Duck Virus Research Articles

Molecular surveillance of avian influenza A viruses in Basrah and Wasit

The aim of this study was to detect influenza A virus in broiler chickens and wild ducks in different geographical regions of Basrah and Wasit provinces, Iraq. This study was authenticated by analysing the viral genome and designing a set of universal primers for the detection of all influenza A subtypes in a single enzymatic reaction through the amplification of a highly conserved region of viral M gene. A total of 157 and 155 oropharyngeal and cloacal swabs from broiler chickens and wild ducks, respectively, were analysed. The study shows that influenza A viruses were prevalent in these birds in all study regions with a significantly higher percentage in wild ducks compared to broiler chickens. The results showed that 92/157 samples (54/75 wild ducks and 38/82 broiler chickens) and 96/155 samples (38/75 wild ducks and 58/80 broiler chickens) in Basrah and Wasit, respectively, were positive for the viral M gene. In addition, there was no significant difference in virus prevalence between Basrah and Wasit provinces.

Seroprevalensi Penyakit Egg Drop Syndrome pada Itik di Desa Tumbak Bayuh, Kecamatan Mengwi, Badung, Bali

Egg Drop Syndrome can cause detrimental impacts on breeders due to reducing production and quality of theaffected eggs.This study aim was to determine the seroprevalece ofantibody against Egg Drop Syndrome (EDS) virus in ducks. Antibody titers examination was done from 75blood samplesof ducks thathave not been vaccinatedagainstEDS virus. The duck samples were collected from Tumbak Bayuh Village, Mengwi, Badung. Serological examination was held at the Virology Laboratory,Faculty of Veterinary Medicine, Udayana University by usingHaemagglutination Inhibition (HI) test. HI test results showed that 24 samples were positive contained antibody of the EDS,while 51 samples were negative. Range of EDS antibody titer observed was from24 to 27 HI units. This results indicates that the ducks have protective antibody titer against EDS virus. The positive serum samples were also tested using HI test against Newcastle Disease (ND) virus with negative result. It can be concluded that the ducks in Tumbak Bayuh Village, Mengwi, Badung have 32% of antibody titer against EDS virus whichmight result from being exposed by EDS virus naturally.

Molecular, antigenic, and pathogenic characterization of H5N8 highly pathogenic avian influenza viruses isolated in the Democratic Republic of Congo in 2017.

In May 2017, high mortality of chickens and Muscovy ducks due to the H5N8 highly pathogenic avian influenza virus (HPAIV) was reported in the Democratic Republic of Congo (DR Congo). In this study, we assessed the molecular, antigenic, and pathogenic features in poultry of the H5N8 HPAIV from the 2017 Congolese outbreaks. Phylogenetic analysis of the eight viral gene segments revealed that all 12 DR Congo isolates clustered in clade 2.3.4.4B together with other H5N8 HPAIVs isolated in Africa and Eurasia, suggesting a possible common origin of these viruses. Antigenically, a slight difference was observed between the Congolese isolates and a representative virus from group C in the same clade. After intranasal inoculation with a representative DR Congo virus, high pathogenicity was observed in chickens and Muscovy ducks but not in Pekin ducks. Viral replication was higher in chickens than in Muscovy duck and Pekin duck organs; however, neurotropism was pronounced in Muscovy ducks. Our data confirmed the high pathogenicity of the DR Congo virus in chickens and Muscovy ducks, as observed in the field. National awareness and strengthening surveillance in the region are needed to better control HPAIVs.

Long-term passage of duck Tembusu virus in BHK-21 cells generates a completely attenuated and immunogenic population with increased genetic diversity

Duck Tembusu virus (TMUV) is an emerging pathogenic flavivirus that causes severe egg-drop and fatal encephalitis in domestic ducks and geese. Although a live-attenuated virus vaccine is effective for disease control, the stability of the attenuation has not been clearly evaluated due to a poor understanding of the attenuation mechanism. Here, a virulent duck TMUV isolate was successively passaged in BHK-21 cells, leading to an approximately 100-fold increase of virus production in cell culture and a complete attenuation of virulence for ducks. The passaged virus induced high titers of TMUV-specific antibody and provided efficient protection against a virulent TMUV challenge after a single-dose vaccination. One hundred and two, and eighteen single-nucleotide polymorphisms (SNPs) at a frequency of >1% were respectively identified in the attenuated virus population and the original isolate by deep sequencing. The increased SNPs numbers suggested that the accumulated variants of virus population may have conferred the phenotypic changes. We cloned and characterized a dominant variant exhibiting similar fitness to the mixed population, and 23 amino acid substitutions were identified across the viral open reading frame. Using reverse genetics, two chimeric viruses were generated by introducing the mutated E or NS5 gene into the backbone of virulent TMUV. We found that mutations in the E gene conferred a fitness advantage in BHK-21 cells and decreased the virus pathogenicity, whereas NS5 mutations reduced the virus infectivity in ducklings without altering the in vitro fitness. In conclusion, increased mutations in a virulent TMUV strain did substantially reduce the virus virulence, and mutations in multiple genes co-contribute to TMUV attenuation.

Organ-specific small non-coding RNA responses in domestic (Sudani) ducks experimentally infected with highly pathogenic avian influenza virus (H5N1)

ABSTRACT The duck represents an important reservoir of influenza viruses for transmission to other avian and mammalian hosts, including humans. The increased pathogenicity of the recently emerging clades of highly pathogenic avian influenza (HPAI) viruses of the H5N1 subtype in ducks features systemic viral spread and organ-to-organ variation in viral transcription and tissue damage. We previously reported that experimental infection of Sudani ducks (Cairina moschata) with an Egyptian HPAI (H5N1) virus (clade 2.2.1.2) features high viral replication and severe tissue damage in lung, but lower viral replication and only mild histological changes in brain. Little is known about the involvement of miRNA in organ-specific responses to H5N1 viruses in ducks, and involvement of the other classes of small noncoding RNA (sncRNA) has not been investigated so far. Following RNA sequencing, we have annotated the duck sncRNome and compared global expression changes of the four major sncRNA classes (miRNAs, piRNAs, snoRNAs, snRNAs) between duck lung and brain during a 120 h time course of infection with this HPAI strain. We find major organ-specific differences in miRNA, piRNA and snoRNA populations even before infection and substantial reprogramming of all sncRNA classes throughout infection, which was less pronounced in brain. Pathway prediction analysis of miRNA targets revealed enrichment of inflammation-, infection- and apoptosis-related pathways in lung, but enrichment of metabolism-related pathways (including tryptophan metabolism) in brain. Thus, organ-specific differences in sncRNA responses may contribute to differences in viral replication and organ damage in ducks infected with isolates from this emerging HPAI clade, and likely other strains.

Genetic characteristics and polymorphisms in the chicken interferon-induced transmembrane protein (IFITM3) gene.

The interferon-induced transmembrane protein 3 (IFITM3) gene is classified as a small interferon-stimulated gene and is associated with a broad spectrum of antiviral functions against several fatal enveloped viruses, including influenza A viruses (IAVs). The rs12252 single nucleotide polymorphism (SNP) of the IFITM3 gene in humans was associated with susceptibility to H1N1 influenza in a 2009 pandemic. In addition, overexpression of the IFITM3 protein potently inhibits the highly pathogenic avian influenza H5N1 virus in ducks and chickens. Although chickens are a major host of influenza viruses and the IFITM3 gene participates in the host antiviral system, studies on chicken IFITM3 gene are very rare. To investigate the genetic characteristics of the chicken IFITM3 gene, we performed direct sequencing and alignment in 108 Dekalb White and 72 Ross breeds. We also investigated the genotype and haplotype frequencies and linkage disequilibrium of the IFITM3 gene polymorphisms and evaluated whether the non-synonymous SNPs are deleterious. We found significantly different genotype, allele and haplotypes frequencies between two chicken breeds, Dekalb White and Ross. Furthermore, we compared and analyzed the promoter structure of the chicken IFITM3 gene with that of several species. We found that birds have a long C-terminal domain and inverted topology of the IFITM3 protein compared to mammals. We also identified fourteen genetic polymorphisms in the chicken IFITM3 gene. L100 M and N125H were predicted as ‘probably damaging’ and L100 M can alter the length of its conserved intracellular loop (CIL). Furthermore, chickens, but not mammals, contain CpG islands (CGIs) in this promoter region.

Variable impact of the hemagglutinin polybasic cleavage site on virulence and pathogenesis of avian influenza H7N7 virus in chickens, turkeys and ducks

Avian influenza viruses (AIV) are classified into 16 hemagglutinin (HA; H1-H16) and 9 neuraminidase (NA; N1-N9) subtypes. All AIV are low pathogenic (LP) in birds, but subtypes H5 and H7 AIV can evolve into highly pathogenic (HP) forms. In the last two decades evolution of HPAIV H7 from LPAIV has been frequently reported. However, little is known about the pathogenesis and evolution of HP H7 from LP ancestors particularly, in non-chicken hosts. In 2015, both LP and HP H7N7 AIV were isolated from chickens in two neighbouring farms in Germany. Here, the virulence of these isogenic H7N7 LP, HP and LP virus carrying a polybasic HA cleavage site (HACS) from HP (designated LP-Poly) was studied in chickens, turkeys and different duck breeds. The LP precursor was avirulent in all birds. In contrast, all inoculated and contact chickens and turkeys died after infection with HP. HP infected Pekin and Mallard ducks remained clinically healthy, while Muscovy ducks exhibited moderate depression and excreted viruses at significantly higher amounts. The polybasic HACS increased virulence in a species-specific manner with intravenous pathogenicity indices of 3.0, 1.9 and 0.2 in chickens, turkeys and Muscovy ducks, respectively. Infection of endothelial cells was only observed in chickens. In summary, Pekin and Mallard were more resistant to HPAIV H7N7 than chickens, turkeys and Muscovy ducks. The polybasic HACS was the main determinant for virulence and endotheliotropism of HPAIV H7N7 in chickens, whereas other viral and/or host factors play an essential role in virulence and pathogenesis in turkeys and ducks.

Adaptation of wild strain of duck plague virus in cell culture systems

Duck virus enteritis (DVE) is an acute, contagious herpes viral disease of ducks, geese and swans and members of the family Anatidae under the order Anseriformes. As per the recent taxonomic classification by ICTV, DEV has been classified into the genus Mardivirus, subfamily Alpha-herpesvirinae of the family Herpesviridae. Vaccination is the only option for the prevention and control of Duck plague. In India vaccination is done with chicken embryo adapted live virus which has many shortcomings. So, in this present situation a safe and potent vaccine development is the need of the hour. The use of chicken embryo fibroblast and a certified cell line may, probably, be the best option to achieve this. Therefore, the present study was undertaken for adaptation and propagation of local strain of duck plague virus in various cell culture systems. During the study a wild strain of DPV (DP/As-Km/0019) which was isolated in Duck Embryo Fibroblast, available in the Department of Microbiology was selected. The selected wild strain was used for adaptation in various cell culture systems viz. Chicken embryo fibroblast cell culture (CEF), Vero cell line and QT-35 cell line. The virus was passaged up to 12th passage levels and the presence of viral antigen was demonstrated by appearance of cytopathic effect (CPE), by Polymerase Chain Reaction (PCR) and by Sandwich ELISA. PCR was able to detect virus from all the cell cultures from 5th passage onwards and virus titre was detected at 10th and 12th passage level by S-ELISA. It was observed that various cell culture systems can be a good candidate for propagation of DPV and further study is required to study its immunogenicity and its feasibility as a vaccine candidate.

Assessment of the Effect of Baicalin on Duck Virus Hepatitis.

Duck virus hepatitis (DVH) caused by duck hepatitis A virus type 1 (DHAV-1) is a malignant disease in ducklings, causing economic losses in the duck industry. However, there is still no antiviral drug against DHAV-1 in the clinic. Our aim is to investigate the anti-DHAV-1 effect of baicalin, which is a flavonoid derived from the Chinese medicinal herb huangqin (Scutellaria baicalensis Georgi). Here, we first detected its anti-DHAV-1 ability in vitro and in vivo. At the same time, the inhibition of baicalin on DHAV-1 reproduction was determined. Finally, we tested and verified the anti-oxidative and immuno-enhancing roles of baicalin on its curative effect on DVH. Baicalin possessed anti-DHAV-1 effect. It improved the cytoactive of DEH which was infected by DHAV-1 as well as reduced the DHAV-1 reproduction in DEH. Under baicalin treatment, mortality of ducklings infected by DHAV-1 decreased, additionally the DHAV-1 level and liver injury in such ducklings were significantly reduced or alleviated. The in vitro mechanism study indicated baicalin inhibited DHAV-1 reproduction via interfering the viral replication and release. Furthermore, the in vivo mechanism study manifested both the anti-oxidative and immuno-enhancing abilities of baicalin, which played crucial roles in its curative effect on DVH. This study may provide a scientific basis for developing baicalin as one or a part of the anti-DHAV-1 drugs.

Will China's H7N9 Control Strategy Continue to Be Effective?

Since the first outbreak of avian influenza A(H7N9) virus in China in early 2013, several interventions to control the transmission of H7N9 virus from poultry to humans have been implemented. Temporarily closing live poultry markets reduced the risk of human infection to an extent, but it did not prevent the spread of the H7N9 virus among poultry, and this spread eventually led to more human cases. Nevertheless, the mass vaccination of poultry after September 2017 has been highly effective in preventing the H7N9 virus infection in both poultry and humans. In light of the emergence of highly pathogenic H7N9 and H7N2 viruses in unimmunized ducks, vaccination among poultry, especially for ducks, should be accompanied with continued surveillance of H7N9 variants and other avian influenza A viruses that could signal a heightened pandemic risk.

Virulence of three European highly pathogenic H7N1 and H7N7 avian influenza viruses in Pekin and Muscovy ducks

BackgroundThere is paucity of data on the virulence of highly pathogenic (HP) avian influenza viruses (AIV) H7 in ducks compared to HPAIV H5. Here, the virulence of HPAIV H7N1 (designated H7N1-FPV34 and H7N1-It99) and H7N7 (designated H7N7-FPV27) was assessed in Pekin and/or Muscovy ducklings after intrachoanal (IC) or intramuscular (IM) infection.ResultsThe morbidity rate ranged from 60 to 100% and mortality rate from 20 to 80% depending on the duck species, virus strain and/or challenge route. All Muscovy ducklings inoculated IC with H7N7-FPV27 or H7N1-FPV34 exhibited mild to severe clinical signs resulting in the death of 2/10 and 8/10 ducklings, respectively. Also, 2/10 and 6/9 of inoculated Muscovy ducklings died after IC or IM infection with H7N1-It99, respectively. Moreover, 5/10 Pekin ducklings inoculated IC or IM with H7N1-It99 died. The level of virus detected in the oropharyngeal swabs was higher than in the cloacal swabs.ConclusionTaken together, HPAIV H7 cause mortality and morbidity in Muscovy and Pekin ducklings. The severity of disease in Muscovy ducklings depended on the virus strain and/or route of infection. Preferential replication of the virus in the respiratory tract compared to the gut merits further investigation.

Molecular Detection of Influenza A virus in Domestic Ducks and Geese in Basra Province, Southern Iraq

Molecular Detection of Influenza A virus in Domestic Ducks and Geese in Basra Province, Southern Iraq

Molecular cloning and mRNA expression of IFIT5 in tissues of ducklings infected with virulent duck hepatitis A virus type 3

Interferon-induced proteins with tetratricopeptide repeats (IFITs) are a family of proteins strongly induced downstream of type I interferon signaling. The function of IFITs has been investigated extensively in mammals. IFIT5 is the sole protein in this family found in birds and little information is available about the function of avian IFIT5. In this study, duck IFIT5 was cloned from peripheral blood mononuclear cells. Multiple amino acid sequence alignment and phylogenetic analysis showed that duck IFIT5 is highly homologous to chicken IFIT5. Tissue specificity analysis demonstrated that duck IFIT5 was ubiquitously expressed in all examined tissues of five-day-old ducklings, with the highest expression levels in heart, followed by thymus, cerebrum, liver, and lung; kidney expressed the lowest. Quantitative real-time PCR (qRT-PCR) analysis revealed that duck IFIT5 expression rapidly increased both in vitro and in vivo after stimulation with polyinosinic:polycytidylic acid [poly (I:C)] and infection with virulent duck hepatitis A virus type 3 (DHAV-3), respectively. Altogether, these results indicate that the expression of duck IFIT5 is positively correlated with viral load and may play an important role in the immune response to DHAV-3 infection. This study lays a foundation for further research into the innate antiviral immune responses of ducklings.

Genetic relationship between poultry and wild bird viruses during the highly pathogenic avian influenza H5N6 epidemic in the Netherlands, 2017-2018.

SummaryIn the Netherlands, three commercial poultry farms and two hobby holdings were infected with highly pathogenic avian influenza (HPAI) H5N6 virus in the winter of 2017–2018. This H5N6 virus is a reassortant of HPAI H5N8 clade 2.3.4.4 group B viruses detected in Eurasia in 2016. H5N6 viruses were also detected in several dead wild birds during the winter. However, wild bird mortality was limited compared to the caused by the H5N8 group B virus in 2016–2017. H5N6 virus was not detected in wild birds after March, but in late summer infected wild birds were found again. In this study, the complete genome sequences of poultry and wild bird viruses were determined to study their genetic relationship. Genetic analysis showed that the outbreaks in poultry were not the result of farm‐to‐farm transmissions, but rather resulted from separate introductions from wild birds. Wild birds infected with viruses related to the first outbreak in poultry were found at short distances from the farm, within a short time frame. However, no wild bird viruses related to outbreaks 2 and 3 were detected. The H5N6 virus isolated in summer shares a common ancestor with the virus detected in outbreak 1. This suggests long‐term circulation of H5N6 virus in the local wild bird population. In addition, the pathogenicity of H5N6 virus in ducks was determined, and compared to that of H5N8 viruses detected in 2014 and 2016. A similar high pathogenicity was measured for H5N6 and H5N8 group B viruses, suggesting that biological or ecological factors in the wild bird population may have affected the mortality rates during the H5N6 epidemic. These observations suggest different infection dynamics for the H5N6 and H5N8 group B viruses in the wild bird population.

Development and application of multiplex PCR method for simultaneous detection of seven viruses in ducks

BackgroundMajor viruses, including duck-origin avian influenza virus, duck-origin Newcastle disease virus, novel duck parvovirus, duck hepatitis A virus, duck Tembusu virus, fowl adenovirus, and duck enteritis virus, pose great harm to ducks and cause enormous economic losses to duck industry. This study aims to establish a multiplex polymerase chain reaction (m-PCR) method for simultaneous detection of these seven viruses.ResultsSpecific primers were designed and synthesized according to the conserved region of seven viral gene sequences. Then, seven recombinant plasmids, as the positive controls, were reconstructed in this study. Within the study, D-optimal design was adopted to optimize PCR parameters. The optimum parameters for m-PCR were annealing temperature at 57 °C, Mg2+ concentration at 4 mM, Taq DNA polymerase concentration at 0.05 U/μL, and dNTP concentration at 0.32 mM. With these optimal parameters, the m-PCR method produced neither cross-reactions among these seven viruses nor nonspecific reactions with other common waterfowl pathogens. The detection limit of m-PCR for each virus was 1 × 104 viral DNA copies/μL. In addition, the m-PCR method could detect a combination of several random viruses in co-infection analysis. Finally, the m-PCR method was successfully applied to clinical samples, and the detection results were consistent with uniplex PCR.ConclusionGiven its rapidity, specificity, sensitivity, and convenience, the established m-PCR method is feasible for simultaneous detection of seven duck-infecting viruses and can be applied to clinical diagnosis of viral infection in ducks.

Innate Immune Responses to Avian Influenza Viruses in Ducks and Chickens.

Mallard ducks are important natural hosts of low pathogenic avian influenza (LPAI) viruses and many strains circulate in this reservoir and cause little harm. Some strains can be transmitted to other hosts, including chickens, and cause respiratory and systemic disease. Rarely, these highly pathogenic avian influenza (HPAI) viruses cause disease in mallards, while chickens are highly susceptible. The long co-evolution of mallard ducks with influenza viruses has undoubtedly fine-tuned many immunological host–pathogen interactions to confer resistance to disease, which are poorly understood. Here, we compare innate responses to different avian influenza viruses in ducks and chickens to reveal differences that point to potential mechanisms of disease resistance. Mallard ducks are permissive to LPAI replication in their intestinal tissues without overtly compromising their fitness. In contrast, the mallard response to HPAI infection reflects an immediate and robust induction of type I interferon and antiviral interferon stimulated genes, highlighting the importance of the RIG-I pathway. Ducks also appear to limit the duration of the response, particularly of pro-inflammatory cytokine expression. Chickens lack RIG-I, and some modulators of the signaling pathway and may be compromised in initiating an early interferon response, allowing more viral replication and consequent damage. We review current knowledge about innate response mediators to influenza infection in mallard ducks compared to chickens to gain insight into protective immune responses, and open questions for future research.

Active surveillance and genetic evolution of avian influenza viruses in Egypt, 2016–2018

ABSTRACT Egypt is a hotspot for avian influenza virus (AIV) due to the endemicity of H5N1 and H9N2 viruses. AIVs were isolated from 329 samples collected in 2016–2018; 48% were H9N2, 37.1% were H5N8, 7.6% were H5N1, and 7.3% were co-infections with 2 of the 3 subtypes. The 32 hemagglutinin (HA) sequences of the H5N1 viruses formed a well-defined lineage within clade 2.2.1.2. The 10 HA sequences of the H5N8 viruses belonged to a subclade within 2.3.4.4. The 11 HA of H9N2 isolates showed high sequence homology with other Egyptian G1-like H9N2 viruses. The prevalence of H5N8 viruses in ducks (2.4%) was higher than in chickens (0.94%). Genetic reassortment was detected in H9N2 viruses. Antigenic analysis showed that H9N2 viruses are homogenous, antigenic drift was detected among H5N1 viruses. AI H5N8 showed higher replication rate followed by H9N2 and H5N1, respectively. H5N8 was more common in Southern Egypt, H9N2 in the Nile Delta, and H5N1 in both areas. Ducks and chickens played a significant role in transmission of H5N1 viruses. The endemicity and co-circulation of H5N1, H5N8, and H9N2 AIV coupled with the lack of a clear control strategy continues to provide avenues for further virus evolution in Egypt.

Identification and characterization of a novel nanobody against duck hepatitis A virus type 1

Duck virus hepatitis (DVH) caused by duck hepatitis A virus type 1 (DHAV-1) is an acute and highly contagious disease affecting young ducklings. The VP1 protein is one of the major structural proteins of DHAV-1 carries critical epitopes responsible for the induction of neutralizing antibodies. In this study, we have successfully constructed an immune phage display VHHs library against DHAV-1 with the size of 6 × 106 colonies. A nanobody (Nb) against VP1 protein of DHAV-1, named Nb25, was identified from the immunized phage display library. Nb25 could react with the conserved linear B-cell epitope of 174PAPTST179 in DHAV-1 VP1, even though Nb25 showed no neutralizing activity to DHAV-1. To the best of our knowledge, this is the first report about preparation of anti-DHAV-1 Nbs and identification of the specific conserved linear B-cell epitope of DHAV-1 with Nb, which will facilitate the serologic diagnosis of DHAV-1 infection.

Outbreaks of Duck Hepatitis A Virus in Egyptian Duckling Flocks.

During 2015, duck farms (n = 27) in Sharkia Province, Egypt, experienced several disease outbreaks leading to mortality and nervous manifestations. Upon necropsy, the affected ducklings showed liver lesions, such as hemorrhage or necrosis, suggestive of duck virus hepatitis (DVH). Reverse transcription-PCR (RT-PCR), on the basis of the 3D gene, found duck livers from 21 farms to be positive for duck hepatitis A virus serotype 1 (DHAV-1). All duck breeds (Pekin, Mallard, and Muscovy) were infected. The virus was isolated in embryonated chicken eggs, which showed embryonic mortality (40%-80%) within 5-7 days, stunting or dwarfing (69.6%), and necrotic liver foci (60.9%). The VP1 gene of 11 DHAV-1 strains was characterized by RT-PCR and Sanger sequencing. All study strains were clustered in a monophyletic branch within subclade B2 of Group 4 and were separated from the Egyptian vaccine strain. Several amino acid (aa) residues, such as V129, S142 (only in four strains), L181, G184, and K217, were related to virus attenuation. However, two aa residues (N193 and E205), found in virulent DHAV-1 strains, were also observed in our strains. This study confirms the circulation of DHAV-1 (subclade B2) in Lower Egypt and elucidates the phylogenetic characters of the VP1 genes, which will be useful in following the local trends of DHAV-1 infections. Further studies are indicated to determine the correlation between these mutations and the virulence of the Egyptian DHAV-1 isolates.

Pathogenicity of two novel human-origin H7N9 highly pathogenic avian influenza viruses in chickens and ducks.

Human infection by low-pathogenic avian influenza viruses of the H7N9 subtype was first reported in March 2013 in China. Subsequently, these viruses caused five outbreaks through September 2017. In the fifth outbreak, H7N9 virus possessing a multiple basic amino acid insertion in the cleavage site of hemagglutinin emerged and caused 4% of all human infections in that period. To date, H7N9 highly pathogenic avian influenza viruses (HPAIVs) have been isolated from poultry, mostly chickens, as well as the environment. To evaluate the relative infectivity of these viruses in poultry, chickens and ducks were subjected to experimental infection with two H7N9 HPAIVs isolated from humans, namely A/Guangdong/17SF003/2016 and A/Taiwan/1/2017. When chickens were inoculated with the HPAIVs at a dose of 106 50% egg infectious dose (EID50), all chickens died within 2-5 days after inoculation, and the viruses replicated in most of the internal organs examined. The 50% lethal doses of A/Guangdong/17SF003/2016 and A/Taiwan/1/2017 in chickens were calculated as 103.3 and 104.7 EID50, respectively. Conversely, none of the ducks inoculated with either virus displayed any clinical signs, and less-efficient virus replication and less shedding were observed in ducks compared to chickens. These findings indicate that chickens, but not ducks, are highly permissive hosts for emerging H7N9 HPAIVs.