, wintertime months. However, little is known about the dynamics of influenza and viral respiratory disease dynamics in the tropics, despite high morbidity and a clear epidemiological link between tropical and temperate countries. In temperate countries, the dynamics of influenza and other respiratory diseases are often analyzed using syndromic surveillance data describing influenza-like illness (ILI) as ILI is highly correlated with virological surveillance for influenza. To obtain a detailed picture of respiratory disease incidence patterns in a large tropical city, we established an mHealth study in community outpatient clinics in Ho Chi Minh City, Vietnam (11N latitude). From August 2009 through December 2015, clinics reported daily case numbers of ILI using standard mobile-phone SMS messaging. A subset of these clinics performed molecular diagnostics for influenza A and B viruses. Unlike the annual patterns seen in temperate countries, ILI activity in Ho Chi Minh City exhibited strong non-annual periodicity and was not correlated with PCR-confirmed influenza. The dominant periodicity in the data was approximately 200 days. This was confirmed by a time series decomposition, a step-wise regression analysis on annual and non-annual covariates, and a forecasting exercise showing that forecasting was 30% to 40% more accurate when a 200-day non-annual cycle was included in the forecast. This suggests, for the first-time, that a non-annual cycle may be an essential driver of ILI dynamics in the tropics. This raises new questions about the seasonality and drivers of respiratory disease transmission in tropical countries.

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The impact of pandemic influenza A (H1N1) 2009 on the circulation of respiratory viruses 2009–2011

Cited by 68 publications

References 8 publications

Viral epidemiology of respiratory infections among children at a tertiary hospital in Southern Brazil

Viral epidemiology of respiratory infections among children at a tertiary hospital in Southern Brazil

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

Non-annual seasonality of influenza-like illness in a tropical urban setting

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