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1.
Emerg Microbes Infect ; 8(1): 1465-1478, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31608791

RESUMO

The ANP32A is responsible for mammalian-restricted influenza virus polymerase activity. However, the mechanism of ANP32A modulation of polymerase activity remains poorly understood. Here, we report that chicken ANP32A (chANP32A) -X1 and -X2 stimulated mammalian-restricted PB2 627E polymerase activity in a dose-dependent manner. Distinct effects of ANP32A constructs suggested that the 180VK181 residues within chANP32A-X1 are necessary but not sufficient to stimulate PB2 627E polymerase activity. The PB2 N567D, T598V, A613V or F636L mutations promoted PB2 627E polymerase activity and chANP32A-X1 showed additive effects, providing further support that species-specific regulation of ANP32A might be only relevant with the PB2 E627K mutation. Rescue of cycloheximide-mediated inhibition showed that ANP32A is species-specific for modulation of vRNA but not mRNA and cRNA, demonstrating chANP32A-X1 compensated for defective cRNPs produced by PB2 627E virus in mammalian cells. The promoter mutations of cRNA enhanced the restriction of PB2 627E polymerase in mammalian cells, which could be restored by chANP32A-X1, indicating that ANP32A is likely to regulate the interaction of viral polymerase with RNA promoter. Coimmunoprecipitation showed that ANP32A did not affect the primary cRNPs assembly. We propose a model that chANP32A-X1 regulates PB2 627E polymerase for suitable interaction with cRNA promoter for vRNA replication.


Assuntos
Vírus da Influenza A Subtipo H1N1/enzimologia , Subtipo H7N9 do Vírus da Influenza A/enzimologia , Vírus da Influenza A Subtipo H9N2/enzimologia , Influenza Aviária/metabolismo , Influenza Humana/metabolismo , Doenças das Aves Domésticas/metabolismo , RNA Replicase/metabolismo , Proteínas de Ligação a RNA/metabolismo , Proteínas Virais/metabolismo , Sequência de Aminoácidos , Animais , Galinhas , Humanos , Vírus da Influenza A Subtipo H1N1/genética , Vírus da Influenza A Subtipo H1N1/fisiologia , Subtipo H7N9 do Vírus da Influenza A/genética , Subtipo H7N9 do Vírus da Influenza A/fisiologia , Vírus da Influenza A Subtipo H9N2/genética , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/genética , Influenza Aviária/virologia , Influenza Humana/genética , Influenza Humana/virologia , Mutação , Doenças das Aves Domésticas/genética , Doenças das Aves Domésticas/virologia , Ligação Proteica , RNA Replicase/genética , RNA Viral/genética , RNA Viral/metabolismo , Proteínas de Ligação a RNA/química , Proteínas de Ligação a RNA/genética , Alinhamento de Sequência , Especificidade da Espécie , Proteínas Virais/genética , Replicação Viral
2.
PLoS Pathog ; 15(7): e1007919, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31265471

RESUMO

Avian influenza virus H9N2 has been endemic in birds in the Middle East, in particular in Egypt with multiple cases of human infections since 1998. Despite concerns about the pandemic threat posed by H9N2, little is known about the biological properties of H9N2 in this epicentre of infection. Here, we investigated the evolutionary dynamics of H9N2 in the Middle East and identified phylogeny-associated PB2 mutations that acted cooperatively to increase H9N2 replication/transcription in human cells. The accumulation of PB2 mutations also correlated with an increase in H9N2 virus growth in the upper and lower airways of mice and in virulence. These mutations clustered on a solvent-exposed region in the PB2-627 domain in proximity to potential interfaces with host factors. These PB2 mutations have been found at high prevalence during evolution of H9N2 in the field, indicating that they have provided a selective advantage for viral adaptation to infect poultry. Therefore, continuous prevalence of H9N2 virus in the Middle East has generated a far more fit or optimized replication phenotype, leading to an expanded viral host range, including to mammals, which may pose public health risks beyond the current outbreaks.


Assuntos
Vírus da Influenza A Subtipo H9N2/genética , Vírus da Influenza A Subtipo H9N2/patogenicidade , Influenza Humana/virologia , Mutação , RNA Replicase/genética , Proteínas Virais/genética , Animais , Evolução Molecular , Feminino , Células HEK293 , Especificidade de Hospedeiro/genética , Humanos , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Humana/epidemiologia , Mamíferos/virologia , Camundongos , Camundongos Endogâmicos BALB C , Oriente Médio/epidemiologia , Modelos Moleculares , Infecções por Orthomyxoviridae/virologia , Filogenia , RNA Replicase/química , RNA Replicase/metabolismo , Vírus Reordenados/genética , Vírus Reordenados/patogenicidade , Vírus Reordenados/fisiologia , Proteínas Virais/química , Proteínas Virais/metabolismo , Virulência/genética , Replicação Viral/genética , Zoonoses/virologia
3.
Vet Microbiol ; 233: 1-4, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31176393

RESUMO

Domestic ducks are considered as the interface between wild aquatic birds and terrestrial poultry and play an important role in the transmission and evolution of avian influenza viruses (AIVs). However, the infectivity of H9N2 AIVs in different domestic duck species has not been systematically evaluated. Here we investigated the infectivity of various genotypes of chicken H9N2 AIVs in Pekin duck (Anas Platyrhynchos), Mallard duck (Anas Platyrhynchos) and Muscovy duck (Cairina Moschata) through intranasal inoculation. We found that Pekin ducks and Mallard ducks were generally resistant to chicken H9N2 virus infection, while Muscovy ducks were relatively susceptible to H9N2 AIVs. All the tested viruses were isolated from oropharynx, trachea and lung tissues of Muscovy ducks. Additionally, genotype 57 (G57) H9N2 AIVs, which was predominant in chickens since 2010, showed increased virus replication in this duck species, indicating an improved interspecies transmission ability of recent H9N2 viruses from chickens to ducks. Our results demonstrated the role of Muscovy ducks in the ecology of H9N2 AIVs. More attentions should be paid to this host during viral surveillances. Additionally, inactivated H9N2 vaccine may be unnecessarily used in Pekin and Mallard ducks.


Assuntos
Patos/virologia , Influenza Aviária/transmissão , Doenças das Aves Domésticas/virologia , Replicação Viral , Animais , Galinhas/virologia , Suscetibilidade a Doenças , Vírus da Influenza A Subtipo H9N2/genética , Vírus da Influenza A Subtipo H9N2/fisiologia , Pulmão/virologia , Orofaringe/virologia , Traqueia/virologia
4.
Br Poult Sci ; 60(5): 493-498, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31116018

RESUMO

1. Infectious bursal disease virus (IBDV) causes immunosuppression in chickens, increasing their susceptibility to other infectious diseases and resulting in vaccination failure. Here, we investigated the immune-depressing effect of IBDV on H9N2 avian influenza viral infection in the broiler chickens. 2. For this purpose, chickens were divided into four groups. In group A, chickens were inoculated with IBDV at 21 days of age and H9N2 avian influenza virus (AIV) 5 days later. Groups B and C only received AIV at 26 days of age and IBDV at 21 days, respectively. The control group (D) were inoculated with normal saline at the same times. Tissue samples from different organs were collected on the days 1, 3, 6, 9, and 12 after H9N2 infection. 3. Macroscopic observation showed IBD lesions in groups A and C, including swollen bursa with the presence of gelatinous exudates, haemorrhages in the thigh muscle, edema, and nephritis. 4. Reverse Transcription-PCR was used to study H9N2 AIV dissemination, and qRT-PCR to determine viral genome copy number in different organs. A considerable titre of AIV was found in the trachea, lungs, cecal tonsils, spleens, and feces of infected chickens. The genome copy number of the virus in the trachea and lungs of group A was significantly higher than that in group B on the first day after inoculation. But in the other days post inoculation, RT-PCR did not detect the AIV genome in group A. Although there might have been some immunosuppression in group A, IBDV could interfere with AIV replication in the chickens of this group. 5. In conclusion, we propose that pre-exposure to IBDV at 3 weeks of age reduces the replication and shedding of H9N2 in broiler chicken.


Assuntos
Infecções por Birnaviridae/veterinária , Galinhas , Vírus da Doença Infecciosa da Bursa/fisiologia , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/virologia , Doenças das Aves Domésticas , Eliminação de Partículas Virais/fisiologia , Animais , Infecções por Birnaviridae/virologia , Coinfecção/veterinária , Coinfecção/virologia , Distribuição Aleatória
5.
Virus Genes ; 55(4): 440-447, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31025287

RESUMO

The untranslated regions within viral segments are the essential promoter elements required for the initiation of viral replication and transcription. The end of the UTR sequence and part of the ORF sequence constitute the packaging signal for progeny viruses. To explore the influence of single-point and multi-site joint mutations in the UTR of the NA gene on the viral expression, we select clones with upregulated expression of the reporter gene and analyze their sequence characteristics. Bioinformatics methods were used to analyze polymorphisms in the untranslated region (UTR) of the neuraminidase gene of the H9N2 influenza A virus. Using the RNA polymerase I reporting system with enhanced green fluorescence protein (EGFP) gene as the reporter gene, libraries containing random mutations at sites within the N2 UTR were constructed using random mutagenesis. The mutants were selected from the randomized mutagenesis libraries for the N2-UTR. The N2-UTR-RNA polymerase I fluorescence reporter system was identified by sequencing and transfected into infected MDCK cells. The expression of the reporter EGFP was observed using fluorescence microscopy, and the relative fluorescence intensity was measured using a multifunctional microplate reader to analyze the expression of the reporter gene (EGFP) qualitatively and quantitatively. Herein, an RNA polymerase reporter system was constructed to rescue the mutated viruses and measure their tissue culture infective dose (TCID50). The results showed that the U13 → C13 mutation in the 3'end of the NA gene promoted the expression of viral RNA and protein, and mutation of other sites within the UTR could differentially regulate viral genomic transcription and translation. These data showed that the U13 → C13 mutation within the variable region of the 3'UTR of the NA gene in the H9N2 influenza virus promotes viral genomic expression and infection.


Assuntos
Vírus da Influenza A Subtipo H9N2/genética , Neuraminidase/genética , Proteínas Virais/genética , Replicação Viral/genética , Regiões 3' não Traduzidas , Animais , Cães , Regulação Viral da Expressão Gênica , Genes Reporter , Proteínas de Fluorescência Verde/genética , Vírus da Influenza A Subtipo H9N2/fisiologia , Células Madin Darby de Rim Canino , Mutagênese , RNA Viral
6.
Virol J ; 16(1): 46, 2019 04 11.
Artigo em Inglês | MEDLINE | ID: mdl-30975159

RESUMO

BACKGROUND: Compared with chickens, ducks are normally resistant to avian influenza virus without clinical signs while they habor almost all subtypes of influenza A viruses. To date, however the mechanism for duck anti-influenza has not been completely understood. The H9N2 avian influenza virus (AIV) is the most prevalent subtype of influenza A virus that infects chickens and ducks in China. However, H9N2 AIV replication and the host immune response in these domestic birds has not been systematically investigated. METHODS: In the present study, we compared the kinetics and magnitudes of antibody responses in chickens and ducks after infection with H9N2 AIV by the intranasal route or intravenous route. Furthermore, we determined the viral replication and distribution in chickens and ducks after infection with H9N2 AIV by the intravenous route. RESULTS: Our results revealed that the antibody response was rapid and robust in ducks than in chickens at early time (2-3dpi) after intravenous infection with H9N2 AIVs, while delayed and lower antibody detected in ducks than in chickens after intranasal infection with H9N2 AIVs. The virus was detected in multiple organs tissues in chickens but not in ducks infected by the intravenous route. CONCLUSIONS: Our results provide the evidence that humoral immune response could play a critical role in duck resistance for influenza, which expands our knowledge on duck anti-influenza characteristics.


Assuntos
Anticorpos Antivirais/sangue , Galinhas/imunologia , Patos/imunologia , Imunidade Humoral , Influenza Aviária/imunologia , Administração Intravenosa , Animais , Galinhas/virologia , Resistência à Doença , Patos/virologia , Vírus da Influenza A Subtipo H9N2/fisiologia , Carga Viral , Replicação Viral
7.
Poult Sci ; 98(9): 3488-3495, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-30941436

RESUMO

H9N2 avian influenza has been prevalent in chicken flocks of China for years. In the first half year of 2018, clinical cases of suspected H9N2 infection were collected from chicken flocks in Shandong province. Nine strains of H9N2 influenza virus were isolated. The pathological changes of the dead chickens were mainly respiratory inflammation, renal swelling, and secondary infection. The microscopic lesions were consistent with the pathogenic characteristics of H9N2 influenza virus. From November 2017 to June 2018, a total of 3,380 serum samples were randomly collected from commercial laying hens in Shandong Province. The H9 antibody levels were tested with the isolated strain (CK/SD/231/17) as the antigen. It showed that the average of antibody titers of H9 avian influenza was 9.24 1og2. Hemagglutination inhibition experiments were conducted on chicken serum with the vaccine virus and the isolated virus (CK/SD/231/17) as the antigens. It was found that the antibody titer measured with the vaccine virus was 1 or 2 titers higher than the isolated strain. It indicated that the antigenicity of H9N2 circulating strain was different from that of vaccine strain. The nucleotide sequences of HA gene of these recent H9N2 avian influenza virus isolates shared homologies from 93.8 to 99.9%. Phylogenetic analysis revealed that the eight gene segments of the viruses were in the same clades with G57 gene reference strain. The amino acid site analysis of influenza resistance showed that the virus was sensitive to neuraminidase inhibitors and resistant to amantadine. Highlights: The protection rate of the H9N2 AIV vaccine almost reached 100% before 2016, but the antibody level of serum samples showed high diversity in this study, which means the poultry were infected. The antigenicity of isolated H9N2 strains was different from that of vaccine strain. Current available vaccines may provide only limited protection.


Assuntos
Galinhas , Genótipo , Vírus da Influenza A Subtipo H9N2/fisiologia , Vacinas contra Influenza/imunologia , Influenza Aviária/imunologia , Doenças das Aves Domésticas/imunologia , Animais , China , Evolução Molecular , Feminino , Imunogenicidade da Vacina/imunologia , Vírus da Influenza A Subtipo H9N2/genética , Influenza Aviária/patologia , Doenças das Aves Domésticas/patologia
8.
Virology ; 529: 135-143, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30703577

RESUMO

H9N2 avian influenza viruses (AIVs) have become panzootic and caused sporadic human cases since 1998. Based on the poultry-related environmental surveillance data in mainland China from 2013 to 2016, a total of 68 representative environment isolates were selected and further investigated systematically. Phylogenetic analysis indicated that Y280-like H9N2 viruses have been predominant during 2013-2016 and acquired multiple specific amino acid substitutions that might favor viral transmission from avian to mammalians. Additionally, the viruses have undergone dramatic evolution and reassortment, resulting in an increased genetic diversity or acting as the gene contributors to new avian viruses. Receptor-binding tests indicated that most of the H9N2 isolates bound to human-type receptor, making them easily cross the species barrier and infect human efficiently. Our results suggested that the H9N2 AIVs prevalent in poultry may pose severe public health threat.


Assuntos
Vírus da Influenza A Subtipo H9N2/genética , Influenza Aviária/virologia , Aves Domésticas/virologia , Animais , China , Microbiologia Ambiental , Genoma Viral , Genótipo , Abrigo para Animais , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/epidemiologia , Vigilância da População , RNA Viral/genética
9.
Virol J ; 16(1): 24, 2019 02 21.
Artigo em Inglês | MEDLINE | ID: mdl-30791956

RESUMO

BACKGROUND: As a low pathogenic influenza virus, avian influenza virus subtype H9N2 (H9N2 AIV) often induces high morbidity in association with secondary bacterial infections in chickens or mammals. To explore this phenomenon, the relationship between intestinal microflora changes and bacterial translocations was studied post H9N2 AIV challenge and post AIV infection plus Ageratum-liquid treatment. METHODS: Illumina sequencing, histological examination and Neongreen-tagged bacteria were used in this study to research the microbiota composition, intestinal barrier, and bacterial translocation in six weeks of BALB/c mice. RESULTS: H9N2 AIV infection caused intestinal dysbacteriosis and mucosal barrier damages. Notably, the villus length was significantly reduced (p < 0.01) at 12 dpi and the crypt depth was significantly increased (p < 0.01) at 5 dpi and 12 dpi with infection, resulting in the mucosal regular villus-length/crypt-depth (V/C) was significantly reduced (p < 0.01) at 5 dpi and 12 dpi. Moreover, degeneration and dissolution of the mucosal epithelial cells, loose of the connective tissue and partial glandular atrophy were found in infection group, indicating that intestinal barrier function was weakened. Eventually, intestinal microbiota (Staphylococcus, E. coli, etc.) overrun the intestinal barrier and migrated to liver and lung tissues of the mice at 5 and 12 dpi. Furthermore, the bacteria transferred in mesentery tissue sites from intestine at 36 h through tracking the Neongreen-tagged bacteria. Then the Neongreen-tagged bacteria were isolated from liver at 48 h post intragastrical administration. Simultaneously, Ageratum-liquid could inhibit the intestinal microbiota disorder post H9N2 AIV challenge via the respiratory tract. In addition, this study also illustrated that Ageratum-liquid could effectively prevent intestinal bacterial translocation post H9N2 AIV infection in mice. CONCLUSION: In this study, we report the discovery that H9N2 AIV infection could damage the ileal mucosal barrier and induce the disturbance of the intestinal flora in BALB/c mice resulting in translocation of intestinal bacteria. In addition, this study indicated that Ageratum-liquid can effectively prevent bacterial translocation following H9N2 infection. These findings are of important theoretical and practical significance in prevention and control of H9N2 AIV infection.


Assuntos
Ageratum/química , Infecções Bacterianas/tratamento farmacológico , Translocação Bacteriana/efeitos dos fármacos , Medicamentos de Ervas Chinesas/farmacologia , Mucosa Intestinal/virologia , Infecções por Orthomyxoviridae/tratamento farmacológico , Animais , Coinfecção/tratamento farmacológico , Microbioma Gastrointestinal , Genoma Bacteriano , Vírus da Influenza A Subtipo H9N2/patogenicidade , Vírus da Influenza A Subtipo H9N2/fisiologia , Mucosa Intestinal/microbiologia , Mucosa Intestinal/patologia , Camundongos , Camundongos Endogâmicos BALB C
10.
Viruses ; 11(1)2019 01 09.
Artigo em Inglês | MEDLINE | ID: mdl-30634394

RESUMO

The polymerase acidic (PA) protein is the third subunit of the influenza A virus polymerase. In recent years, studies have shown that PA plays an important role in overcoming the host species barrier and host adaptation of the avian influenza virus (AIV). The objective of this study was to elucidate the role of the PA subunit on the replication and airborne transmission of the H9N2 subtype AIV. By reverse genetics, a reassortant rSD01-PA was derived from the H9N2 subtype AIV A/Chicken/Shandong/01/2008 (SD01) by introducing the PA gene from the pandemic influenza A H1N1 virus A/swine/Shandong/07/2011 (SD07). Specific pathogen-free (SPF) chickens and guinea pigs were selected as the animal models for replication and aerosol transmission studies. Results show that rSD01-PA lost the ability of airborne transmission among SPF chickens because of the single substitution of the PA gene. However, rSD01-PA could infect guinea pigs through direct contact, while the parental strain SD01 could not, even though the infection of rSD01-PA could not be achieved through aerosol. In summary, our results indicate that the protein encoded by the PA gene plays a key role in replication and airborne transmission of the H9N2 subtype AIV.


Assuntos
Vírus da Influenza A Subtipo H1N1/genética , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/transmissão , Doenças das Aves Domésticas/transmissão , RNA Replicase/genética , Proteínas Virais/genética , Replicação Viral , Substituição de Aminoácidos , Animais , Galinhas/virologia , Replicação do DNA , Modelos Animais de Doenças , Feminino , Cobaias , Vírus da Influenza A Subtipo H9N2/enzimologia , Vírus da Influenza A Subtipo H9N2/genética , Influenza Aviária/virologia , Pulmão/virologia , Doenças das Aves Domésticas/virologia , RNA Replicase/metabolismo , Vírus Reordenados/genética , Genética Reversa , Organismos Livres de Patógenos Específicos , Proteínas Virais/metabolismo
11.
Virology ; 526: 1-12, 2019 01 02.
Artigo em Inglês | MEDLINE | ID: mdl-30316042

RESUMO

The non-structural protein 1 (NS1) of different influenza A virus (IAV) strains can differentially regulate the activity of c-Jun terminal kinase (JNK) and PI-3 kinase (PI3K). Whether varying JNK and PI3K activation impacts autophagy and IAV replication differently remains uncertain. Here we report that H5N1 (A/mallard/Huadong/S/2005) influenza A virus induced functional autophagy, as evidenced by increased LC3 lipidation and decreased p62 levels, and the presence of autolysosomes in chicken fibroblast cells. H9N2 (A/chicken/Shanghai/F/98) virus weakly induced autophagy, whereas H1N1 virus (A/PR/8/34, PR8) blocked autophagic flux. H5N1 virus activated JNK but inhibited the PI-3 kinase pathway. In contrast, N9N2 virus infection led to modest JNK activation and strong PI-3 kinase activation; whereas H1N1 virus activated the PI-3 kinase pathway but did not activate JNK. SP600125, a JNK inhibitor, inhibited H5N1 virus-induced autophagy and virus replication in a DF-1 chicken fibroblast cell line. Our study uncovered a previously unrecognized role of JNK in IAV replication and autophagy.


Assuntos
Autofagia , Vírus da Influenza A/fisiologia , Influenza Aviária/enzimologia , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Replicação Viral , Animais , Antracenos/farmacologia , Autofagia/efeitos dos fármacos , Células Cultivadas , Galinhas , Ativação Enzimática/efeitos dos fármacos , Interações Hospedeiro-Patógeno , Vírus da Influenza A Subtipo H1N1/fisiologia , Virus da Influenza A Subtipo H5N1/fisiologia , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/fisiopatologia , Influenza Aviária/virologia , Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores , Fosfatidilinositol 3-Quinases/metabolismo , Inibidores de Proteínas Quinases/farmacologia , Transdução de Sinais , Especificidade da Espécie , Proteínas não Estruturais Virais/metabolismo , Replicação Viral/efeitos dos fármacos
12.
Emerg Microbes Infect ; 7(1): 166, 2018 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-30301950

RESUMO

Outbreaks of avian influenza virus continue to pose threats to human health. Animal models such as the mouse, ferret, and macaque are used to understand the pathogenesis of avian influenza virus infection in humans. We previously reported that the tree shrew (Tupaia belangeri, family Tupaiidae), which is regarded as a "low-level primate", has α2,3- and α2,6-linked sialic acid receptor distributions similar to those of humans and is potentially a useful mammalian model for studying mild human influenza (H1N1) virus infection. In this study, we used the tree shrew experimental model to investigate the pathogenesis of avian influenza A (H9N2) virus infection and the effect of the E627K mutation in the PB2 gene, an adaptation to mammalian hosts. Evidence of disease, virus titers in the upper and lower respiratory tract, histopathology and induction of proinflammatory cytokines are described. We also established ex vivo culture models of tree shrew respiratory tissues to study the tropism and replication of the H9N2 virus. Our results demonstrated that the tree shrew is a viable new in vivo experimental model for avian influenza research that provides results comparable to those observed in ferrets. The disease spectrum and pathogenesis in tree shrews correlate well with what is observed in humans.


Assuntos
Modelos Animais de Doenças , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Humana/virologia , Tupaiidae , Animais , Citocinas/genética , Citocinas/imunologia , Feminino , Furões , Humanos , Vírus da Influenza A Subtipo H9N2/genética , Influenza Humana/genética , Influenza Humana/imunologia , Influenza Humana/patologia , Masculino , Tupaiidae/virologia , Tropismo Viral , Replicação Viral
13.
Poult Sci ; 97(11): 3793-3800, 2018 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-30169762

RESUMO

Circulating H7N9 influenza viruses in live poultry markets continue to pose a threat to human health. Free-range poultry, one of the sources for these markets, are common in China as well as in many developing countries. Because the H9N2 virus could be a source of internal genes for the H7N9 virus, we conducted surveillance in free-range poultry and live poultry markets to study the evolution of H7N9 and H9N2 viruses in Eastern China. We found 28 samples positive for the H9N2 virus (a rate of 3.2%), but no positive samples for the H7N9 virus. Six representative H9N2 isolates were sequenced and analyzed, and the results showed that these viruses shared high nucleotide identities (99.0 to 100%) and were in a same branch in the phylogenetic trees. All these 6 viruses are closely clustered with Zhejiang H9N2 chicken isolates, and belonged to genotype G57, along with some novel H7N9 strains and H9N2 strains circulating in humans in China. We hope that surveillance of AIVs in free-range poultry will be strengthened for further identification more genetic diversity.


Assuntos
Subtipo H7N9 do Vírus da Influenza A/fisiologia , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/epidemiologia , Doenças das Aves Domésticas/epidemiologia , Animais , Galinhas , China/epidemiologia , Columbidae , Patos , Gansos , Subtipo H7N9 do Vírus da Influenza A/genética , Vírus da Influenza A Subtipo H9N2/genética , Influenza Aviária/virologia , Filogenia , Doenças das Aves Domésticas/virologia , Análise de Sequência de RNA , Proteínas Virais/análise
14.
Vet Microbiol ; 223: 100-106, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30173734

RESUMO

Airborne transmission plays an important role in dissemination of H9N2 subtype avian influenza virus. Annexin II (A2)-mediated activation of plasminogen (PLG) promotes cleavage of the influenza virus HA protein and viral replication, resulting in enhanced pathogenesis. In this study, airborne transmission competent and defective strains of H9N2 influenza virus, SH7 and SH14, respectively, were used to investigate the effect of A2 on airborne spread. The results showed that A2 protein was increased in SH7 virions compared with SH14 particles, the binding ability of the SH7-infected MDCK cells to PLG was significantly higher than the SH14-infected cells, and influence efficiency of the PLG on replicated ability of SH7 virus was significantly stronger than that of SH14 virus, who spread without airborne route, indicating that the annexin 2 (A2) can bind PLG and contributes to SH7 with high replication ability. Furthermore, the copies of SH7 in the airborne infected chickens under inhibited by 6-AHA were significantly decreased, suggesting that the release of H9N2 avian influenza virus were reduced by inhibiting the conversion of PLG to PL, ultimately resulting in reduced airborne transmission of H9N2 avian influenza virus. In summary, A2-mediated conversion of PLG to PL plays a role in the airborne transmission capacity of H9N2 avian influenza viruses, and this interaction may represent potential targets for prevention and treatment of influenza virus infection.


Assuntos
Anexina A2/metabolismo , Galinhas/virologia , Fibrinolisina/metabolismo , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/transmissão , Doenças das Aves Domésticas/transmissão , Animais , Cães , Influenza Aviária/virologia , Células Madin Darby de Rim Canino , Plasminogênio/metabolismo , Doenças das Aves Domésticas/virologia , Organismos Livres de Patógenos Específicos , Replicação Viral
15.
Vet Microbiol ; 222: 11-17, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30080665

RESUMO

H4 and H9 avian influenza viruses (AIVs) are two of the most prevalent influenza viruses worldwide. The co-existence of H4 and H9 viruses in multiple avian species provides an opportunity for the generation of novel reassortants and for viral evolution. The diversity of the biological characteristics of the reassortants enhances the potential threat to the poultry industry and to public health. To evaluate the reassortment of these viruses and the potential public risk of the reassortants, we co-infected chickens with H4N6 and H9N2 viruses derived from poultry and tested the replication and virulence of the reassortant viruses in mice. A high frequency of reassortment was detected in chickens after co-infection with these two viruses and nine reassortants of six genotypes were purified from the chicken samples. Two H9N2 reassortants containing the PA of the parent H4N6 virus showed higher virulence than the parent H9N2 virus, revealing the significant role of the H4N6 wt virus PA gene in viral reassortment. Analysis of the polymerase activity of the ribonucleoprotein (RNP) complex in vitro suggested that the PA of H4N6 wt origin enhanced polymerase activity. Our results indicate that co-infection of an avian individual with the H4N6 and H9N2 viruses leads to a high frequency of reassortment and generates some reassortants that have higher virulence than the wild-type viruses in mammals. These results highlight the potential public risk of the avian influenza reassortants and the importance of surveillance of the co-existence of the H4N6 and H9N2 viruses in avian species and other animals.


Assuntos
Galinhas/virologia , Coinfecção/veterinária , Vírus da Influenza A Subtipo H9N2/genética , Vírus da Influenza A/genética , Infecções por Orthomyxoviridae/veterinária , Vírus Reordenados/genética , Animais , Coinfecção/virologia , Evolução Molecular , Feminino , Humanos , Vírus da Influenza A Subtipo H9N2/fisiologia , Vírus da Influenza A/fisiologia , Influenza Aviária/epidemiologia , Influenza Aviária/virologia , Influenza Humana/epidemiologia , Influenza Humana/prevenção & controle , Influenza Humana/virologia , Camundongos , Camundongos Endogâmicos BALB C , Mutação , Infecções por Orthomyxoviridae/epidemiologia , Infecções por Orthomyxoviridae/virologia , Filogenia , Saúde Pública , Vírus Reordenados/isolamento & purificação , Vírus Reordenados/patogenicidade , Ribonucleoproteínas/genética , Virulência , Replicação Viral
16.
Vet Res ; 49(1): 83, 2018 Aug 29.
Artigo em Inglês | MEDLINE | ID: mdl-30157967

RESUMO

Since 1997, G1-lineage H9N2 avian influenza viruses have been circulating in Asia and later on in the Middle East, and they have been associated to mild respiratory disease, drops in egg production and moderate mortality in chickens, in particular in the presence of concurrent infections. In this study, we investigated the importance of the G1-lineage H9N2 A/chicken/Israel/1163/2011 virus as a primary pathogen in layers, analyzing its tropism and binding affinity for the oviduct tissues, and investigating the long-term impact on egg production. Besides causing a mild respiratory infection, the virus replicated in the oviduct of 60% of the hens causing different degrees of salpingitis throughout the organ, in particular at the level of the infundibulum, where the detection of the virus was associated with severe heterophilic infiltrate, and necrosis of the epithelium. Binding affinity assays confirmed that the infundibulum was the most receptive region of the oviduct. The drop in egg production was at its peek at 2 weeks post-infection (pi) (60% decrease) and continued up to 80 days pi (35% decrease). On day 80 pi, non-laying birds showed egg yolk peritonitis, and histopathological analyses described profound alteration of the infundibulum architecture, duct ectasia and thinning of the epithelium, while the rest of the oviduct and ovary appeared normal. Our results show that this H9N2 virus is a primary pathogen in layer hens, and that its replication in the infundibulum is responsible for acute and chronic lesions that limits the effective functionality of the oviduct, compromising the commercial life of birds.


Assuntos
Galinhas , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/virologia , Oviductos/virologia , Hipófise/patologia , Doenças das Aves Domésticas/virologia , Reprodução , Animais , Feminino , Influenza Aviária/patologia , Influenza Aviária/fisiopatologia , Óvulo , Hipófise/virologia , Doenças das Aves Domésticas/patologia , Doenças das Aves Domésticas/fisiopatologia , Tropismo
17.
Influenza Other Respir Viruses ; 12(6): 814-817, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-29989679

RESUMO

The H9N2 influenza viruses that have become established in Bangladeshi live poultry markets possess five gene segments of the highly pathogenic H7N3 avian influenza virus. We assessed the replication, transmission, and disease potential of three H9N2 viruses in chickens and New World quail. Each virus replicated to high titers and transmitted by the airborne route to contacts in both species. Infected chickens showed no disease signs, and the viruses differed in their disease potential in New World quail. New World quail were more susceptible than chickens to H9N2 viruses and shed virus after airborne transmission for 10 days. Consequently, New World quail are a potential threat in the maintenance and spread of influenza virus in live poultry markets.


Assuntos
Galinhas , Vírus da Influenza A Subtipo H9N2/isolamento & purificação , Influenza Aviária/virologia , Codorniz , Animais , Bangladesh , Suscetibilidade a Doenças , Transmissão de Doença Infecciosa , Vírus da Influenza A Subtipo H9N2/patogenicidade , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/patologia , Infecções por Orthomyxoviridae , Replicação Viral
18.
Biomed Environ Sci ; 31(4): 306-310, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29773094

RESUMO

To investigate the susceptibility of Chukars to duck avian influenza virus H9N2 and explore their role in interspecies transmission of influenza viruses. Chukars were inoculated with duck avian influenza viruses H9N2. The present study demonstrated that inflammatory lesions and virus antigen were present in the trachea, bronchus, and parabronchus, and the viruses could be isolated from throat swabs and lung tissue homogenate supernatants. At 14 d post virus inoculation, anti-H9 influenza virus antibody in the serum was detected. The results indicated that Chukars are susceptible to duck avian influenza virus and serve as an intermediate host, thereby facilitating viral gene evolution and supporting the need for continued surveillance of epidemiology and evolution of the influenza virus in Chukars.


Assuntos
Galliformes , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/virologia , Replicação Viral/fisiologia , Animais , Vírus da Influenza A Subtipo H9N2/patogenicidade , Sistema Respiratório/patologia , Sistema Respiratório/virologia
19.
Br Poult Sci ; 59(4): 389-395, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29768944

RESUMO

1. The effect of Zataria multiflora essential oil on replication rate of the H9N2 virus in target organs was determined by real-time PCR. One-day-old broiler chicks were randomly divided into six groups and were challenged with H9N2 influenza. Two groups received either 20 or 40 µl/kg body weight/day Zataria multiflora essential oils (ZM) seven days before the challenge while two other groups received the essential oil at the same dosage but after H9N2 challenge. One group received 4 mg/kg body weight/day of the anti-viral compound amantadine after challenge and the last group received no treatment and served as the control. 2. Groups that received the ZM, before or after H9N2 challenge, and the amantadine treated group showed reduced viral replication in the respiratory and gastrointestinal tracts compared to the control. Supplementation with ZM improved weight gain and FCR in broilers in comparison with the control. 3. The results showed that ZM had a positive effect on reducing viral replication in both the intestine and trachea of H9N2 influenza infected broiler chickens, that led to milder clinical symptoms and better performance.


Assuntos
Galinhas , Vírus da Influenza A Subtipo H9N2/efeitos dos fármacos , Lamiaceae/química , Óleos Voláteis/metabolismo , Replicação Viral/efeitos dos fármacos , Amantadina/farmacologia , Ração Animal/análise , Animais , Antivirais/farmacologia , Dieta/veterinária , Suplementos Nutricionais/análise , Relação Dose-Resposta a Droga , Trato Gastrointestinal/virologia , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/tratamento farmacológico , Influenza Aviária/fisiopatologia , Influenza Aviária/virologia , Óleos Voláteis/administração & dosagem , Doenças das Aves Domésticas/tratamento farmacológico , Doenças das Aves Domésticas/fisiopatologia , Doenças das Aves Domésticas/virologia , Distribuição Aleatória , Sistema Respiratório/virologia , Replicação Viral/fisiologia
20.
Viruses ; 10(5)2018 05 18.
Artigo em Inglês | MEDLINE | ID: mdl-29783653

RESUMO

Avian influenza virus subtype H9N2 (H9N2 AIV) has caused significant losses to the poultry industry due to the high mortality associated with secondary infections attributable to E. coli. This study tries to address the underlying secondary mechanisms after H9N2 AIV infection. Initially, nine day-old specific pathogen-free chickens were assigned to control (uninfected) and H9N2-infected groups, respectively. Using Illumina sequencing, histological examination, and quantitative real-time PCR, it was found that H9N2 AIV caused intestinal microbiota disorder, injury, and inflammatory damage to the intestinal mucosa. Notably, the genera Escherichia, especially E. coli, significantly increased (p < 0.01) at five days post-infection (dpi), while Lactobacillus, Enterococcus, and other probiotic organisms were significantly reduced (p < 0.01). Simultaneously, the mRNA expression of tight junction proteins (ZO-1, claudin 3, and occludin), TFF2, and Muc2 were significantly reduced (p < 0.01), indicating the destruction of the intestinal epithelial cell tight junctions and the damage of mucin layer construction. Moreover, the mRNA expression of proinflammatory cytokines IFN-γ, IL-22, IFN-α, and IL-17A in intestinal epithelial cells were significantly upregulated, resulting in the inflammatory response and intestinal injury. Our findings may provide a theoretical basis for observed gastroenteritis-like symptoms such as diarrhea and secondary E. coli infection following H9N2 AIV infection.


Assuntos
Galinhas/virologia , Microbioma Gastrointestinal , Vírus da Influenza A Subtipo H9N2/fisiologia , Influenza Aviária/microbiologia , Mucosa Intestinal/lesões , Animais , Citocinas/genética , Citocinas/metabolismo , DNA Bacteriano/genética , Enterite/metabolismo , Escherichia coli/metabolismo , Influenza Aviária/imunologia , Influenza Aviária/metabolismo , Metagenômica , RNA Mensageiro/metabolismo , RNA Ribossômico 16S/genética , Organismos Livres de Patógenos Específicos
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