Pathogenic Responses among Young Adults during the 1918 Influenza Pandemic

Shanks, G. Dennis; Brundage, John F.

doi:10.3201/eid1802.102042

Cited by 97 publications

(84 citation statements)

References 30 publications

(47 reference statements)

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“…This animal and another from this group displayed signs of severe inflammation of the lungs upon histological examination, and it cannot be excluded that priming by infection with the seasonal influenza A/H3N2 virus predisposed animals to the development of more severe disease after intratracheal infection with the A(H1N1) pdm09 virus. It is possible that the induction of cross-reactive virus-specific T cells played a role in this immunopathological process (50)(51)(52).…”

Section: Discussionmentioning

confidence: 99%

Infection of the Upper Respiratory Tract with Seasonal Influenza A(H3N2) Virus Induces Protective Immunity in Ferrets against Infection with A(H1N1)pdm09 Virus after Intranasal, but Not Intratracheal, Inoculation

Bodewes

Kreijtz

Amerongen

et al. 2013

J Virol

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Section: Discussionmentioning

confidence: 99%

Infection of the Upper Respiratory Tract with Seasonal Influenza A(H3N2) Virus Induces Protective Immunity in Ferrets against Infection with A(H1N1)pdm09 Virus after Intranasal, but Not Intratracheal, Inoculation

Bodewes

Kreijtz

Amerongen

et al. 2013

J Virol

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“…First, a mechanism akin to original antigenic sin (OAS) (36) may have interfered with immune responses in some of those infected in 1918 (33,37), peaking in those exposed to the 1889 virus. Although OAS has been traditionally considered a within-subtype phenomenon (36,(38)(39)(40), it is plausible that interactions between heterosubtypic viruses could also occur (41).…”

Section: Significancementioning

confidence: 99%

Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus

Worobey

Han

Rambaut

2014

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

230

249

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The source, timing, and geographical origin of the 1918-1920 pandemic influenza A virus have remained tenaciously obscure for nearly a century, as have the reasons for its unusual severity among young adults. Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by ∼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged ∼20 to ∼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from ∼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections.phylogeny | cohort immunity | pathogenicity | virulence | reassortment

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“…Recent genomic studies of the 1918 pandemic H1N1 viruses suggest that there were at least two H1 viruses circulating during the pandemic that may have differed antigenically (Worobey et al, 2014), raising the possibility of antigen-dependent enhancement. Differential exposure in early life to distinct influenza viruses, even heterosubtypic strains, has been hypothesized to explain the unusual young adult mortality peak in 1918 (Shanks & Brundage, 2012;Worobey et al, 2014). The evidence here that VAERD due to mismatched HA immunity could be blocked by homologous NA immunity is an especially intriguing observation given that there were three separate waves of the 1918 influenza pandemic, one in early 1918 with little mortality despite much morbidity, followed by the second and third waves in late 1918-early 1919 that killed millions (Taubenberger & Morens, 2006), suggesting that they were caused by different virus strains with antigenically distinct HA and NA.…”

Section: Discussionmentioning

confidence: 99%

Vaccine-associated enhanced respiratory disease is influenced by haemagglutinin and neuraminidase in whole inactivated influenza virus vaccines

Rajão

Chen

Pérez

et al. 2016

Journal of General Virology

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Multiple subtypes and many antigenic variants of influenza A virus (IAV) co-circulate in swine in the USA, complicating effective use of commercial vaccines to control disease and transmission. Whole inactivated virus (WIV) vaccines may provide partial protection against IAV with substantial antigenic drift, but have been shown to induce vaccine-associated enhanced respiratory disease (VAERD) when challenged with an antigenic variant of the same haemagglutinin (HA) subtype. This study investigated the role the immune response against HA, neuraminidase (NA) and nucleoprotein (NP) may play in VAERD by reverse engineering vaccine and challenge viruses on a common backbone and using them in a series of vaccination/challenge trials. Mismatched HA between vaccine and challenge virus was necessary to induce VAERD. However, vaccines containing a matched NA abrogated the VAERD phenomenon induced by the HA mismatch and this was correlated with NA-inhibiting (NI) antibodies. Divergence between the two circulating swine N2 lineages (92 % identity) resulted in a loss of NI cross-reactivity and also resulted in VAERD with the mismatched HA. The NP lineage selected for use in the WIV vaccine strains did not affect protection or pathology. Thus the combination of HA and NA in the vaccine virus strains played a substantial role in vaccine protection versus immunopathology, suggesting that vaccines that target the HA protein alone could be more prone to VAERD due to the absence of cross-protective NI antibodies.

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Pathogenic Responses among Young Adults during the 1918 Influenza Pandemic

Abstract: These responses after secondary exposures caused bacterial pneumonia and most deaths.

Cited by 97 publications

References 30 publications

Infection of the Upper Respiratory Tract with Seasonal Influenza A(H3N2) Virus Induces Protective Immunity in Ferrets against Infection with A(H1N1)pdm09 Virus after Intranasal, but Not Intratracheal, Inoculation

Infection of the Upper Respiratory Tract with Seasonal Influenza A(H3N2) Virus Induces Protective Immunity in Ferrets against Infection with A(H1N1)pdm09 Virus after Intranasal, but Not Intratracheal, Inoculation

Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus

Vaccine-associated enhanced respiratory disease is influenced by haemagglutinin and neuraminidase in whole inactivated influenza virus vaccines

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