Does homologous reinfection drive multiple-wave influenza outbreaks? Accounting for immunodynamics in epidemiological models

Camacho, Anton; Cazelles, Bernard

doi:10.1016/j.epidem.2013.09.003

Cited by 23 publications

(20 citation statements)

References 39 publications

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“…Several populations have experienced severe follow-up waves of A(H1N1)pdm09 infection in the postpandemic season in the absence of any reported antigenic drift (15,16), with waning humoral immunity raised as a potential explanation (17). Our results, using longitudinal data from individuals, are the first to provide robust evidence that repeat pandemic waves prior to antigenic drift (18) are not driven by waning humoral immunity.…”

Section: Discussionsupporting

confidence: 57%

Longevity and Determinants of Protective Humoral Immunity after Pandemic Influenza Infection

Sridhar

Begom

Höschler

et al. 2015

Am J Respir Crit Care Med

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Rationale: Antibodies to influenza hemagglutinin are the primary correlate of protection against infection. The strength and persistence of this immune response influences viral evolution and consequently the nature of influenza epidemics. However, the durability and immune determinants of induction of humoral immunity after primary influenza infection remain unclear.Objectives: The spread of a novel H1N1 (A[H1N1]pdm09) virus in 2009 through an unexposed population offered a natural experiment to assess the nature and longevity of humoral immunity after a single primary influenza infection.Methods: We followed A(H1N1)pdm09-seronegative adults through two influenza seasons (2009-2011) as they developed A(H1N1)pdm09 influenza infection or were vaccinated. Antibodies to A(H1N1)pdm09 virus were measured by hemagglutinationinhibition assay in individuals with paired serum samples collected preinfection and postinfection or vaccination to assess durability of humoral immunity. Preexisting A(H1N1)pdm09-specific multicytokine-secreting CD4 and CD8 T cells were quantified by multiparameter flow cytometry to test the hypothesis that higher frequencies of CD4 1 T-cell responses predict stronger antibody induction after infection or vaccination.Measurements and Main Results: Antibodies induced by natural infection persisted at constant high titer for a minimum of approximately 15 months. Contrary to our initial hypothesis, the fold increase in A(H1N1)pdm09-specific antibody titer after infection was inversely correlated to the frequency of preexisting circulating A(H1N1)pdm09-specific CD4 1 IL-2 1 IFN-g 2 TNF-a 2 T cells (r = 20.4122; P = 0.03).Conclusions: The longevity of protective humoral immunity after influenza infection has important implications for influenza transmission dynamics and vaccination policy, and identification of its predictive cellular immune correlate could guide vaccine development and evaluation.

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Section: Discussionsupporting

confidence: 57%

Longevity and Determinants of Protective Humoral Immunity after Pandemic Influenza Infection

Sridhar

Begom

Höschler

et al. 2015

Am J Respir Crit Care Med

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“…[3]. These population-level observations of viral interference arise from the interplay between (1) immunodynamics (ie, host-level viral interference), (2) heterogeneity between hosts (ie, differences in immunity to virus strains between individuals), and (3) transmission dynamics (ie, within or between different age groups) [43]. For influenza, these processes have been investigated in some detail.…”

Section: Discussionmentioning

confidence: 99%

Investigating Viral Interference Between Influenza A Virus and Human Respiratory Syncytial Virus in a Ferret Model of Infection

Chan

Carolan

Korenkov

et al. 2018

The Journal of Infectious Diseases

102

148

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Epidemiological studies have observed that the seasonal peak incidence of influenza virus infection is sometimes separate from the peak incidence of human respiratory syncytial virus (hRSV) infection, with the peak incidence of hRSV infection delayed. This is proposed to be due to viral interference, whereby infection with one virus prevents or delays infection with a different virus. We investigated viral interference between hRSV and 2009 pandemic influenza A(H1N1) virus (A[H1N1]pdm09) in the ferret model. Infection with A(H1N1)pdm09 prevented subsequent infection with hRSV. Infection with hRSV reduced morbidity attributed to infection with A(H1N1)pdm09 but not infection, even when an increased inoculum dose of hRSV was used. Notably, infection with A(H1N1)pdm09 induced higher levels of proinflammatory cytokines, chemokines, and immune mediators in the ferret than hRSV. Minimal cross-reactive serological responses or interferon γ-expressing cells were induced by either virus ≥14 days after infection. These data indicate that antigen-independent mechanisms may drive viral interference between unrelated respiratory viruses that can limit subsequent infection or disease.

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“…In the Tristan da Cunha isolate, for example, there is a 45% prevalence of atopy and a 36% prevalence of asthma (Mantle and Tyrrell, 1973; Zamel et al, 1996; Camacho et al, 2011; Camacho and Cazelles, 2013). By comparison, the prevalence of asthma in most out-bred populations rarely exceeds 10%.…”

Section: Introductionmentioning

confidence: 99%

“…By comparison, the prevalence of asthma in most out-bred populations rarely exceeds 10%. The severity of the Tristan da Cunha atopy phenotype may be reflected in events such as the Tristan da Cunha influenza epidemic of 1971 (Mantle and Tyrrell, 1973; Zamel et al, 1996; Camacho et al, 2011; Camacho and Cazelles, 2013). …”

Section: Introductionmentioning

confidence: 99%

Cysteinyl Leukotrienes Pathway Genes, Atopic Asthma and Drug Response: From Population Isolates to Large Genome-Wide Association Studies

et al. 2016

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Genetic variants associated with asthma pathogenesis and altered response to drug therapy are discussed. Many studies implicate polymorphisms in genes encoding the enzymes responsible for leukotriene synthesis and intracellular signaling through activation of seven transmembrane domain receptors, such as the cysteinyl leukotriene 1 (CYSLTR1) and 2 (CYSLTR2) receptors. The leukotrienes are polyunsaturated lipoxygenated eicosatetraenoic acids that exhibit a wide range of pharmacological and physiological actions. Of the three enzymes involved in the formation of the leukotrienes, arachidonate 5 lipoxygenase 5 (ALOX5), leukotriene C4 synthase (LTC4S), and leukotriene hydrolase (LTA4H) are all polymorphic. These polymorphisms often result in variable production of the CysLTs (LTC4, LTD4, and LTE4) and LTB4. Variable number tandem repeat sequences located in the Sp1-binding motif within the promotor region of the ALOX5 gene are associated with leukotriene burden and bronchoconstriction independent of asthma risk. A 444A > C SNP polymorphism in the LTC4S gene, encoding an enzyme required for the formation of a glutathione adduct at the C-6 position of the arachidonic acid backbone, is associated with severe asthma and altered response to the CYSLTR1 receptor antagonist zafirlukast. Genetic variability in the CysLT pathway may contribute additively or synergistically to altered drug responses. The 601 A > G variant of the CYSLTR2 gene, encoding the Met201Val CYSLTR2 receptor variant, is associated with atopic asthma in the general European population, where it is present at a frequency of ∼2.6%. The variant was originally found in the founder population of Tristan da Cunha, a remote island in the South Atlantic, in which the prevalence of atopy is approximately 45% and the prevalence of asthma is 36%. In vitro work showed that the atopy-associated Met201Val variant was inactivating with respect to ligand binding, Ca2+ flux and inositol phosphate generation. In addition, the CYSLTR1 gene, located at Xq13-21.1, has been associated with atopic asthma. The activating Gly300Ser CYSLTR1 variant is discussed. In addition to genetic loci, risk for asthma may be influenced by environmental factors such as smoking. The contribution of CysLT pathway gene sequence variants to atopic asthma is discussed in the context of other genes and environmental influences known to influence asthma.

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Does homologous reinfection drive multiple-wave influenza outbreaks? Accounting for immunodynamics in epidemiological models

Cited by 23 publications

References 39 publications

Longevity and Determinants of Protective Humoral Immunity after Pandemic Influenza Infection

Longevity and Determinants of Protective Humoral Immunity after Pandemic Influenza Infection

Investigating Viral Interference Between Influenza A Virus and Human Respiratory Syncytial Virus in a Ferret Model of Infection

Cysteinyl Leukotrienes Pathway Genes, Atopic Asthma and Drug Response: From Population Isolates to Large Genome-Wide Association Studies

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