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1.
J Virol ; 96(14): e0027822, 2022 07 27.
Artigo em Inglês | MEDLINE | ID: mdl-35862690

RESUMO

The incursions of H7 subtype low-pathogenicity avian influenza virus (LPAIV) from wild birds into poultry and its mutations to highly pathogenic avian influenza virus (HPAIV) have been an ongoing concern in North America. Since 2000, 10 phylogenetically distinct H7 virus outbreaks from wild birds have been detected in poultry, six of which mutated to HPAIV. To study the molecular evolution of the H7 viruses that occurs when changing hosts from wild birds to poultry, we performed analyses of the North American H7 hemagglutinin (HA) genes to identify amino acid changes as the virus circulated in wild birds from 2000 to 2019. Then, we analyzed recurring HA amino acid changes and gene constellations of the viruses that spread from wild birds to poultry. We found six HA amino acid changes occurring during wild bird circulation and 10 recurring changes after the spread to poultry. Eight of the changes were in and around the HA antigenic sites, three of which were supported by positive selection. Viruses from each H7 outbreak had a unique genotype, with no specific genetic group associated with poultry outbreaks or mutation to HPAIV. However, the genotypes of the H7 viruses in poultry outbreaks tended to contain minor genetic groups less observed in wild bird H7 viruses, suggesting either a biased sampling of wild bird AIVs or a tendency of having reassortment with minor genetic groups prior to the virus's introduction to poultry. IMPORTANCE Wild bird-origin H7 subtype avian influenza viruses are a constant threat to commercial poultry, both directly by the disease they cause and indirectly through trade restrictions that can be imposed when the virus is detected in poultry. It is important to understand the genetic basis of why the North American lineage H7 viruses have repeatedly crossed the species barrier from wild birds to poultry. We examined the amino acid changes in the H7 viruses associated with poultry outbreaks and tried to determine gene reassortment related to poultry adaptation and mutations to HPAIV. The findings in this study increase the understanding of the evolutionary pathways of wild bird AIV before infecting poultry and the HA changes associated with adaptation of the virus in poultry.


Assuntos
Evolução Molecular , Glicoproteínas de Hemaglutininação de Vírus da Influenza , Vírus da Influenza A , Influenza Aviária , Doenças das Aves Domésticas , Aminoácidos/genética , Animais , Animais Selvagens , Aves , Glicoproteínas de Hemaglutininação de Vírus da Influenza/genética , Vírus da Influenza A/genética , América do Norte , Filogenia , Aves Domésticas , Doenças das Aves Domésticas/virologia
2.
Avian Pathol ; 52(3): 219-228, 2023 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-36999798

RESUMO

Highly pathogenic (HP) avian influenza viruses (AIVs) of the clade 2.3.4.4 goose/Guangdong/1996 H5 lineage continue to be a problem in poultry and wild birds in much of the world. The recent incursion of a H5N1 clade 2.3.4.4b HP AIV from this lineage into North America has resulted in widespread outbreaks in poultry and consistent detections of the virus across diverse families of birds and occasionally mammals. To characterize the pathobiology of this virus in mallards (Anas platyrhynchos), which are a primary reservoir of AIV, a challenge study was conducted with 2-week-old birds. The 50% bird infectious dose was determined to be < 2 log10 50% egg infectious doses (EID50) and all exposed ducks, including ducks co-housed with inoculated ducks, were infected. Infection appeared to be subclinical for 58.8% (20/34) of the ducks, one duck was lethargic, about 20% developed neurological signs and were euthanized, and 18% developed corneal opacity. The mallards shed virus by both the oral and cloacal routes within 24-48 h post-infection. Oral shedding substantially decreased by 6-7 days post-infection, but 65% of the ducks continued to shed virus cloacally through 14 days post-exposure (DPE) for the direct inoculates and 13 DPE for contact-exposed ducks. Based on the high transmissibility, high virus shed titres, and mild-to-moderate disease, mallards could serve as efficient reservoirs to amplify and disseminate recent North American clade 2.3.4.4b viruses.


Assuntos
Virus da Influenza A Subtipo H5N1 , Vírus da Influenza A , Influenza Aviária , Animais , Patos , Animais Selvagens , Aves Domésticas , Mamíferos
3.
J Virol ; 95(18): e0095521, 2021 08 25.
Artigo em Inglês | MEDLINE | ID: mdl-34232725

RESUMO

Highly pathogenic avian influenza (HPAI) viruses from the H5Nx Goose/Guangdong/96 lineage continue to cause outbreaks in domestic and wild bird populations. Two distinct genetic groups of H5N8 HPAI viruses, hemagglutinin (HA) clades 2.3.4.4A and 2.3.4.4B, caused intercontinental outbreaks in 2014 to 2015 and 2016 to 2017, respectively. Experimental infections using viruses from these outbreaks demonstrated a marked difference in virulence in mallards, with the H5N8 virus from 2014 causing mild clinical disease and the 2016 H5N8 virus causing high mortality. To assess which gene segments are associated with enhanced virulence of H5N8 HPAI viruses in mallards, we generated reassortant viruses with 2014 and 2016 viruses. For single-segment reassortants in the genetic backbone of the 2016 virus, pathogenesis experiments in mallards revealed that morbidity and mortality were reduced for all eight single-segment reassortants compared to the parental 2016 virus, with significant reductions in mortality observed with the polymerase basic protein 2 (PB2), nucleoprotein (NP), and matrix (M) reassortants. No differences in morbidity and mortality were observed with reassortants that either have the polymerase complex segments or the HA and neuraminidase (NA) segments of the 2016 virus in the genetic backbone of the 2014 virus. In vitro assays showed that the NP and polymerase acidic (PA) segments of the 2014 virus lowered polymerase activity when combined with the polymerase complex segments of the 2016 virus. Furthermore, the M segment of the 2016 H5N8 virus was linked to filamentous virion morphology. Phylogenetic analyses demonstrated that gene segments related to the more virulent 2016 H5N8 virus have persisted in the contemporary H5Nx HPAI gene pool until 2020. IMPORTANCE Outbreaks of H5Nx HPAI viruses from the goose/Guangdong/96 lineage continue to occur in many countries and have resulted in substantial impact on wild birds and poultry. Epidemiological evidence has shown that wild waterfowl play a major role in the spread of these viruses. While HPAI virus infection in gallinaceous species causes high mortality, a wide range of disease outcomes has been observed in waterfowl species. In this study, we examined which gene segments contribute to severe disease in mallards infected with H5N8 HPAI viruses. No virus gene was solely responsible for attenuating the high virulence of a 2016 H5N8 virus, but the PB2, NP, and M segments significantly reduced mortality. The findings herein advance our knowledge on the pathobiology of avian influenza viruses in waterfowl and have potential implications on the ecology and epidemiology of H5Nx HPAI in wild bird populations.


Assuntos
Patos/virologia , Vírus da Influenza A Subtipo H5N8/classificação , Vírus da Influenza A Subtipo H5N8/patogenicidade , Influenza Aviária/transmissão , Influenza Aviária/virologia , Doenças das Aves Domésticas/virologia , Proteínas Virais/genética , Animais , Vírus da Influenza A Subtipo H5N8/genética , Filogenia , Doenças das Aves Domésticas/genética , Virulência
4.
J Virol ; 95(5)2021 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-33268526

RESUMO

The H5N8 highly pathogenic avian influenza (HPAI) clade 2.3.4.4 virus spread to North America by wild birds and reassorted to generate the H5N2 HPAI virus that caused the poultry outbreak in the United States in 2015. In previous studies, we showed that H5N2 viruses isolated from poultry in the later stages of the outbreak had higher infectivity and transmissibility in chickens than the wild bird index H5N2 virus. Here, we determined the genetic changes that contributed to the difference in host virus fitness by analyzing sequence data from all of the viruses detected during the H5N2 outbreak, and studying the pathogenicity of reassortant viruses generated with the index wild bird virus and a chicken virus from later in the outbreak. Viruses with the wild bird virus backbone and either PB1, NP, or the entire polymerase complex of the chicken isolate, caused higher and earlier mortality in chickens, with three mutations (PB1 E180D, M317V, and NP I109T) identified to increase polymerase activity in chicken cells. The reassortant virus with the HA and NA from the chicken virus, where mutations in functionally known gene regions were acquired as the virus circulated in turkeys (HA S141P and NA S416G) and later in chickens (HA M66I, L322Q), showed faster virus growth, bigger plaque size and enhanced heat persistence in vitro, and increased pathogenicity and transmissibility in chickens. Collectively, these findings demonstrate an evolutionary pathway in which a HPAI virus from wild birds can accumulate genetic changes to increase fitness in poultry.IMPORTANCE H5Nx highly pathogenic avian influenza (HPAI) viruses of the A/goose/Guangdong/1/96 lineage continue to circulate widely affecting both poultry and wild birds. These viruses continue to change and reassort, which affects their fitness to different avian hosts. In this study, we defined mutations associated with increased virus fitness in chickens as the clade 2.3.4.4. H5N2 HPAI virus circulated in different avian species. We identified mutations in the PB1, NP, HA, and NA virus proteins that were highly conserved in the poultry isolates and contributed to the adaptation of this virus in chickens. This knowledge is important for understanding the epidemiology of H5Nx HPAI viruses and specifically the changes related to adaptation of these viruses in poultry.

5.
Vet Pathol ; 59(1): 75-81, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-34794360

RESUMO

Selected lymphoid and reproductive tissues were examined from groups of 3-week-old chickens and 62-week-old hens that were inoculated choanally and conjunctivally with 106 EID50 of a virulent Newcastle disease virus (NDV) isolate from the California 2018-2020 outbreak, and euthanized at 1, 2, and 3 days postinfection. In the 3-week-old chickens, immunohistochemistry for NDV and for T and B cell lymphocytes, as well as in situ hybridization for IL-1ß, IL-6, IFN-γ, and TNF-α revealed extensive expression of IL-1ß and IL-6 in lymphoid tissues, often coinciding with NDV antigen. IFN-γ was only expressed infrequently in the same lymphoid tissues, and TNF-α was rarely expressed. T-cell populations initially expanded but by day 3 their numbers were below control levels. B cells underwent a similar expansion but remained elevated in some tissues, notably spleen, cecal tonsils, and cloacal bursa. Cytokine expression in the 62-week-old hens was overall lower than in the 3-week-old birds, and there was more prolonged infiltration of both T and B cells in the older birds. The strong pro-inflammatory cytokine response in young chickens is proposed as the reason for more severe disease.


Assuntos
Citocinas , Doença de Newcastle , Doenças das Aves Domésticas , Animais , Galinhas , Citocinas/genética , Feminino , Expressão Gênica , Doença de Newcastle/genética , Doença de Newcastle/imunologia , Doenças das Aves Domésticas/genética , Doenças das Aves Domésticas/imunologia
6.
Emerg Infect Dis ; 26(12): 3074-3076, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33219803

RESUMO

We challenged chickens, turkeys, ducks, quail, and geese with severe acute respiratory syndrome coronavirus 2 or Middle East respiratory syndrome coronavirus. We observed no disease and detected no virus replication and no serum antibodies. We concluded that poultry are unlikely to serve a role in maintenance of either virus.


Assuntos
Anseriformes , Infecções por Coronavirus/veterinária , Galliformes , Coronavírus da Síndrome Respiratória do Oriente Médio , Doenças das Aves Domésticas/virologia , SARS-CoV-2 , Animais , Anticorpos Antivirais , COVID-19/veterinária , COVID-19/virologia , Infecções por Coronavirus/virologia , Suscetibilidade a Doenças/veterinária , Suscetibilidade a Doenças/virologia , Patos , Gansos , Replicação Viral
7.
Emerg Infect Dis ; 26(12): 2966-2969, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33030423

RESUMO

An outbreak of low-pathogenicity avian influenza A(H7N3) virus of North American wild bird lineage occurred on commercial turkey farms in North Carolina and South Carolina, USA, during March-April 2020. The virus mutated to the highly pathogenic form in 1 house on 1 farm via recombination with host 28S rRNA.


Assuntos
Influenza Aviária , Doenças das Aves Domésticas , Aves Domésticas , Animais , Aves , Surtos de Doenças , Vírus da Influenza A Subtipo H7N3 , Influenza Aviária/epidemiologia , North Carolina , Aves Domésticas/virologia , Doenças das Aves Domésticas/epidemiologia , Estados Unidos/epidemiologia
8.
Proc Biol Sci ; 287(1934): 20201680, 2020 09 09.
Artigo em Inglês | MEDLINE | ID: mdl-32901574

RESUMO

In this investigation, we used a combination of field- and laboratory-based approaches to assess if influenza A viruses (IAVs) shed by ducks could remain viable for extended periods in surface water within three wetland complexes of North America. In a field experiment, replicate filtered surface water samples inoculated with duck swabs were tested for IAVs upon collection and again after an overwintering period of approximately 6-7 months. Numerous IAVs were molecularly detected and isolated from these samples, including replicates maintained at wetland field sites in Alaska and Minnesota for 181-229 days. In a parallel laboratory experiment, we attempted to culture IAVs from filtered surface water samples inoculated with duck swabs from Minnesota each month during September 2018-April 2019 and found monthly declines in viral viability. In an experimental challenge study, we found that IAVs maintained in filtered surface water within wetlands of Alaska and Minnesota for 214 and 226 days, respectively, were infectious in a mallard model. Collectively, our results support surface waters of northern wetlands as a biologically important medium in which IAVs may be both transmitted and maintained, potentially serving as an environmental reservoir for infectious IAVs during the overwintering period of migratory birds.


Assuntos
Patos/virologia , Vírus da Influenza A , Influenza Aviária/virologia , Áreas Alagadas , Animais , América do Norte
9.
J Virol ; 93(14)2019 07 15.
Artigo em Inglês | MEDLINE | ID: mdl-31068421

RESUMO

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.IMPORTANCE Not 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.


Assuntos
Galinhas/virologia , Patos/virologia , Glicoproteínas de Hemaglutininação de Vírus da Influenza/genética , Vírus da Influenza A Subtipo H7N3/fisiologia , Influenza Aviária , Mutação de Sentido Incorreto , Doenças das Aves Domésticas , Proteínas do Core Viral/genética , Substituição de Aminoácidos , Animais , Influenza Aviária/genética , Influenza Aviária/transmissão , México , Doenças das Aves Domésticas/genética , Doenças das Aves Domésticas/transmissão , Doenças das Aves Domésticas/virologia
10.
BMC Vet Res ; 16(1): 351, 2020 Sep 23.
Artigo em Inglês | MEDLINE | ID: mdl-32967673

RESUMO

BACKGROUND: Aquatic waterfowl, particularly those in the order Anseriformes and Charadriiformes, are the ecological reservoir of avian influenza viruses (AIVs). Dabbling ducks play a recognized role in the maintenance and transmission of AIVs. Furthermore, the pathogenesis of highly pathogenic AIV (HPAIV) in dabbling ducks is well characterized. In contrast, the role of diving ducks in HPAIV maintenance and transmission remains unclear. In this study, the pathogenesis of a North American A/Goose/1/Guangdong/96-lineage clade 2.3.4.4 group A H5N2 HPAIV, A/Northern pintail/Washington/40964/2014, in diving sea ducks (surf scoters, Melanitta perspicillata) was characterized. RESULTS: Intrachoanal inoculation of surf scoters with A/Northern pintail/Washington/40964/2014 (H5N2) HPAIV induced mild transient clinical disease whilst concomitantly shedding high virus titers for up to 10 days post-inoculation (dpi), particularly from the oropharyngeal route. Virus shedding, albeit at low levels, continued to be detected up to 14 dpi. Two aged ducks that succumbed to HPAIV infection had pathological evidence for co-infection with duck enteritis virus, which was confirmed by molecular approaches. Abundant HPAIV antigen was observed in visceral and central nervous system organs and was associated with histopathological lesions. CONCLUSIONS: Collectively, surf scoters, are susceptible to HPAIV infection and excrete high titers of HPAIV from the respiratory and cloacal tracts whilst being asymptomatic. The susceptibility of diving sea ducks to H5 HPAIV highlights the need for additional research and surveillance to further understand the contribution of diving ducks to HPAIV ecology.


Assuntos
Patos , Vírus da Influenza A Subtipo H5N2/patogenicidade , Influenza Aviária/virologia , Animais , Antígenos Virais , Coinfecção/veterinária , Coinfecção/virologia , Feminino , Infecções por Herpesviridae/veterinária , Influenza Aviária/patologia , Masculino , Mardivirus/isolamento & purificação , Eliminação de Partículas Virais
11.
Vet Res ; 50(1): 89, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31675983

RESUMO

In the 2014-2015 Eurasian lineage clade 2.3.4.4A H5 highly pathogenic avian influenza (HPAI) outbreak in the U.S., backyard flocks with minor gallinaceous poultry and large commercial poultry (chickens and turkeys) operations were affected. The pathogenesis of the first H5N8 and reassortant H5N2 clade 2.3.4.4A HPAI U.S. isolates was investigated in six gallinaceous species: chickens, Japanese quail, Bobwhite quail, Pearl guinea fowl, Chukar partridges, and Ring-necked pheasants. Both viruses caused 80-100% mortality in all species, except for H5N2 virus that caused 60% mortality in chickens. The surviving challenged birds remained uninfected based on lack of clinical disease and lack of seroconversion. Among the infected birds, chickens and Japanese quail in early clinical stages (asymptomatic and listless) lacked histopathologic findings. In contrast, birds of all species in later clinical stages (moribund and dead) had histopathologic lesions and systemic virus replication consistent with HPAI virus infection in gallinaceous poultry. These birds had widespread multifocal areas of necrosis, sometimes with heterophilic or lymphoplasmacytic inflammatory infiltrate, and viral antigen in parenchymal cells of most tissues. In general, lesions and antigen distribution were similar regardless of virus and species. However, endotheliotropism was the most striking difference among species, with only Pearl guinea fowl showing widespread replication of both viruses in endothelial cells of most tissues. The expression of IFN-γ and IL-10 in Japanese quail, and IL-6 in chickens, were up-regulated in later clinical stages compared to asymptomatic birds.


Assuntos
Galliformes , Imunidade Inata , Vírus da Influenza A/fisiologia , Influenza Aviária/imunologia , Influenza Aviária/virologia , Doenças das Aves Domésticas/imunologia , Doenças das Aves Domésticas/virologia , Animais , Estados Unidos
12.
Emerg Infect Dis ; 24(10): 1840-1848, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-30226167

RESUMO

Eurasia highly pathogenic avian influenza virus (HPAIV) H5 clade 2.3.4.4 emerged in North America at the end of 2014 and caused outbreaks affecting >50 million poultry in the United States before eradication in June 2015. We investigated the underlying ecologic and epidemiologic processes associated with this viral spread by performing a comparative genomic study using 268 full-length genome sequences and data from outbreak investigations. Reassortant HPAIV H5N2 circulated in wild birds along the Pacific flyway before several spillover events transmitting the virus to poultry farms. Our analysis suggests that >3 separate introductions of HPAIV H5N2 into Midwest states occurred during March-June 2015; transmission to Midwest poultry farms from Pacific wild birds occurred ≈1.7-2.4 months before detection. Once established in poultry, the virus rapidly spread between turkey and chicken farms in neighboring states. Enhanced biosecurity is required to prevent the introduction and dissemination of HPAIV across the poultry industry.


Assuntos
Vírus da Influenza A/classificação , Vírus da Influenza A/genética , Influenza Aviária/transmissão , Influenza Aviária/virologia , Doenças das Aves Domésticas/transmissão , Doenças das Aves Domésticas/virologia , Animais , Teorema de Bayes , Surtos de Doenças , Genoma Viral , História do Século XXI , Vírus da Influenza A/patogenicidade , Influenza Aviária/epidemiologia , Influenza Aviária/história , América do Norte/epidemiologia , Filogenia , Aves Domésticas , Doenças das Aves Domésticas/epidemiologia , Doenças das Aves Domésticas/história , RNA Viral , Vírus Reordenados
13.
J Virol ; 91(21)2017 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-28794040

RESUMO

In 2014 and 2015, the United States experienced an unprecedented outbreak of Eurasian clade 2.3.4.4 H5 highly pathogenic avian influenza (HPAI) virus. Initial cases affected mainly wild birds and mixed backyard poultry species, while later outbreaks affected mostly commercial chickens and turkeys. The pathogenesis, transmission, and intrahost evolutionary dynamics of initial Eurasian H5N8 and reassortant H5N2 clade 2.3.4.4 HPAI viruses in the United States were investigated in minor gallinaceous poultry species (i.e., species for which the U.S. commercial industries are small), namely, Japanese quail, bobwhite quail, pearl guinea fowl, chukar partridges, and ring-necked pheasants. Low mean bird infectious doses (<2 to 3.7 log10) support direct introduction and infection of these species as observed in mixed backyard poultry during the early outbreaks. Pathobiological features and systemic virus replication in all species tested were consistent with HPAI virus infection. Sustained virus shedding with transmission to contact-exposed birds, alongside long incubation periods, may enable unrecognized dissemination and adaptation to other gallinaceous species, such as chickens and turkeys. Genome sequencing of excreted viruses revealed numerous low-frequency polymorphisms and 20 consensus-level substitutions in all genes and species, but especially in Japanese quail and pearl guinea fowl and in internal proteins PB1 and PB2. This genomic flexibility after only one passage indicates that influenza viruses can continue to evolve in galliform species, increasing their opportunity to adapt to other species. Our findings suggest that these gallinaceous poultry are permissive for infection and sustainable transmissibility with the 2014 initial wild bird-adapted clade 2.3.4.4 virus, with potential acquisition of mutations leading to host range adaptation.IMPORTANCE The outbreak of clade 2.3.4.4 H5 highly pathogenic avian influenza (HPAI) virus that occurred in the United States in 2014 and 2015 represents the worst livestock disease event in the country, with unprecedented socioeconomic and commercial consequences. Epidemiological and molecular investigations can identify transmission pathways of the HPAI virus. However, understanding the pathogenesis, transmission, and intrahost evolutionary dynamics of new HPAI viruses in different avian species is paramount. The significance of our research is in examining the susceptibility of minor gallinaceous species to HPAI virus, as this poultry sector also suffers from HPAI epizootics, and identifying the biological potential of these species as an epidemiological link between the waterfowl reservoir and the commercial chicken and turkey populations, with the ultimate goal of refining surveillance in these populations to enhance early detection, management, and control in future HPAI virus outbreaks.


Assuntos
Surtos de Doenças/veterinária , Vírus da Influenza A Subtipo H5N2/patogenicidade , Vírus da Influenza A Subtipo H5N8/patogenicidade , Influenza Aviária/transmissão , Influenza Aviária/virologia , Doenças das Aves Domésticas/transmissão , Doenças das Aves Domésticas/virologia , Animais , Galinhas , Coturnix , Influenza Aviária/epidemiologia , Doenças das Aves Domésticas/epidemiologia , Estados Unidos/epidemiologia , Virulência , Eliminação de Partículas Virais
14.
Vet Res ; 49(1): 82, 2018 Aug 29.
Artigo em Inglês | MEDLINE | ID: mdl-30157963

RESUMO

In March 2017, H7N9 highly pathogenic avian influenza (HPAI) virus was detected in 2 broiler breeder farms in the state of Tennessee, USA. Subsequent surveillance detected the low pathogenicity avian influenza (LPAI) virus precursor in multiple broiler breeder farms and backyard poultry in Tennessee and neighboring states. The pathogenesis of the H7N9 LPAI virus was investigated in commercial broiler breeders, the bird type mostly affected in this outbreak. Infectivity, transmissibility, and pathogenesis of the H7N9 HPAI and LPAI viruses were also studied in 4-week-old specific pathogen free (SPF) leghorn chickens. The mean bird infectious doses (BID50) for the LPAI isolate was 5.6 log10 mean egg infectious dose (EID50) for broiler breeders and 4.3 log10 EID50 for SPF layer chickens, and no transmission to contact-exposed birds was observed. In both bird types, virus shedding was almost exclusively from the oropharyngeal route. These findings suggest sub-optimal adaptation for sustained transmission with the H7N9 LPAI isolate, indicating that factors other than the birds genetic background may explain the epidemiology of the outbreak. The BID50 for the HPAI isolate in SPF layer chickens was more than 2 logs lower (<2 log10 EID50) than the LPAI isolate. Also, the HPAI virus was shed by both the oropharyngeal and cloacal routes and transmitted to contacts. Greater susceptibility and easier transmission of the H7N9 HPAI virus are features of the HP phenotype that could favor the spread of HPAI over LPAI viruses during outbreaks.


Assuntos
Galinhas , Subtipo H7N9 do Vírus da Influenza A/fisiologia , Subtipo H7N9 do Vírus da Influenza A/patogenicidade , Influenza Aviária/transmissão , Influenza Aviária/virologia , Doenças das Aves Domésticas/transmissão , Doenças das Aves Domésticas/virologia , Animais , Organismos Livres de Patógenos Específicos , Tennessee , Virulência
15.
J Virol ; 90(21): 9967-9982, 2016 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-27558429

RESUMO

Wild aquatic birds have been associated with the intercontinental spread of H5 subtype highly pathogenic avian influenza (HPAI) viruses of the A/goose/Guangdong/1/96 (Gs/GD) lineage during 2005, 2010, and 2014, but dispersion by wild waterfowl has not been implicated with spread of other HPAI viruses. To better understand why Gs/GD H5 HPAI viruses infect and transmit more efficiently in waterfowl than other HPAI viruses, groups of mallard ducks were challenged with one of 14 different H5 and H7 HPAI viruses, including a Gs/GD lineage H5N1 (clade 2.2) virus from Mongolia, part of the 2005 dispersion, and the H5N8 and H5N2 index HPAI viruses (clade 2.3.4.4) from the United States, part of the 2014 dispersion. All virus-inoculated ducks and contact exposed ducks became infected and shed moderate to high titers of the viruses, with the exception that mallards were resistant to Ck/Pennsylvania/83 and Ck/Queretaro/95 H5N2 HPAI virus infection. Clinical signs were only observed in ducks challenged with the H5N1 2005 virus, which all died, and with the H5N8 and H5N2 2014 viruses, which had decreased weight gain and fever. These three viruses were also shed in higher titers by the ducks, which could facilitate virus transmission and spread. This study highlights the possible role of wild waterfowl in the spread of HPAI viruses. IMPORTANCE: The spread of H5 subtype highly pathogenic avian influenza (HPAI) viruses of the Gs/GD lineage by migratory waterfowl is a serious concern for animal and public health. H5 and H7 HPAI viruses are considered to be adapted to gallinaceous species (chickens, turkeys, quail, etc.) and less likely to infect and transmit in wild ducks. In order to understand why this is different with certain Gs/GD lineage H5 HPAI viruses, we compared the pathogenicity and transmission of several H5 and H7 HPAI viruses from previous poultry outbreaks to Gs/GD lineage H5 viruses, including H5N1 (clade 2.2), H5N8 and H5N2 (clade 2.3.4.4) viruses, in mallards as a representative wild duck species. Surprisingly, most HPAI viruses examined in this study replicated well and transmitted among mallards; however, the three Gs/GD lineage H5 HPAI viruses replicated to higher titers, which could explain the transmission of these viruses in susceptible wild duck populations.


Assuntos
Patos/virologia , Vírus da Influenza A/patogenicidade , Influenza Aviária/transmissão , Influenza Aviária/virologia , Animais , Animais Selvagens/virologia , Surtos de Doenças , Aves Domésticas/virologia , Doenças das Aves Domésticas/virologia
16.
Vet Res ; 48(1): 33, 2017 06 07.
Artigo em Inglês | MEDLINE | ID: mdl-28592320

RESUMO

In late 2014, a H5N8 highly pathogenic avian influenza (HPAI) virus, clade 2.3.4.4, spread by migratory waterfowl into North America reassorting with low pathogenicity AI viruses to produce a H5N2 HPAI virus. Since domestic waterfowl are common backyard poultry frequently in contact with wild waterfowl, the infectivity, transmissibility, and pathogenicity of the United States H5 HPAI index viruses (H5N8 and H5N2) was investigated in domestic ducks and geese. Ducks infected with the viruses had an increase in body temperature but no or mild clinical signs. Infected geese did not show increase in body temperature and most only had mild clinical signs; however, some geese presented severe neurological signs. Ducks became infected and transmitted the viruses to contacts when inoculated with high virus doses [(104 and 106 50% embryo infective dose (EID50)], but not with a lower dose (102 EID50). Geese inoculated with the H5N8 virus became infected regardless of the virus dose given, and transmitted the virus to direct contacts. Only geese inoculated with the higher doses of the H5N2 and their contacts became infected, indicating differences in infectivity between the two viruses and the two waterfowl species. Geese shed higher titers of virus and for a longer period of time than ducks. In conclusion, the H5 HPAI viruses can infect domestic waterfowl and easily transmit to contact birds, with geese being more susceptible to infection and disease than ducks. The disease is mostly asymptomatic, but infected birds shed virus for several days representing a risk to other poultry species.


Assuntos
Patos/virologia , Gansos/virologia , Vírus da Influenza A Subtipo H5N2/patogenicidade , Vírus da Influenza A Subtipo H5N8/patogenicidade , Influenza Aviária/transmissão , Doenças das Aves Domésticas/virologia , Animais , Vírus da Influenza A Subtipo H5N2/genética , Vírus da Influenza A Subtipo H5N8/genética , Influenza Aviária/epidemiologia , Influenza Aviária/virologia , Doenças das Aves Domésticas/epidemiologia , Doenças das Aves Domésticas/transmissão , RNA Viral/genética , Estados Unidos/epidemiologia
17.
Vet Res ; 47(1): 116, 2016 11 21.
Artigo em Inglês | MEDLINE | ID: mdl-27871330

RESUMO

In 2014-2015, the US experienced an unprecedented outbreak of H5 clade 2.3.4.4 highly pathogenic avian influenza (HPAI) virus. The H5N2 HPAI virus outbreak in the Midwest in 2015 affected commercial turkey and layer farms, but not broiler farms. To assess any potential genetic resistance of broilers and/or age-related effects, we investigated the pathogenesis and transmission of A/turkey/Minnesota/12582/2015 (H5N2) (Tk/MN/15) virus in commercial 5-week-old broilers, 8-week-old broilers, and >30-week-old broiler breeders. The mean bird lethal dose (BLD50) was 5.0 log10 mean egg infectious dose (EID50) for all age groups. The mean death time (MDT) was statistically not different among the three age groups, ranging between 3.2 and 4.8 days. All broilers that became infected shed high levels of virus with transmission to contacts and demonstrated severe pathology. Mortality and virus shedding results indicated that age is not a determinant factor in susceptibility of broilers to H5N2 clade 2.3.4.4 HPAI virus. Previously, the Tk/MN/15 virus had a BLD50 of 3.6 log10 EID50 and MDT of 2 days in White Leghorn chickens and a BLD50 of 5.0 log10 EID50 and MDT of 5.9 days in turkeys, suggesting that the broiler breed is less susceptible to Midwestern H5N2 virus than the layer breed but similarly susceptible to turkeys. Therefore, genetic resistance of broilers to infection may have accounted only partially for the lack of affected broiler farms in the Midwestern outbreaks, with other contributing factors such as fewer outside to on farm exposure to contacts, type of production management system or enhanced biosecurity.


Assuntos
Suscetibilidade a Doenças/veterinária , Vírus da Influenza A Subtipo H5N2 , Influenza Aviária/virologia , Doenças das Aves Domésticas/virologia , Fatores Etários , Animais , Galinhas/imunologia , Galinhas/virologia , Suscetibilidade a Doenças/imunologia , Vírus da Influenza A Subtipo H5N2/genética , Vírus da Influenza A Subtipo H5N2/imunologia , Vírus da Influenza A Subtipo H5N2/patogenicidade , Influenza Aviária/imunologia , Influenza Aviária/patologia , Lisofosfolipídeos , Doenças das Aves Domésticas/imunologia , Doenças das Aves Domésticas/patologia , Eliminação de Partículas Virais
18.
Arch Virol ; 161(3): 605-12, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26650037

RESUMO

Since the first detection of H15 avian influenza viruses (AIVs) in Australia in 1979, only seven H15 strains have been reported. A new H15 AIV was detected in Ukraine in 2010, carrying the unique HA-NA subtype combination H15N7. This virus replicated efficiently in chicken eggs, and antisera against it reacted strongly with the homologous antigen, but with lower titers when using the reference Australian antigen. The amino acid motifs of the HA cleavage site and receptor-binding site were different from those in the Australian viruses. The new virus, together with an H15 virus from Siberia from 2008, constitutes a new clade of H15 AIV isolates.


Assuntos
Variação Genética , Genótipo , Vírus da Influenza A/classificação , Vírus da Influenza A/genética , Influenza Aviária/virologia , Animais , Ásia , Galinhas , Europa (Continente) , Vírus da Influenza A/isolamento & purificação , Vírus da Influenza A/fisiologia , Óvulo/virologia , Sorogrupo , Replicação Viral
19.
Arch Virol ; 161(12): 3345-3353, 2016 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-27581808

RESUMO

Here, we report the circulation of highly related virulent Newcastle disease viruses (NDV) in Bulgaria and Ukraine from 2002 until 2013. All of these NDV isolates have the same virulence-associated cleavage site ("113RQKR↓F117"), and selected ones have intracerebral pathogenicity index values ranging from 1.61 to 1.96. These isolates are most closely related to viruses circulating in Eastern Europe, followed by viruses isolated in Asia during the same period of time. Interestingly, the majority of the viruses were isolated from backyard poultry, suggesting the possibility of a "domestic" or "urban" cycle of maintenance. The molecular characterization of the nucleotide sequence of the complete fusion protein gene of the studied viruses suggests continued circulation of virulent NDV of sub-genotype VIId in Eastern Europe, with occasional introductions from Asia. Furthermore, the high level of genetic similarity among those isolates suggests that the NDV isolates of sub-genotype VIId from Bulgaria and Ukraine may have been part of a broader epizootic process in Eastern Europe rather than separate introductions from Asia or Africa. The continuous monitoring of backyard poultry flocks for the presence of circulating virulent NDV strains will allow early identification of Newcastle disease outbreaks.


Assuntos
Galinhas/virologia , Genótipo , Doença de Newcastle/virologia , Vírus da Doença de Newcastle/classificação , Vírus da Doença de Newcastle/isolamento & purificação , Doenças das Aves Domésticas/virologia , Animais , Bulgária/epidemiologia , Análise por Conglomerados , Epidemiologia Molecular , Vírus da Doença de Newcastle/genética , Vírus da Doença de Newcastle/patogenicidade , Filogenia , Doenças das Aves Domésticas/epidemiologia , Análise de Sequência de DNA , Homologia de Sequência , Ucrânia/epidemiologia , Proteínas Virais de Fusão/genética
20.
BMC Vet Res ; 12(1): 260, 2016 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-27876034

RESUMO

BACKGROUND: From December 2014 through June 2015, the US experienced the most costly highly pathogenic avian influenza (HPAI) outbreak to date. Most cases in commercial poultry were caused by an H5N2 strain which was a reassortant with 5 Eurasian lineage genes, including a clade 2.3.4.4 goose/Guangdong/1996 lineage hemagglutinin, and 3 genes from North American wild waterfowl low pathogenicity avian influenza viruses. The outbreak primarily affected turkeys and table-egg layer type chickens. Three isolates were selected for characterization in turkeys: the US index isolate from December 2014 (A/northern pintail/WA/40964/2014), and two poultry isolates from April 2015 (A/chicken/IA/13388/2015 and A/turkey/MN/12528/2015). RESULTS: Four week old broad-breasted white turkeys were inoculated with one of three doses (102, 104 or 106 50% egg infectious doses [EID50] per bird) of each of the isolates to evaluate infectious dose and pathogenesis. The mean bird infectious dose of A/northern pintail/WA/40964/2014 and A/turkey/MN/12528/2015 was 105 EID50 per bird, but was 103 EID50 per bird for A/chicken/IA/13388/2015, suggesting the latter had greater adaptation to gallinaceous birds. All three isolates had unusually long mean death time of 5.3-5.9 days post challenge, and the primary clinical signs were severe lethargy and neurological signs which started no more than 24 h before death (the average pre-clinical period was 4 days). Infected turkeys also shed high levels of virus by both the oropharyngeal and cloacal routes. CONCLUSIONS: The unusually long mean death times, high levels of virus in feces, and increased adaptation of the later viruses may have contributed to the rapid spread of the virus during the peak of the outbreak.


Assuntos
Vírus da Influenza A Subtipo H5N2/fisiologia , Influenza Aviária/patologia , Influenza Aviária/virologia , Perus , Animais , Interações Hospedeiro-Patógeno , Vírus da Influenza A Subtipo H5N2/patogenicidade , Fatores de Tempo
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