Reproducibility of Serologic Assays for Influenza Virus A (H5N1)

Stephenson, Iain; Heath, Alan; Major, Diane; Newman, Robert W.; Höschler, Katja; Junzi, Wang; Katz, Jacqueline M.; Weir, Jerry P.; Zambon, Maria; Wood, John M.

doi:10.3201/eid1508.081754

Cited by 121 publications

(119 citation statements)

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“…However, this does not rule out the possibility that some serologic assays fail to identify antibodies in older individuals, or reflect antibodies among older individuals in countries without high routine seasonal influenza vaccination coverage 62. Differences in laboratory methodology rather than real differences in pre‐existing immunity would also explain the observation that reported cumulative incidence was not higher in ≥65 year olds in Asia where pre‐pandemic seroprevalence was found to be lower 62. We also observed low‐level pre‐pandemic seropositivity in children (<5%) and adolescents (<10%) in some countries, which may again be due to assay differences between laboratories.…”

Section: Discussionmentioning

confidence: 98%

“…Therefore, given the small numbers of studies in individual regions, these patterns may reflect differences in laboratory methodology. However, this does not rule out the possibility that some serologic assays fail to identify antibodies in older individuals, or reflect antibodies among older individuals in countries without high routine seasonal influenza vaccination coverage 62. Differences in laboratory methodology rather than real differences in pre‐existing immunity would also explain the observation that reported cumulative incidence was not higher in ≥65 year olds in Asia where pre‐pandemic seroprevalence was found to be lower 62.…”

Section: Discussionmentioning

confidence: 99%

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Estimating age‐specific cumulative incidence for the 2009 influenza pandemic: a meta‐analysis of A(H1N1)pdm09 serological studies from 19 countries

Kerkhove¹,

Hirve

Koukounari

et al. 2013

Influenza Resp Viruses

162

139

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BackgroundThe global impact of the 2009 influenza A(H1N1) pandemic (H1N1pdm) is not well understood.ObjectivesWe estimate overall and age‐specific prevalence of cross‐reactive antibodies to H1N1pdm virus and rates of H1N1pdm infection during the first year of the pandemic using data from published and unpublished H1N1pdm seroepidemiological studies.MethodsPrimary aggregate H1N1pdm serologic data from each study were stratified in standardized age groups and evaluated based on when sera were collected in relation to national or subnational peak H1N1pdm activity. Seropositivity was assessed using well‐described and standardized hemagglutination inhibition (HI titers ≥32 or ≥40) and microneutralization (MN ≥ 40) laboratory assays. The prevalence of cross‐reactive antibodies to the H1N1pdm virus was estimated for studies using sera collected prior to the start of the pandemic (between 2004 and April 2009); H1N1pdm cumulative incidence was estimated for studies in which collected both pre‐ and post‐pandemic sera; and H1N1pdm seropositivity was calculated from studies with post‐pandemic sera only (collected between December 2009–June 2010).ResultsData from 27 published/unpublished studies from 19 countries/administrative regions – Australia, Canada, China, Finland, France, Germany, Hong Kong SAR, India, Iran, Italy, Japan, Netherlands, New Zealand, Norway, Reunion Island, Singapore, United Kingdom, United States, and Vietnam – were eligible for inclusion. The overall age‐standardized pre‐pandemic prevalence of cross‐reactive antibodies was 5% (95%CI 3–7%) and varied significantly by age with the highest rates among persons ≥65 years old (14% 95%CI 8–24%). Overall age‐standardized H1N1pdm cumulative incidence was 24% (95%CI 20–27%) and varied significantly by age with the highest in children 5–19 (47% 95%CI 39–55%) and 0–4 years old (36% 95%CI 30–43%).ConclusionsOur results offer unique insight into the global impact of the H1N1 pandemic and highlight the need for standardization of seroepidemiological studies and for their inclusion in pre‐pandemic preparedness plans. Our results taken together with recent global pandemic respiratory‐associated mortality estimates suggest that the case fatality ratio of the pandemic virus was approximately 0·02%.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Estimating age‐specific cumulative incidence for the 2009 influenza pandemic: a meta‐analysis of A(H1N1)pdm09 serological studies from 19 countries

Kerkhove¹,

Hirve

Koukounari

et al. 2013

Influenza Resp Viruses

162

139

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“…69,70,77 The immunogenicity of the two-dose schedule of the two influenza 2009 H1N1 vaccines was assessed by HI assay, according to standard methods, [78][79][80] …”

Section: Discussionmentioning

confidence: 99%

A randomised, partially observer blind, multicentre, head-to-head comparison of a two-dose regimen of Baxter and GlaxoSmithKline H1N1 pandemic vaccines, administered 21 days apart

Nicholson

Abrams²,

Batham³

et al. 2010

Health Technol Assess

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A randomised, partially observer-blind, multicentre, head-to-head comparison of a two-dose regimen of Baxter and GlaxoSmithKline H1N1 pandemic vaccines, administered 21 days apart KG Participants: Three hundred and forty-seven subjects were identified and randomised to AS03 A -adjuvanted split-virion H1N1 vaccine or whole-virion (WV) vaccine in age groups [≥ 18-44 years (n = 140), ≥ 45-64 years (n = 136) and ≥ 65 years (n = 71)]. Interventions: Vaccine was administered by intramuscular injection into the deltoid muscle of the non-dominant arm. One hundred and seventy-five randomised subjects were allocated AS03 A -adjuvanted split H1N1 vaccine; one hundred and sixty-nine subjects had a second dose of the same vaccine 21 days later. One hundred and seventy-two subjects were allocated WV vaccine; one hundred and seventy-one subjects had a second dose of the same vaccine 21 days later. Serum samples for antibody measurements were collected on days 0 (before the first vaccination), 7, 14, 21 (before the second vaccination), 28, 35, 42 and 180. Subjects were observed for local and systemic reactions for 30 minutes after each injection, and for the next 7 days they recorded, in self-completed diaries, the severity of solicited local (pain, bruising, erythema and swelling) and systemic symptoms (chills, malaise, muscle aches, nausea and headache), oral temperature and use of analgesic medications. Main outcome measures: Vaccine immunogenicity using the CHMP and the FDA licensing criteria. Antibody titres were measured using haemagglutination inhibition (HI) and microneutralisation (MN) assays at baseline and 7, 14 and 21 days after each vaccination and at day 180. The three immunogenicity criteria end points were the seroprotection rate, the seroconversion rate and the mean-fold titre elevation. Results: Both vaccine doses were given in 340 subjects (98%). Data from 680 (99%) of 687 issued diary cards were returned. Sera were obtained from 340 (98.0%), 333 (96.0%), 341 (98.3%), 331 (95.4%), Abstract 196 329 (94.8%) and 332 (95.7%) subjects on days 7, 14, 21, 28, 35 and 42, respectively. Three hundred and fortysix and 345 subjects were included in the safety and immunogenicity analyses, respectively. Prevaccination antibody was detected by HI (titre ≥ 1 : 8) and MN (titre ≥ 1 : 10) in 14% and 31% of subjects, respectively. Among the 298 (85.9%) subjects without baseline antibody on HI assay, a titre of ≥ 1 : 40 (seroprotection) was achieved after a single dose of AS03 A -adjuvanted vaccine and WV vaccine by day 21 in 93.0% and 65.5%, respectively, of subjects between 18 and 44 years, 76.4% and 36.1% of subjects between 45 and 64 years, and 53.1% and 30.0% of subjects ≥ 65 years. Among all 347 subjects, a titre of ≥ 1 : 40 was achieved after a single dose of AS03 A -adjuvanted vaccine and WV vaccine by day 21 in 94.0% and 71.4%, respectively, of subjects between 18 and 44 years, 77.3% and 38.8% of subjects between 45 and 64 years, and 51.4% and 32.4% of subjects ≥ 65 years. The age-adjusted odds ratio (OR) for ...

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“…Although a survey in two affected villages in Cambodia found serological evidence of subclinical A/H5N1 infection in seven (1 %) out of 674 subjects [24], evidence from active surveillance and serological surveys of populations known to be exposed to A/H5N1 generally indicates that large numbers of cases are not being missed [19,21,[25][26][27][28][29][30][31][32][33]. While the sensitivity and reproducibility of serological assays for A/H5N1 infection is variable, many serological studies have used the gold standard of microneutralization assay with Western blot confirmation and therefore provide the best estimate currently available of A/H5N1 infection prevalence [34,35]. The apparent low incidence of infection following exposure to sick poultry and the low risk in some intensely exposed groups indicates a substantial species barrier, but a barrier that seems to be much weaker in a small number of individuals and families [36].…”

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confidence: 99%

What is the evidence of a role for host genetics in susceptibility to influenza A/H5N1?

et al. 2010

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SUMMARYThe apparent family clustering of avian influenza A/H5N1 has led several groups to postulate the existence of a host genetic influence on susceptibility to A/H5N1, yet the role of host factors on the risk of A/H5N1 disease has received remarkably little attention compared to the efforts focused on viral factors. We examined the epidemiological patterns of human A/H5N1 cases, their possible explanations, and the plausibility of a host genetic effect on susceptibility to A/H5N1 infection. The preponderance of familial clustering of cases and the relative lack of non-familial clusters, the occurrence of related cases separated by time and place, and the paucity of cases in some highly exposed groups such as poultry cullers, are consistent with a host genetic effect. Animal models support the biological plausibility of genetic susceptibility to A/H5N1. Although the evidence is circumstantial, host genetic factors are a parsimonious explanation for the unusual epidemiology of human A/H5N1 cases and warrant further investigation.

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Reproducibility of Serologic Assays for Influenza Virus A (H5N1)

Abstract: Results for clade 1 viruses were more consistent among laboratories when a standard antibody was used.

Cited by 121 publications

References 12 publications

Estimating age‐specific cumulative incidence for the 2009 influenza pandemic: a meta‐analysis of A(H1N1)pdm09 serological studies from 19 countries

Estimating age‐specific cumulative incidence for the 2009 influenza pandemic: a meta‐analysis of A(H1N1)pdm09 serological studies from 19 countries

A randomised, partially observer blind, multicentre, head-to-head comparison of a two-dose regimen of Baxter and GlaxoSmithKline H1N1 pandemic vaccines, administered 21 days apart

What is the evidence of a role for host genetics in susceptibility to influenza A/H5N1?

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