Influenza A(H10N7) Virus in Dead Harbor Seals, Denmark

Krog, Jesper Schak; Hansen, Mette Sif; Holm, Elisabeth; Hjulsager, Charlotte Kristiane; Chriél, Mariann; Pedersen, Karl; Andresen, Lars Ole; Abildstrøm, Morten; Jensen, Trine Hammer; Larsen, Lars Erik

doi:10.3201/eid2104.141484

Cited by 87 publications

(42 citation statements)

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“…In addition, necro-suppurative and/or granulomatous and eosinophilic inflammation was present most likely due to secondary bacterial infections and parasitic infestations. Our findings share morphological findings that have been described in seals infected with Seal/H10N7 from Sweden and Denmark, however, immunohistochemical staining for virus antigen has not been described [1,2]. Lesions and cell type tropism of Seal/H10N7 infection in harbor seals is in accordance with previously described natural infections of harbor seals with LPAI H3N8 influenza virus in which virus and lesions were mainly present in the bronchi [7], and of harbor seals naturally infected with LPAI H7N7 that developed necrotizing bronchitis, bronchiolitis and hemorrhagic alveolitis [27].…”

Section: Discussionsupporting

confidence: 89%

“…Concurrent infections with bacteria were also described in Sweden and Denmark since all animals had severe growth in the lungs of Pseudomonas aeruginosa, Streptococcus equi ssp. zooepidemicus or Escherichia coli [1,2]. The presence of severe lesions due to bacterial co-infections was also seen in the 1918 and 1957 influenza pandemics in humans since antibiotics were not available at that time [30].…”

Section: Discussionmentioning

confidence: 99%

“…In 2014 and the beginning of 2015, there was an epidemic of a novel H10N7 influenza A virus (Seal/H10N7) among harbor seals (Phoca vitulina) resulting in increased mortalities along the coasts of Sweden, Denmark, Germany and The Netherlands [1][2][3][4][5]. Most probably this epidemic was caused by a spill-over of a low pathogenic avian influenza virus (LPAI) originating from wild aquatic birds, since this Seal/H10N7 is genetically closely related to various influenza viruses detected in wild birds [3,5].…”

Section: Introductionmentioning

confidence: 99%

“…Ferrets infected with this H3N8 virus demonstrated virus titers of above 10 6 TCID 50 /g in the nasal turbinates and the lungs [11]. The few pathological investigations on seals that died during this Seal/H10N7 outbreak report similar lesions, consisting of necro-suppurative bronchopneumonia with a bacterial co-infection [1,2]. The whole spectrum of virus-associated histological changes, the distribution of viral antigen and the target cell tropism of Seal/H10N7 in harbor seals are unknown.…”

Section: Introductionmentioning

confidence: 99%

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Influenza A (H10N7) Virus Causes Respiratory Tract Disease in Harbor Seals and Ferrets

Brand¹,

Wohlsein²,

Herfst³

et al. 2016

PLoS ONE

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Avian influenza viruses sporadically cross the species barrier to mammals, including humans, in which they may cause epidemic disease. Recently such an epidemic occurred due to the emergence of avian influenza virus of the subtype H10N7 (Seal/H10N7) in harbor seals (Phoca vitulina). This epidemic caused high mortality in seals along the north-west coast of Europe and represented a potential risk for human health. To characterize the spectrum of lesions and to identify the target cells and viral distribution, findings in 16 harbor seals spontaneously infected with Seal/H10N7 are described. The seals had respiratory tract inflammation extending from the nasal cavity to bronchi associated with intralesional virus antigen in respiratory epithelial cells. Virus infection was restricted to the respiratory tract. The fatal outcome of the viral infection in seals was most likely caused by secondary bacterial infections. To investigate the pathogenic potential of H10N7 infection for humans, we inoculated the seal virus intratracheally into six ferrets and performed pathological and virological analyses at 3 and 7 days post inoculation. These experimentally inoculated ferrets displayed mild clinical signs, virus excretion from the pharynx and respiratory tract inflammation extending from bronchi to alveoli that was associated with virus antigen expression exclusively in the respiratory epithelium. Virus was isolated only from the respiratory tract. In conclusion, Seal/H10N7 infection in naturally infected harbor seals and experimentally infected ferrets shows that respiratory epithelial cells are the permissive cells for viral replication. Fatal outcome in seals was caused by secondary bacterial pneumonia similar to that in fatal human cases during influenza pandemics. Productive infection of ferrets indicates that seal/H10N7 may possess a zoonotic potential. This outbreak of LPAI from wild birds to seals demonstrates the risk of such occasions for mammals and thus humans.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Influenza A (H10N7) Virus Causes Respiratory Tract Disease in Harbor Seals and Ferrets

Brand¹,

Wohlsein²,

Herfst³

et al. 2016

PLoS ONE

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“…Three human cases of H10N8 virus have been reported in China so far, two of which were fatal (1)(2)(3). Furthermore, an avian H10N7 strain was found to be the etiological agent responsible for the massive die-off harbor seals in the Baltic Sea, an epidemic that killed more than 10% of the local seal population (4)(5)(6). The receptor binding profile of H10 viruses is currently debated (7)(8)(9)(10)(11)(12), but the subtype has been proven to cause productive infections in humans (13,14).…”

mentioning

confidence: 99%

Hemagglutinin Stalk- and Neuraminidase-Specific Monoclonal Antibodies Protect against Lethal H10N8 Influenza Virus Infection in Mice

Wohlbold

Chromikova

Tan

et al. 2016

J Virol

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Between November 2013 and February 2014, China reported three human cases of H10N8 influenza virus infection in the Jiangxi province, two of which were fatal. Using hybridoma technology, we isolated a panel of H10-and N8-directed monoclonal antibodies (MAbs) and further characterized the binding reactivity of these antibodies (via enzyme-linked immunosorbent assay) to a range of purified virus and recombinant protein substrates. The H10-directed MAbs displayed functional hemagglutination inhibition (HI) and neutralization activity, and the N8-directed antibodies displayed functional neuraminidase inhibition (NI) activity against H10N8. Surprisingly, the HI-reactive H10 antibodies, as well as a previously generated, group 2 hemagglutinin (HA) stalk-reactive antibody, demonstrated NI activity against H10N8 and an H10N7 strain; this phenomenon was absent when virus was treated with detergent, suggesting the anti-HA antibodies inhibited neuraminidase enzymatic activity through steric hindrance. We tested the prophylactic efficacy of one representative H10-reactive, N8-reactive, and group 2 HA stalk-reactive antibody in vivo using a BALB/c challenge model. All three antibodies were protective at a high dose (5 mg/kg). At a low dose (0.5 mg/kg), only the anti-N8 antibody prevented weight loss. Together, these data suggest that antibody targets other than the globular head domain of the HA may be efficacious in preventing influenza virus-induced morbidity and mortality. IMPORTANCEAvian H10N8 and H10N7 viruses have recently crossed the species barrier, causing morbidity and mortality in humans and other mammals. Although these reports are likely isolated incidents, it is possible that more cases may emerge in future winter seasons, similar to H7N9. Furthermore, regular transmission of avian influenza viruses to humans increases the risk of adaptive mutations and reassortment events, which may result in a novel virus with pandemic potential. Currently, no specific therapeutics or vaccines are available against the H10N8 influenza virus subtype. We generated a panel of H10-and N8-reactive MAbs. Although these antibodies may practically be developed into therapeutic agents, characterizing the protective potential of MAbs that have targets other than the HA globular head domain will provide insight into novel antibody-mediated mechanisms of protection and help to better understand correlates of protection for influenza A virus infection. R ecently, avian influenza A viruses of the H10 subtype have been reported to infect seals and humans and have generated concern over their pandemic potential. Three human cases of H10N8 virus have been reported in China so far, two of which were fatal (1-3). Furthermore, an avian H10N7 strain was found to be the etiological agent responsible for the massive die-off harbor seals in the Baltic Sea, an epidemic that killed more than 10% of the local seal population (4-6). The receptor binding profile of H10 viruses is currently debated (7-12), but the subtype has been proven to cause ...

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Sporadic influenza A virus infections of miscellaneous mammal species

Kroeze

Kuiken

2016

Animal Influenza

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Influenza A(H10N7) Virus in Dead Harbor Seals, Denmark

Abstract: Since April 2014, an outbreak of influenza in harbor seals has been ongoing in northern Europe. In Denmark during June–August, 152 harbor seals on the island of Anholt were found dead from severe pneumonia. We detected influenza A(H10N7) virus in 2 of 4 seals examined.

Cited by 87 publications

References 12 publications

Influenza A (H10N7) Virus Causes Respiratory Tract Disease in Harbor Seals and Ferrets

Influenza A (H10N7) Virus Causes Respiratory Tract Disease in Harbor Seals and Ferrets

Hemagglutinin Stalk- and Neuraminidase-Specific Monoclonal Antibodies Protect against Lethal H10N8 Influenza Virus Infection in Mice

Sporadic influenza A virus infections of miscellaneous mammal species

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