#Human #infection with a novel #reassortant #Eurasian-avian lineage #swine #H1N1 virus in northern #China (Emerg Microbes Infect., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Emerg Microbes Infect. 2019;8(1):1535-1545. doi: 10.1080/22221751.2019.1679611.

Human infection with a novel reassortant Eurasian-avian lineage swine H1N1 virus in northern China.

Li X1, Guo L1, Liu C2, Cheng Y3, Kong M1, Yang L3, Zhuang Z1, Liu J3, Zou M1, Dong X1, Su X1, Gu Q1.

Author information: 1 Tianjin Centers for Disease Control and Prevention, Tianjin, People’s Republic of China. 2 Jizhou District Center for Disease Control and Prevention, Tianjin, People’s Republic of China. 3 Chinese National Influenza Center, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of China.

 

Abstract

Influenza A virus infections occur in different species, causing mild to severe respiratory symptoms that lead to a heavy disease burden. Eurasian avian-like swine influenza A(H1N1) viruses (EAS-H1N1) are predominant in pigs and occasionally infect humans. An influenza A(H1N1) virus was isolated from a boy who was suffering from fever and headache and designated as A/Tianjin-baodi/1606/2018(H1N1). Full-genome sequencing and phylogenetic analysis revealed that A/Tianjin-baodi/1606/2018(H1N1) is a novel reassortant EAS-H1N1 containing gene segments from EAS-H1N1 (HA and NA), classical swine H1N1(NS) and A(H1N1)pdm09(PB2, PB2, PA, NP and M) viruses. The isolation and analysis of A/Tianjin-baodi/1606/2018(H1) provide further evidence that EAS-H1N1 poses a threat to human health and greater attention should be paid to surveillance of influenza virus infection in pigs and humans.

KEYWORDS: EAS-H1N1; Influenza A virus; Phylogenetic analysis; molecular characteristics; triple-reassortant

PMID: 31661383 PMCID: PMC6830285 DOI: 10.1080/22221751.2019.1679611 [Indexed for MEDLINE] Free PMC Article

Keywords: Influenza A; Swine Influenza; H1N1; H1N1pdm09; Reassortant strain; Human; China.

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Emergence of an #Eurasian #avian-like #swine #influenza A (#H1N1) virus from #mink in #China (Vet Microbiol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Vet Microbiol. 2020 Jan;240:108509. doi: 10.1016/j.vetmic.2019.108509. Epub 2019 Nov 22.

Emergence of an Eurasian avian-like swine influenza A (H1N1) virus from mink in China.

Liu J1, Li Z1, Cui Y1, Yang H1, Shan H1, Zhang C2.

Author information: 1 College of Veterinary Medicine, Qingdao Agricultural University, Qingdao, China. 2 College of Veterinary Medicine, Qingdao Agricultural University, Qingdao, China. Electronic address: zhangchuanmei100@163.com.

 

Abstract

We evaluated the phenotype and genotype of a fatal influenza/canine distemper virus coinfection found in farmed mink in China. We identified a novel subtype H1N1 influenza virus strain from the lungs of infected mink designated A/Mink/Shandong/1121/2017 (H1N1). The results of phylogenetic analysis of 8 gene fragments of the H1N1 strain showed the virus was a swine origin triple-reassortant H1N1 influenza virus: with the 2009 pandemic H1N1 segments (PB2, PB1, PA, NP and M), Eurasian avian-like H1N1 swine segments (HA and NA) and classical swine (NS) lineages. The EID50/0.2 mL of this strain was 10-6.2 and pathogenicity tests were 100 % lethal in a mouse model of infection. We found that while not lethal and lacking any overt signs of infection in mink, the virus could proliferate in the upper respiratory tracts and the animals were converted to seropositive for the HA protein.

Copyright © 2019 Elsevier B.V. All rights reserved.

KEYWORDS: Eurasian avian-like swine influenza virus; H1N1; Mink influenza virus; Phylogenetic analysis; Reassortment

PMID: 31902506 DOI: 10.1016/j.vetmic.2019.108509

Keywords: Avian Influenza; Swine Influenza; H1N1pdm09; H1N1; Reassortant strain; Wildlife; China.

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#Genetic and #serologic #surveillance of #canine (CIV) and #equine (EIV) #influenza virus in Nuevo León State, #México (PeerJ., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

PeerJ. 2019 Dec 17;7:e8239. doi: 10.7717/peerj.8239. eCollection 2019.

Genetic and serologic surveillance of canine (CIV) and equine (EIV) influenza virus in Nuevo León State, México.

Plata-Hipólito CB1, Cedillo-Rosales S2, Obregón-Macías N3, Hernández-Luna CE4, Rodríguez-Padilla C1, Tamez-Guerra RS1, Contreras-Cordero JF1.

Author information: 1 Universidad Autónoma de Nuevo León, Facultad de Ciencias Biológicas, Laboratorio de Inmunología y Virología, San Nicolás de los Garza, Nuevo León, México. 2 Universidad Autónoma de Nuevo León, Facultad de Medicina Veterinaria y Zootecnia, Departamento de Virología, Escobedo, Nuevo León, México. 3 Universidad Autónoma de Nuevo León, Facultad de Medicina Veterinaria y Zootecnia, Departamento de Grandes Especies, Escobedo, Nuevo León, México. 4 Universidad Autónoma de Nuevo León, Facultad de Ciencias Biológicas, Departamento de Química, San Nicolás de los Garza, Nuevo León, México.

 

Abstract

BACKGROUND:

Despite the uncontrolled distribution of the Influenza A virus through wild birds, the detection of canine influenza virus and equine influenza virus in Mexico was absent until now. Recently, outbreaks of equine and canine influenza have been reported around the world; the virus spreads quickly among animals and there is potential for zoonotic transmission.

METHODS:

Amplification of the Influenza A virus matrix gene from necropsies, nasal and conjunctival swabs from trash service horses and pets/stray dogs was performed through RT-PCR. The seroprevalence was carried out through Sandwich enzyme-linked immunosorbent assay system using the M1 recombinant protein and polyclonal antibodies anti-M1.

RESULTS:

The matrix gene was amplified from 13 (19.11%) nasal swabs, two (2.94%) conjunctival swabs and five (7.35%) lung necropsies, giving a total of 20 (29.41%) positive samples in a pet dog population. A total of six (75%) positive samples of equine nasal swab were amplified. Sequence analysis showed 96-99% identity with sequences of Influenza A virus matrix gene present in H1N1, H1N2 and H3N2 subtypes. The phylogenetic analysis of the sequences revealed higher identity with matrix gene sequences detected from zoonotic isolates of subtype H1N1/2009. The detection of anti-M1 antibodies in stray dogs showed a prevalence of 123 (100%) of the sampled population, whereas in horses, 114 (92.68%) positivity was obtained.

CONCLUSION:

The results unveil the prevalence of Influenza A virus in the population of horses and dogs in the state of Nuevo Leon, which could indicate a possible outbreak of equine and Canine Influenza in Mexico. We suggest that the prevalence of Influenza virus in companion animals be monitored to investigate its epizootic and zoonotic potential, in addition to encouraging the regulation of vaccination in these animal species in order to improve their quality of life.

© 2019 Plata-Hipólito et al.

KEYWORDS: Canine Influenza Virus (CIV); Equine Influenza Virus (EIV); Matrix gene (M); Polyclonal antibodies

PMID: 31871842 PMCID: PMC6924343 DOI: 10.7717/peerj.8239

Keywords: Influenza A; Equine Influenza; Canine Avian Influenza; H1N1pdm09; H1N2; H3N2; H1N1; Reassortant strains; Dogs; Horses; Mexico; Serology.

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The 1918 #Influenza #Pandemic and Its #Legacy (Cold Spring Harb Perspect Med., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Cold Spring Harb Perspect Med. 2019 Dec 23. pii: a038695. doi: 10.1101/cshperspect.a038695. [Epub ahead of print]

The 1918 Influenza Pandemic and Its Legacy.

Taubenberger JK1, Morens DM2.

Author information: 1 Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. 2 Office of the Director, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

 

Abstract

Just over a century ago in 1918-1919, the “Spanish” influenza pandemic appeared nearly simultaneously around the world and caused extraordinary mortality-estimated at 50-100 million fatalities-associated with unexpected clinical and epidemiological features. The pandemic’s sudden appearance and high fatality rate were unprecedented, and 100 years later still serve as a stark reminder of the continual threat influenza poses. Sequencing and reconstruction of the 1918 virus have allowed scientists to answer many questions about its origin and pathogenicity, although many questions remain. Several of the unusual features of the 1918-1919 pandemic, including age-specific mortality patterns and the high frequency of severe pneumonias, are still not fully understood. The 1918 pandemic virus initiated a pandemic era still ongoing. The descendants of the 1918 virus remain today as annually circulating and evolving influenza viruses causing significant mortality each year. This review summarizes key findings and unanswered questions about this deadliest of human events.

Copyright © 2019 Cold Spring Harbor Laboratory Press; all rights reserved.

PMID: 31871232 DOI: 10.1101/cshperspect.a038695

Keywords: Influenza A; H1N1; Pandemic Influenza; Spanish Flu.

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The #matrix segment of the “#Spanishflu” virus originated from intragenic #recombination between #avian and #human #influenza A viruses (Transbound Emerg Dis., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Transbound Emerg Dis. 2019 Sep;66(5):2188-2195. doi: 10.1111/tbed.13282. Epub 2019 Jul 15.

The matrix segment of the “Spanish flu” virus originated from intragenic recombination between avian and human influenza A viruses.

He CQ1, He M1, He HB1, Wang HM1, Ding NZ1.

Author information: 1 The Key Laboratory of Animal Resistant Biology of Shandong, College of Life Science, Shandong Normal University, Jinan, China.

 

Abstract

The 1918 Spanish flu virus has claimed more than 50 million lives. However, the mechanism of its high pathogenicity remains elusive; and the origin of the virus is controversial. The matrix (M) segment regulates the replication of influenza A virus, thereby affecting its virulence and pathogenicity. This study found that the M segment of the Spanish flu virus is a recombinant chimera originating from avian influenza virus and human influenza virus. The unique mosaic M segment might confer the virus high replication capacity, showing that the recombination might play an important role in inducing high pathogenicity of the virus. In addition, this study also suggested that the NA and NS segments of the virus were generated by reassortment between mammalian and avian viruses. Direct phylogenetic evidence was also provided for its avian origin.

© 2019 Blackwell Verlag GmbH.

PMID: 31241237 DOI: 10.1111/tbed.13282 [Indexed for MEDLINE]

Keywords: Avian Influenza; Pandemic Influenza; Reassortant strain; H1N1; Spanish Flu.

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#Childhood immune #imprinting to #influenza A shapes birth year-specific #risk during seasonal #H1N1 and #H3N2 #epidemics (PLOS Pathog., abstract)

[Source: PLOS Pathogens, full page: (LINK). Abstract, edited.]

OPEN ACCESS /  PEER-REVIEWED / RESEARCH ARTICLE

Childhood immune imprinting to influenza A shapes birth year-specific risk during seasonal H1N1 and H3N2 epidemics

Katelyn M. Gostic , Rebecca Bridge, Shane Brady, Cécile Viboud, Michael Worobey, James O. Lloyd-Smith

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Published: December 19, 2019 / DOI: https://doi.org/10.1371/journal.ppat.1008109

 

Abstract

Across decades of co-circulation in humans, influenza A subtypes H1N1 and H3N2 have caused seasonal epidemics characterized by different age distributions of cases and mortality. H3N2 causes the majority of severe, clinically attended cases in high-risk elderly cohorts, and the majority of overall deaths, whereas H1N1 causes fewer deaths overall, and cases shifted towards young and middle-aged adults. These contrasting age profiles may result from differences in childhood imprinting to H1N1 and H3N2 or from differences in evolutionary rate between subtypes. Here we analyze a large epidemiological surveillance dataset to test whether childhood immune imprinting shapes seasonal influenza epidemiology, and if so, whether it acts primarily via homosubtypic immune memory or via broader, heterosubtypic memory. We also test the impact of evolutionary differences between influenza subtypes on age distributions of cases. Likelihood-based model comparison shows that narrow, within-subtype imprinting shapes seasonal influenza risk alongside age-specific risk factors. The data do not support a strong effect of evolutionary rate, or of broadly protective imprinting that acts across subtypes. Our findings emphasize that childhood exposures can imprint a lifelong immunological bias toward particular influenza subtypes, and that these cohort-specific biases shape epidemic age distributions. As a consequence, newer and less “senior” antibody responses acquired later in life do not provide the same strength of protection as responses imprinted in childhood. Finally, we project that the relatively low mortality burden of H1N1 may increase in the coming decades, as cohorts that lack H1N1-specific imprinting eventually reach old age.

 

Author summary

Influenza viruses of subtype H1N1 and H3N2 both cause seasonal epidemics in humans, but with different age-specific impacts. H3N2 causes a greater proportion of cases in older adults than H1N1, and more deaths overall. People tend to gain the strongest immune memory of influenza viruses encountered in childhood, and so differences in H1N1 and H3N2’s age-specific impacts may reflect that individuals born in different eras of influenza circulation have been imprinted with different immunological risk profiles. Another idea is that H3N2 may be more able to infect immunologically experienced adults because it evolves slightly faster than H1N1 and can more quickly escape immune memory. We analyzed a large epidemiological data set and found that birth year-specific differences in childhood immune imprinting, not differences in evolutionary rate, explain differences in H1N1 and H3N2’s age-specific impacts. These results can help epidemiologists understand how epidemic risk from specific influenza subtypes is distributed across the population and predict how population risk may shift as differently imprinted birth years grow older. Further, these results provide immunological clues to which facets of immune memory become biased in childhood, and then later play a strong role in protection during seasonal influenza epidemics.

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Citation: Gostic KM, Bridge R, Brady S, Viboud C, Worobey M, Lloyd-Smith JO (2019) Childhood immune imprinting to influenza A shapes birth year-specific risk during seasonal H1N1 and H3N2 epidemics. PLoS Pathog 15(12): e1008109. https://doi.org/10.1371/journal.ppat.1008109

Editor: Sabra L. Klein, Johns Hopkins Bloomberg School of Public Health, UNITED STATES

Received: July 9, 2019; Accepted: September 25, 2019; Published: December 19, 2019

This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

Data Availability: All relevant data are available as Supporting Information files. All data are also archived alongside the full suite of code used to perform analyses and generate plots, at https://zenodo.org/badge/latestdoi/160883450.

Funding: KMG was supported by the National Institutes of Health (F31AI134017, T32-GM008185). JOLS was supported by NSF grants OCE-1335657 and DEB-1557022, SERDP RC-2635, and DARPA PREEMPT D18AC00031. MW was supported by the David and Lucile Packard Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

Keywords: Seasonal Influenza; Immunology; H1N1; H3N2.

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Re-evaluation of the #evolution of #influenza #H1 viruses using direct PCA (Sci Rep., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Sci Rep. 2019 Dec 17;9(1):19287. doi: 10.1038/s41598-019-55254-z.

Re-evaluation of the evolution of influenza H1 viruses using direct PCA.

Konishi T1.

Author information: 1 Graduate School of Bioresource Sciences, Akita Prefectural University, Akita, Japan. konishi@akita-pu.ac.jp.

 

Abstract

The history of influenza H1 virus was re-evaluated by applying a new methodology to sequencing data; this objective method enables comparisons among viral types. The approach led to the segregation of all segments of swine and human viruses into three distinct groups: two of them included the pandemic 1977 and 2009 human viruses, and the remaining group may be new in humans. These three groups might have originated from avian viruses and drifted out independently. Genome shifts occurred occasionally among swine viruses; however, distances between avian and swine/human viruses negated the existence of direct shifts from avian viruses. In humans, only one or two viruses appeared each year, which suggests the presence of competition among viruses that migrated freely. All segments drifted continuously under certain rules and constant velocity. Viruses that had caused an outbreak did not appear again over subsequent decades, which may mean populations had become immune to such viruses. In contrast, the viruses in livestock were rather conserved and maintained unique strains in small, separate areas. Such collections of swine strains included human segments, which could become an epidemic in the future.

PMID: 31848356 DOI: 10.1038/s41598-019-55254-z

Keywords: Influenza; H1N1; Seasonal Influenza; Swine Influenza; Pigs.

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