The pathogenesis of H7N8 low and highly pathogenic avian influenza viruses from the United States 2016 outbreak in chickens, turkeys and mallards

Pantin‐Jackwood, Mary J.; Stephens, Christopher B.; Bertran, Kateri; Swayne, David E.; Spackman, Erica

doi:10.1371/journal.pone.0177265

Cited by 48 publications

(58 citation statements)

References 35 publications

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“…Therefore, this discrepancy is likely caused by differences in susceptibility in individual birds. The transmission results obtained in this (47)(48)(49)(50). However, LPAI viruses that are known to be well adapted to chickens, including the Asian H9N2 and H7N9 viruses, readily transmitted in chickens in our model (51).…”

Section: Discussionmentioning

confidence: 70%

Loss of Fitness of Mexican H7N3 Highly Pathogenic Avian Influenza Virus in Mallards after Circulating in Chickens

Youk

Lee

Leyson

et al. 2019

J Virol

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Outbreaks of highly pathogenic avian influenza (HPAI) virus subtype H7N3 have been occurring in commercial chickens in Mexico since its first introduction in 2012. In order to determine changes in virus pathogenicity and adaptation in avian species, three H7N3 HPAI viruses from 2012, 2015, and 2016 were evaluated in chickens and mallards. All three viruses caused high mortality in chickens when given at medium to high doses and replicated similarly. No mortality or clinical signs and similar infectivity were observed in mallards inoculated with the 2012 and 2016 viruses. However, the 2012 H7N3 HPAI virus replicated well in mallards and transmitted to contacts, whereas the 2016 virus replicated poorly and did not transmit to contacts, which indicates that the 2016 virus is less adapted to mallards.In vitro, the 2016 virus grew slower and to lower titers than did the 2012 virus in duck fibroblast cells. Full-genome sequencing showed 115 amino acid differences between the 2012 and the 2016 viruses, with some of these changes previously associated with changes in replication in avian species, including hemagglutinin (HA) A125T, nucleoprotein (NP) M105V, and NP S377N. In conclusion, as the Mexican H7N3 HPAI virus has passaged through large populations of chickens in a span of several years and has retained its high pathogenicity for chickens, it has decreased in fitness in mallards, which could limit the potential spread of this HPAI virus by waterfowl.IMPORTANCENot much is known about changes in host adaptation of avian influenza (AI) viruses in birds after long-term circulation in chickens or other terrestrial poultry. Although the origin of AI viruses affecting poultry is wild aquatic birds, the role of these birds in further dispersal of poultry-adapted AI viruses is not clear. Previously, we showed that HPAI viruses isolated early from poultry outbreaks could still infect and transmit well in mallards. In this study, we demonstrate that the Mexican H7N3 HPAI virus after four years of circulation in chickens replicates poorly and does not transmit in mallards but remains highly pathogenic in chickens. This information on changes in host adaptation is important for understanding the epidemiology of AI viruses and the role that wild waterfowl may play in disseminating viruses adapted to terrestrial poultry.

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Section: Discussionmentioning

confidence: 70%

Loss of Fitness of Mexican H7N3 Highly Pathogenic Avian Influenza Virus in Mallards after Circulating in Chickens

Youk

Lee

Leyson

et al. 2019

J Virol

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“…Shibata et al (2018a) tested chicken, Pekin duck and Muscovy duck meat that had been illegally imported by international flight passengers and detected H5N1 HPAIV and H5N6 HPAIV as well as H9N2 LPAIV and H1N2 LPAIV. As mentioned previously, no virus could be detected in muscle tissues of infected chickens (Pantin-Jackwood et al, 2017). Chickens and ducks were inoculated via the intranasal route with the obtained H9N2 LPAIV, which could be recovered from the trachea 3 days after the inoculation of the chickens (4/4) but not from inoculated ducks (0/4).…”

Section: Assessment Of Lpaiv Transmission Via Raw Poultry Meatmentioning

confidence: 86%

“…Shibata et al (2018a) detected H9N2 virus titres of up to 3.5 log 10 /g in a mixture of tissues including muscle and other organs. Pantin-Jackwood et al (2017) detected viral RNA of H7N8 LPAIV in turkeys (2/2) exposed via the intra-choanal route. Virus titres of 4.8 log 10 EID 50 /g were determined based on RRT-PCR, although it is not clear what would be the corresponding titre of viable virus.…”

Section: Commercial and Non-commercial Poultrymentioning

confidence: 98%

Assessment of low pathogenic avian influenza virus transmission via raw poultry meat and raw table eggs

Gonzáles¹,

Roberts²,

Śmietanka³

et al. 2018

EFS2

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A rapid qualitative assessment has been done by performing a theoretical analysis on the transmission of low pathogenic avian influenza (LPAI) via fresh meat from poultry reared or kept in captivity for the production of meat (raw poultry meat) or raw table eggs. A predetermined transmission pathway followed a number of steps from a commercial or non‐commercial poultry establishment within the EU exposed to LPAI virus (LPAIV) to the onward virus transmission to animals and humans. The combined probability of exposure and subsequent LPAIV infection via raw poultry meat containing LPAIV is negligible for commercial poultry and humans exposed via consumption whereas it is very unlikely for non‐commercial poultry, wild birds and humans exposed via handling and manipulation. The probability of LPAIV transmission from an individual infected via raw poultry meat containing LPAIV is negligible for commercial poultry and humans, whereas it is very unlikely for non‐commercial poultry and wild birds. The combined probability of exposure and subsequent LPAIV infection via raw table eggs containing LPAIV is negligible for commercial poultry and humans and extremely unlikely to negligible for non‐commercial poultry and wild birds. The probability of LPAIV transmission from an individual infected via raw table eggs containing LPAIV is negligible for commercial poultry and humans and very unlikely to negligible for non‐commercial poultry and wild birds. Although the presence of LPAIV in raw poultry meat and table eggs is very unlikely to negligible, there is in general a high level of uncertainty on the estimation of the subsequent probabilities of key steps of the transmission pathways for poultry and wild birds, mainly due to the limited number of studies available, for instance on the viral load required to infect a bird via raw poultry meat or raw table eggs containing LPAIV.

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“…Little or no mortality is normally observed during most H7 LPAIV turkey outbreaks 39 – 41 , but up to 40% mortality has been reported in association with secondary bacterial infections and husbandry factors 42 , 43 . Experimental infection of high health status turkeys with H7 LPAIVs resulted in up to 40–60% mortality for three of 12 North American isolates 44 , but without the extensive systemic dissemination described in the current study (Figs 4 and 5 , Table 1 ).…”

Section: Discussionmentioning

confidence: 99%

Unexpected infection outcomes of China-origin H7N9 low pathogenicity avian influenza virus in turkeys

Slomka

Seekings

Mahmood

et al. 2018

Sci Rep

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The China-origin H7N9 low pathogenicity avian influenza virus (LPAIV) emerged as a zoonotic threat in 2013 where it continues to circulate in live poultry markets. Absence of overt clinical signs in poultry is a typical LPAIV infection outcome, and has contributed to its insidious maintenance in China. This study is the first description of H7N9 LPAIV (A/Anhui/1/13) infection in turkeys, with efficient transmission to two additional rounds of introduced contact turkeys which all became infected during cohousing. Surprisingly, mortality was observed in six of eight (75%) second-round contact turkeys which is unusual for LPAIV infection, with unexpected systemic dissemination to many organs beyond the respiratory and enteric tracts, but interestingly no accompanying mutation to highly pathogenic AIV. The intravenous pathogenicity index score for a turkey-derived isolate (0.39) affirmed the LPAIV phenotype. However, the amino acid change L235Q in the haemagglutinin gene occurred in directly-infected turkeys and transmitted to the contacts, including those that died and the two which resolved infection to survive to the end of the study. This polymorphism was indicative of a reversion from mammalian to avian adaptation for the H7N9 virus. This study underlined a new risk to poultry in the event of H7N9 spread beyond China.

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The pathogenesis of H7N8 low and highly pathogenic avian influenza viruses from the United States 2016 outbreak in chickens, turkeys and mallards

Cited by 48 publications

References 35 publications

Loss of Fitness of Mexican H7N3 Highly Pathogenic Avian Influenza Virus in Mallards after Circulating in Chickens

Loss of Fitness of Mexican H7N3 Highly Pathogenic Avian Influenza Virus in Mallards after Circulating in Chickens

Assessment of low pathogenic avian influenza virus transmission via raw poultry meat and raw table eggs

Unexpected infection outcomes of China-origin H7N9 low pathogenicity avian influenza virus in turkeys

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