scholarly journals Co-infection of chickens with H9N2 and H7N9 avian influenza viruses leads to emergence of reassortant H9N9 virus with increased fitness for poultry and enhanced zoonotic potential

2021 ◽  
Author(s):  
Sushant Bhat ◽  
Joe James ◽  
Jean-Remy Sadeyen ◽  
Sahar Mahmood ◽  
Holly J Everest ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Influenza A ◽  
Genetic Material ◽  
Influenza Viruses ◽  
Experimental Simulation ◽  
List Type ◽  
Zoonotic Potential ◽  
Avian Influenza Viruses ◽  
Replication Fitness ◽  
Reassortant Viruses

SUMMARYAn H7N9 low pathogenicity avian influenza virus (LPAIV) emerged through genetic reassortment between H9N2 and other LPAIVs circulating in birds in China. This virus causes inapparent clinical disease in chickens, but zoonotic transmission results in severe and fatal disease in humans. We evaluated the consequences of reassortment between the H7N9 and the contemporary H9N2 viruses of G1 lineage that are enzootic in poultry across the Indian sub-continent and the Middle East. Co-infection of chickens with these viruses resulted in emergence of novel reassortant H9N9 viruses carrying genes derived from both H9N2 and H7N9 viruses. These reassortant H9N9 viruses showed significantly increased replication fitness, enhanced pathogenicity in chicken embryos and the potential to transmit via contact among ferrets. Our study highlights that the co-circulation of H7N9 and H9N2 viruses could represent a threat for the generation of novel reassortant viruses with greater virulence in poultry and an increased zoonotic potential. Graphical AbstractIn BriefH9N2 viruses have a high propensity to reassort with other avian influenza viruses. We found that co-infection of chickens with H9N2 and H7N9 led to the emergence of reassortant viruses including the H9N9 subtype. Some reassortant H9N9 viruses exhibited increased replication fitness, increased pathogenicity in the chicken embryo, greater avidity for human and avian cell receptors, lower pH fusion and contact-transmission to ferrets. This study demonstrated the ability of viruses that already exist in nature to exchange genetic material, highlighting the potential emergence of viruses from these subtypes with increased zoonotic potential. There are nine H9 influenza A subtypes carrying different neuraminidase (NA) genes, including H9N9 viruses, while they are not common they do exist in nature as wildtypes (CDC).HighlightsCo-infection of chickens with H7N9 and H9N2 led to emergence of reassortant H9N9 virusesReassortant H9N9 viruses had an increased replication rate in avian and human cellsReassortant H9N9 viruses had a lower pH fusion and significantly higher receptor binding to α 2,3 sialoglycansReassortant H9N9 replicated in ferrets at similar levels compared to H7N9 and transmitted via direct contactFerrets exposed to reassortant H9N9 by aerosol contact were also found to be seropositiveExperimental simulation of events that may occur naturally with circulating viruses has demonstrated the risk of emergence of viruses with increased zoonotic potential.

scholarly journals Genetic Analysis of Avian Influenza Viruses: Cocirculation of Avian Influenza Viruses with Allele A and B Nonstructural Gene in Northern Pintail (Anas acuta) Ducks Wintering in Japan

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Alam Jahangir ◽  
Sakchai Ruenphet ◽  
Nadia Sultana ◽  
Dany Shoham ◽  
Kazuaki Takehara
Keyword(s):  
Avian Influenza ◽  
Asian American ◽  
Influenza A ◽  
Genetic Material ◽  
Influenza Viruses ◽  
Influenza A Viruses ◽  
Avian Influenza Viruses ◽  
Anas Acuta ◽  
Northern Pintail ◽  
Ns Gene

The pandemic influenza virus strains of 1918 (H1N1), 1957 (H2N2), 1968 (H3N2), and 2009 (H1N1) have genes related to avian influenza viruses (AIVs). The nonstructural (NS) gene of AIVs plays a significant role in host-viral interaction. However, little is known about the degree of diversity of this gene in Northern pintail (Anas acuta) ducks wintering in Japan. This study describes characteristics of pintail-originated H1N1, H1N2, H1N3, H5N2, H5N3, H5N9, and H7N7 viruses. Most of the viruses were revealed to be avian strains and not related to pandemic and seasonal flu strains. Nevertheless, the NP genes of 62.5% (5/8) viruses were found closely related to a A/swine/Korea/C12/08, indicating exchange of genetic material and ongoing mammalian-linked evolution of AIVs. Besides, all the viruses, except Aomori/422/07 H1N1, contain PSIQSR*GLF motif usually found in avian, porcine, and human H1 strains. The Aomori/422/07 H1N1 has a PSVQSR*GLF motif identical to a North American strain. This findings linked to an important intercontinental, Asian-American biogeographical interface. Phylogenetically all the viruses were clustered in Eurasian lineage. Cocirculation of allele A and B (NS gene) viruses was evident in the study implying the existence of a wide reservoir of influenza A viruses in pintail wintering in Japan.

scholarly journals Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

2020 ◽  
Vol 117 (34) ◽  
pp. 20814-20825 ◽  
Author(s):  
Samantha J. Lycett ◽  
Anne Pohlmann ◽  
Christoph Staubach ◽  
Valentina Caliendo ◽  
Mark Woolhouse ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Severe Disease ◽  
Wild Birds ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
Highly Pathogenic ◽  
Time Resolved ◽  
Bird Populations ◽  
Pathogenic Avian Influenza ◽  
Reassortant Viruses

Highly pathogenic avian influenza (HPAI) viruses of the H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasionally in humans. In recent years, H5 HPAI viruses of this lineage infecting poultry in Asia have spilled over into wild birds and spread via bird migration to countries in Europe, Africa, and North America. In 2016/2017, this spillover resulted in the largest HPAI epidemic on record in Europe and was associated with an unusually high frequency of reassortments between H5 HPAI viruses and cocirculating low-pathogenic avian influenza viruses. Here, we show that the seven main H5 reassortant viruses had various combinations of gene segments 1, 2, 3, 5, and 6. Using detailed time-resolved phylogenetic analysis, most of these gene segments likely originated from wild birds and at dates and locations that corresponded to their hosts’ migratory cycles. However, some gene segments in two reassortant viruses likely originated from domestic anseriforms, either in spring 2016 in east China or in autumn 2016 in central Europe. Our results demonstrate that, in addition to domestic anseriforms in Asia, both migratory wild birds and domestic anseriforms in Europe are relevant sources of gene segments for recent reassortant H5 HPAI viruses. The ease with which these H5 HPAI viruses reassort, in combination with repeated spillovers of H5 HPAI viruses into wild birds, increases the risk of emergence of a reassortant virus that persists in wild bird populations yet remains highly pathogenic for poultry.

scholarly journals The Polymerase Acidic Protein Gene of Influenza A Virus Contributes to Pathogenicity in a Mouse Model

2009 ◽  
Vol 83 (23) ◽  
pp. 12325-12335 ◽  
Author(s):  
Min-Suk Song ◽  
Philippe Noriel Q. Pascua ◽  
Jun Han Lee ◽  
Yun Hee Baek ◽  
Ok-Jun Lee ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Mammalian Cells ◽  
Influenza A ◽  
Lethal Dose ◽  
Influenza Viruses ◽  
Mammalian Host ◽  
Viral Gene ◽  
Avian Influenza Viruses ◽  
Range Restriction ◽  
Viral Genes

ABSTRACT Adaptation of influenza A viruses to a new host species usually involves the mutation of one or more of the eight viral gene segments, and the molecular basis for host range restriction is still poorly understood. To investigate the molecular changes that occur during adaptation of a low-pathogenic avian influenza virus subtype commonly isolated from migratory birds to a mammalian host, we serially passaged the avirulent wild-bird H5N2 strain A/Aquatic bird/Korea/W81/05 (W81) in the lungs of mice. The resulting mouse-adapted strain (ma81) was highly virulent (50% mouse lethal dose = 2.6 log10 50% tissue culture infective dose) and highly lethal. Nonconserved mutations were observed in six viral genes (those for PB2, PB1, PA, HA, NA, and M). Reverse genetic experiments substituting viral genes and mutations demonstrated that the PA gene was a determinant of the enhanced virulence in mice and that a Thr-to-Iso substitution at position 97 of PA played a key role. In growth kinetics studies, ma81 showed enhanced replication in mammalian but not avian cell lines; the PA97I mutation in strain W81 increased its replicative fitness in mice but not in chickens. The high virulence associated with the PA97I mutation in mice corresponded to considerably enhanced polymerase activity in mammalian cells. Furthermore, this characteristic mutation is not conserved among avian influenza viruses but is prevalent among mouse-adapted strains, indicating a host-dependent mutation. To our knowledge, this is the first study that the isoleucine residue at position 97 in PA plays a key role in enhanced virulence in mice and is implicated in the adaptation of avian influenza viruses to mammalian hosts.

scholarly journals Pathogenesis and Transmission Assessments of Two H7N8 Influenza A Viruses Recently Isolated from Turkey Farms in Indiana Using Mouse and Ferret Models

2016 ◽  
Vol 90 (23) ◽  
pp. 10936-10944 ◽  
Author(s):  
Xiangjie Sun ◽  
Jessica A. Belser ◽  
Joanna A. Pulit-Penaloza ◽  
Hui Zeng ◽  
Amanda Lewis ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Influenza A ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
Highly Pathogenic ◽  
Pathogenic Avian Influenza ◽  
Domestic Poultry ◽  
Commercial Turkey

ABSTRACTAvian influenza A H7 viruses have caused multiple outbreaks in domestic poultry throughout North America, resulting in occasional infections of humans in close contact with affected birds. In early 2016, the presence of H7N8 highly pathogenic avian influenza (HPAI) viruses and closely related H7N8 low-pathogenic avian influenza (LPAI) viruses was confirmed in commercial turkey farms in Indiana. These H7N8 viruses represent the first isolation of this subtype in domestic poultry in North America, and their virulence in mammalian hosts and the potential risk for human infection are largely unknown. In this study, we assessed the ability of H7N8 HPAI and LPAI viruses to replicatein vitroin human airway cells andin vivoin mouse and ferret models. Both H7N8 viruses replicated efficientlyin vitroandin vivo, but they exhibited substantial differences in disease severity in mammals. In mice, while the H7N8 LPAI virus largely remained avirulent, the H7N8 HPAI virus exhibited greater infectivity, virulence, and lethality. Both H7N8 viruses replicated similarly in ferrets, but only the H7N8 HPAI virus caused moderate weight loss, lethargy, and mortality. The H7N8 LPAI virus displayed limited transmissibility in ferrets placed in direct contact with an inoculated animal, while no transmission of H7N8 HPAI virus was detected. Our results indicate that the H7N8 avian influenza viruses from Indiana are able to replicate in mammals and cause severe disease but with limited transmission. The recent appearance of H7N8 viruses in domestic poultry highlights the need for continued influenza surveillance in wild birds and close monitoring of the potential risk to human health.IMPORTANCEH7 influenza viruses circulate in wild birds in the United States, but when the virus emerges in domestic poultry populations, the frequency of human exposure and the potential for human infections increases. An H7N8 highly pathogenic avian influenza (HPAI) virus and an H7N8 low-pathogenic avian influenza (LPAI) virus were recently isolated from commercial turkey farms in Indiana. To determine the risk that these influenza viruses pose to humans, we assessed their pathogenesis and transmissionin vitroand in mammalian models. We found that the H7N8 HPAI virus exhibited enhanced virulence, and although transmission was only observed with the H7N8 LPAI virus, the ability of this H7 virus to transmit in a mammalian host and quickly evolve to a more virulent strain is cause for concern. Our findings offer important insight into the potential for emerging H7 avian influenza viruses to acquire the ability to cause disease and transmit among mammals.

scholarly journals The PB1 Gene from H9N2 Avian Influenza Virus Showed High Compatibility and Increased Mutation Rate after Reassorting with a Human H1N1 Influenza Virus

2021 ◽  
Author(s):  
Hongrui Cui ◽  
Guangsheng Che ◽  
Mart CM de Jong ◽  
Xuesong Li ◽  
Qinfang Liu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
H1n1 Virus ◽  
Polymerase Activity ◽  
Influenza Viruses ◽  
Luciferase Reporter ◽  
Avian Influenza Viruses ◽  
Reassortant Virus ◽  
Rnp Complex ◽  
Reassortant Viruses

Abstract BackgroundReassortment between human and avian influenza viruses (AIV) may result in novel viruses with new characteristics that may threaten human health when causing the next flu pandemic. A particular risk may be posed by avian influenza viruses of subtype H9N2 that are currently massively circulating in domestic poultry in Asia and have been shown to infect humans. In this study, we investigate the characteristics and compatibility of a human H1N1 virus with avian H9N2 derived genes. MethodsThe polymerase activity of the viral ribonucleoprotein (RNP) complex from different reassortments was tested in luciferase reporter assays. Reassortant viruses were generated by reverse genetics in which genes of the human WSN-H1N1 virus (A/WSN/1933) were replaced by genes of the avian A2093-H9N2 virus (A/chicken/Jiangsu/A2093/2011). We replaced both the Hemagglutinin (HA) and Neuraminidase (NA) genes in combination with one of the genes involved in the RNP complex (either PB2, PB1, PA or NP). The growth kinetics and virulence of reassortant viruses were tested on cell lines and mice. The reassortant viruses were then passaged for five generations in MDCK cells and mice lungs. The HA gene of progeny viruses from different passaging paths was analyzed using Next Generation Sequencing (NGS). ResultsWe discovered that the avian PB1 gene increased the polymerase activity of the RNP complex. Reassortant viruses were able to replicate in MDCK and DF1 cells and mice. Analysis of the NGS data showed a higher substitution rate for the PB1-reassortant virus. In particular, for the PB1-reassortant virus, increased virulence for mice was measured by increased body weight loss after infection in mice. ConclusionsThe higher polymerase activity and increased mutation frequency measured for the PB1-reassortant virus suggests that the avian PB1 gene may drive the evolution and adaptation of novel reassortant viruses to the human host. This study provides novel insights in the characteristics of novel viruses that may arise by reassortment of human and avian influenza viruses. Surveillance for infections with H9N2 viruses and the emergence of novel reassortant viruses in humans is important for pandemic preparedness.

scholarly journals Detecting influenza and emerging avian influenza virus by influenza and pneumonia surveillance systems in a large city in China, 2005 to 2016

2019 ◽  
Author(s):  
Xiaorong Guo ◽  
Dong Yang ◽  
Ruchun Liu ◽  
Yaman Li ◽  
Qingqing Hu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Influenza A ◽  
Influenza Viruses ◽  
Surveillance Systems ◽  
Avian Influenza Viruses ◽  
Influenza A H1n1 ◽  
Death Cases ◽  
Positive Results

Abstract Background: Detecting avian influenza virus has become an important public health strategy for controlling the emerging infectious disease. This study aimed to analyze the efficiency of two surveillance systems in detecting the emerging avian influenza viruses. Methods: A modified influenza surveillance system (ISS) and a new built pneumonia surveillance system (PSS) have been used to monitor the viruses in Changsha City, China. The ISS is based on monitoring outpatients in two sentinel hospitals to detect mild influenza and avian influenza cases, and PSS is based on monitoring inpatients in all 49 hospitals to detect severe and death influenza cases. Results: During the study period, 3551917 outpatients were monitored by the ISS system, among which 126076 were influenza-like illness (ILI) cases, with the ILI% of 3.55%. Totally, 14913 throat swabs were collected by the ISS system, among which 2016 were tested positive of influenza or avian influenza virus. Among the positive results, 621 were H3N2, 135 were seasonal H1N1, 610 were influenza A/H1N1 (pandemic in 2009), 106 were untyped influenza A, 540 were B, 1 was H5N6, 1 was H7N9, and 2 were H9N2 virus. 5491560 inpatient people were monitored by the PSS system, among which 6.61% (362743/5491560) were pneumonia cases. 10.55% (38260/362743) of reported pneumonia was severe or death cases. 3401 throat swab or lower respiratory tract samples were collected, among which 2094 were tested positive of influenza or avian influenza virus. Among the positive results, 78 were H3N2, 17 were seasonal H1N1, 1871 were influenza A/H1N1, 103 were untyped influenza A, 16 were B, 1 was H5N6, and 8 were H7N9 virus. Of 15 avian influenza cases reported from January, 2005 to September, 2016, 26.7% (4/15) were mild cases detected by the ISS system, while 60.0% (9/15) were severe or death cases detected by the PSS system. Two H5N1 severe cases were missed by the ISS system in January, 2009 when the PSS system was not available. Conclusion: The two systems seem to be of high efficiency in detecting the emerging avian influenza viruses but need to be verified in other cities or countries.

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