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Prof. Kin-Chow Chang
University of Nottingham

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0 Antiviral
0 Antiviral agents
0 Antiviral Innate Immunity
0 virus and innate immunity
0 virus and host immunity

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Antiviral
virus and host immunity

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Journal article
Published: 13 May 2021 in Nature Microbiology
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The retinoic acid-inducible gene I (RIG-I) receptor senses cytoplasmic viral RNA and activates type I interferons (IFN-I) and downstream antiviral immune responses. How RIG-I binds to viral RNA and how its activation is regulated remains unclear. Here, using IFI16 knockout cells and p204-deficient mice, we demonstrate that the DNA sensor IFI16 enhances IFN-I production to inhibit influenza A virus (IAV) replication. IFI16 positively upregulates RIG-I transcription through direct binding to and recruitment of RNA polymerase II to the RIG-I promoter. IFI16 also binds to influenza viral RNA via its HINa domain and to RIG-I protein with its PYRIN domain, thus promoting IAV-induced K63-linked polyubiquitination and RIG-I activation. Our work demonstrates that IFI16 is a positive regulator of RIG-I signalling during influenza virus infection, highlighting its role in the RIG-I-like-receptor-mediated innate immune response to IAV and other RNA viruses, and suggesting its possible exploitation to modulate the antiviral response. IFI16 enhances the type I IFN response to inhibit influenza virus replication by two mechanisms: it directly binds viral RNA to promote RIG-I activation and upregulates RIG-I expression via recruiting RNA polymerase II and binding to the RIG-I promoter.

ACS Style

Zhimin Jiang; Fanhua Wei; Yuying Zhang; Tong Wang; Weihua Gao; Shufang Yu; Honglei Sun; Juan Pu; Yipeng Sun; Mingyang Wang; Qi Tong; Chengjiang Gao; Kin-Chow Chang; Jinhua Liu. IFI16 directly senses viral RNA and enhances RIG-I transcription and activation to restrict influenza virus infection. Nature Microbiology 2021, 6, 932 -945.

AMA Style

Zhimin Jiang, Fanhua Wei, Yuying Zhang, Tong Wang, Weihua Gao, Shufang Yu, Honglei Sun, Juan Pu, Yipeng Sun, Mingyang Wang, Qi Tong, Chengjiang Gao, Kin-Chow Chang, Jinhua Liu. IFI16 directly senses viral RNA and enhances RIG-I transcription and activation to restrict influenza virus infection. Nature Microbiology. 2021; 6 (7):932-945.

Chicago/Turabian Style

Zhimin Jiang; Fanhua Wei; Yuying Zhang; Tong Wang; Weihua Gao; Shufang Yu; Honglei Sun; Juan Pu; Yipeng Sun; Mingyang Wang; Qi Tong; Chengjiang Gao; Kin-Chow Chang; Jinhua Liu. 2021. "IFI16 directly senses viral RNA and enhances RIG-I transcription and activation to restrict influenza virus infection." Nature Microbiology 6, no. 7: 932-945.

Journal article
Published: 10 March 2021 in Journal of Virology
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Infection of the CNS is a serious complication of human cases of AIV infection. The viral and host factors associated with neurovirulence of AIV infection are not well understood.

ACS Style

Xuxiao Zhang; Juan Pu; Yipeng Sun; Yuhai Bi; Zhimin Jiang; GuanLong Xu; Hongyu Zhang; Jing Cao; Kin-Chow Chang; Jinhua Liu; Honglei Sun. Neurovirulence of Avian Influenza Virus Is Dependent on the Interaction of Viral NP Protein with FMRP in the Murine Brain. Journal of Virology 2021, 95, 1 .

AMA Style

Xuxiao Zhang, Juan Pu, Yipeng Sun, Yuhai Bi, Zhimin Jiang, GuanLong Xu, Hongyu Zhang, Jing Cao, Kin-Chow Chang, Jinhua Liu, Honglei Sun. Neurovirulence of Avian Influenza Virus Is Dependent on the Interaction of Viral NP Protein with FMRP in the Murine Brain. Journal of Virology. 2021; 95 (7):1.

Chicago/Turabian Style

Xuxiao Zhang; Juan Pu; Yipeng Sun; Yuhai Bi; Zhimin Jiang; GuanLong Xu; Hongyu Zhang; Jing Cao; Kin-Chow Chang; Jinhua Liu; Honglei Sun. 2021. "Neurovirulence of Avian Influenza Virus Is Dependent on the Interaction of Viral NP Protein with FMRP in the Murine Brain." Journal of Virology 95, no. 7: 1.

Journal article
Published: 03 February 2021 in Viruses
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The long-term control strategy of SARS-CoV-2 and other major respiratory viruses needs to include antivirals to treat acute infections, in addition to the judicious use of effective vaccines. Whilst COVID-19 vaccines are being rolled out for mass vaccination, the modest number of antivirals in use or development for any disease bears testament to the challenges of antiviral development. We recently showed that non-cytotoxic levels of thapsigargin (TG), an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) Ca2+ ATPase pump, induces a potent host innate immune antiviral response that blocks influenza A virus replication. Here we show that TG is also highly effective in blocking the replication of respiratory syncytial virus (RSV), common cold coronavirus OC43, SARS-CoV-2 and influenza A virus in immortalized or primary human cells. TG’s antiviral performance was significantly better than remdesivir and ribavirin in their respective inhibition of OC43 and RSV. Notably, TG was just as inhibitory to coronaviruses (OC43 and SARS-CoV-2) and influenza viruses (USSR H1N1 and pdm 2009 H1N1) in separate infections as in co-infections. Post-infection oral gavage of acid-stable TG protected mice against a lethal influenza virus challenge. Together with its ability to inhibit the different viruses before or during active infection, and with an antiviral duration of at least 48 h post-TG exposure, we propose that TG (or its derivatives) is a promising broad-spectrum inhibitor against SARS-CoV-2, OC43, RSV and influenza virus.

ACS Style

Sarah Al-Beltagi; Cristian Preda; Leah Goulding; Joe James; Juan Pu; Paul Skinner; Zhimin Jiang; Belinda Wang; Jiayun Yang; Ashley Banyard; Kenneth Mellits; Pavel Gershkovich; Christopher Hayes; Jonathan Nguyen-Van-Tam; Ian Brown; Jinhua Liu; Kin-Chow Chang. Thapsigargin Is a Broad-Spectrum Inhibitor of Major Human Respiratory Viruses: Coronavirus, Respiratory Syncytial Virus and Influenza A Virus. Viruses 2021, 13, 234 .

AMA Style

Sarah Al-Beltagi, Cristian Preda, Leah Goulding, Joe James, Juan Pu, Paul Skinner, Zhimin Jiang, Belinda Wang, Jiayun Yang, Ashley Banyard, Kenneth Mellits, Pavel Gershkovich, Christopher Hayes, Jonathan Nguyen-Van-Tam, Ian Brown, Jinhua Liu, Kin-Chow Chang. Thapsigargin Is a Broad-Spectrum Inhibitor of Major Human Respiratory Viruses: Coronavirus, Respiratory Syncytial Virus and Influenza A Virus. Viruses. 2021; 13 (2):234.

Chicago/Turabian Style

Sarah Al-Beltagi; Cristian Preda; Leah Goulding; Joe James; Juan Pu; Paul Skinner; Zhimin Jiang; Belinda Wang; Jiayun Yang; Ashley Banyard; Kenneth Mellits; Pavel Gershkovich; Christopher Hayes; Jonathan Nguyen-Van-Tam; Ian Brown; Jinhua Liu; Kin-Chow Chang. 2021. "Thapsigargin Is a Broad-Spectrum Inhibitor of Major Human Respiratory Viruses: Coronavirus, Respiratory Syncytial Virus and Influenza A Virus." Viruses 13, no. 2: 234.

Research article
Published: 01 January 2021 in Emerging Microbes & Infections
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Pandemic influenza, typically caused by the reassortment of human and avian influenza viruses, can result in severe or fatal infections in humans. Timely identification of potential pandemic viruses must be a priority in influenza virus surveillance. However, the range of host species responsible for the generation of novel pandemic influenza viruses remains unclear. In this study, we conducted serological surveys for avian and human influenza virus infections in farmed mink and determined the susceptibility of mink to prevailing avian and human virus subtypes. The results showed that farmed mink were commonly infected with human (H3N2 and H1N1/pdm) and avian (H7N9, H5N6, and H9N2) influenza A viruses. Correlational analysis indicated that transmission of human influenza viruses occurred from humans to mink, and that feed source was a probable route of avian influenza virus transmission to farmed mink. Animal experiments showed that mink were susceptible and permissive to circulating avian and human influenza viruses, and that human influenza viruses (H3N2 and H1N1/pdm), but not avian viruses, were capable of aerosol transmission among mink. These results indicate that farmed mink could be highly permissive “mixing vessels” for the reassortment of circulating human and avian influenza viruses. Therefore, to reduce the risk of emergence of novel pandemic viruses, feeding mink with raw poultry by-products should not be permitted, and epidemiological surveillance of influenza viruses in mink farms should be urgently implemented.

ACS Style

Honglei Sun; Fangtao Li; Qingzhi Liu; Jianyong Du; Litao Liu; Haoran Sun; Chong Li; Jiyu Liu; Xin Zhang; Jizhe Yang; Yuhong Duan; Yuhai Bi; Juan Pu; Yipeng Sun; Qi Tong; Yongqiang Wang; Xiangjun Du; Yuelong Shu; Kin-Chow Chang; Jinhua Liu. Mink is a highly susceptible host species to circulating human and avian influenza viruses. Emerging Microbes & Infections 2021, 10, 472 -480.

AMA Style

Honglei Sun, Fangtao Li, Qingzhi Liu, Jianyong Du, Litao Liu, Haoran Sun, Chong Li, Jiyu Liu, Xin Zhang, Jizhe Yang, Yuhong Duan, Yuhai Bi, Juan Pu, Yipeng Sun, Qi Tong, Yongqiang Wang, Xiangjun Du, Yuelong Shu, Kin-Chow Chang, Jinhua Liu. Mink is a highly susceptible host species to circulating human and avian influenza viruses. Emerging Microbes & Infections. 2021; 10 (1):472-480.

Chicago/Turabian Style

Honglei Sun; Fangtao Li; Qingzhi Liu; Jianyong Du; Litao Liu; Haoran Sun; Chong Li; Jiyu Liu; Xin Zhang; Jizhe Yang; Yuhong Duan; Yuhai Bi; Juan Pu; Yipeng Sun; Qi Tong; Yongqiang Wang; Xiangjun Du; Yuelong Shu; Kin-Chow Chang; Jinhua Liu. 2021. "Mink is a highly susceptible host species to circulating human and avian influenza viruses." Emerging Microbes & Infections 10, no. 1: 472-480.

Journal article
Published: 27 September 2020 in Viruses
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Influenza A virus is a major global pathogen of humans, and there is an unmet need for effective antivirals. Current antivirals against influenza A virus directly target the virus and are vulnerable to mutational resistance. Harnessing an effective host antiviral response is an attractive alternative. We show that brief exposure to low, non-toxic doses of thapsigargin (TG), an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) Ca2+ ATPase pump, promptly elicits an extended antiviral state that dramatically blocks influenza A virus production. Crucially, oral administration of TG protected mice against lethal virus infection and reduced virus titres in the lungs of treated mice. TG-induced ER stress unfolded protein response appears as a key driver responsible for activating a spectrum of host antiviral defences that include an enhanced type I/III interferon response. Our findings suggest that TG is potentially a viable host-centric antiviral for the treatment of influenza A virus infection without the inherent problem of drug resistance.

ACS Style

Leah V. Goulding; Jiayun Yang; Zhimin Jiang; Hongyu Zhang; Daniel Lea; Richard D. Emes; Tania Dottorini; Juan Pu; Jinhua Liu; Kin-Chow Chang. Thapsigargin at Non-Cytotoxic Levels Induces a Potent Host Antiviral Response that Blocks Influenza A Virus Replication. Viruses 2020, 12, 1093 .

AMA Style

Leah V. Goulding, Jiayun Yang, Zhimin Jiang, Hongyu Zhang, Daniel Lea, Richard D. Emes, Tania Dottorini, Juan Pu, Jinhua Liu, Kin-Chow Chang. Thapsigargin at Non-Cytotoxic Levels Induces a Potent Host Antiviral Response that Blocks Influenza A Virus Replication. Viruses. 2020; 12 (10):1093.

Chicago/Turabian Style

Leah V. Goulding; Jiayun Yang; Zhimin Jiang; Hongyu Zhang; Daniel Lea; Richard D. Emes; Tania Dottorini; Juan Pu; Jinhua Liu; Kin-Chow Chang. 2020. "Thapsigargin at Non-Cytotoxic Levels Induces a Potent Host Antiviral Response that Blocks Influenza A Virus Replication." Viruses 12, no. 10: 1093.

Journal article
Published: 29 June 2020 in Proceedings of the National Academy of Sciences
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Pigs are considered as important hosts or “mixing vessels” for the generation of pandemic influenza viruses. Systematic surveillance of influenza viruses in pigs is essential for early warning and preparedness for the next potential pandemic. Here, we report on an influenza virus surveillance of pigs from 2011 to 2018 in China, and identify a recently emerged genotype 4 (G4) reassortant Eurasian avian-like (EA) H1N1 virus, which bears 2009 pandemic (pdm/09) and triple-reassortant (TR)-derived internal genes and has been predominant in swine populations since 2016. Similar to pdm/09 virus, G4 viruses bind to human-type receptors, produce much higher progeny virus in human airway epithelial cells, and show efficient infectivity and aerosol transmission in ferrets. Moreover, low antigenic cross-reactivity of human influenza vaccine strains with G4 reassortant EA H1N1 virus indicates that preexisting population immunity does not provide protection against G4 viruses. Further serological surveillance among occupational exposure population showed that 10.4% (35/338) of swine workers were positive for G4 EA H1N1 virus, especially for participants 18 y to 35 y old, who had 20.5% (9/44) seropositive rates, indicating that the predominant G4 EA H1N1 virus has acquired increased human infectivity. Such infectivity greatly enhances the opportunity for virus adaptation in humans and raises concerns for the possible generation of pandemic viruses.

ACS Style

Honglei Sun; Yihong Xiao; Jiyu Liu; Dayan Wang; Fangtao Li; Chenxi Wang; Chong Li; Junda Zhu; Jingwei Song; Haoran Sun; Zhimin Jiang; Litao Liu; Xin Zhang; Kai Wei; Dongjun Hou; Juan Pu; Yipeng Sun; Qi Tong; Yuhai Bi; Kin-Chow Chang; Sidang Liu; George F. Gao; Jinhua Liu. Prevalent Eurasian avian-like H1N1 swine influenza virus with 2009 pandemic viral genes facilitating human infection. Proceedings of the National Academy of Sciences 2020, 117, 17204 -17210.

AMA Style

Honglei Sun, Yihong Xiao, Jiyu Liu, Dayan Wang, Fangtao Li, Chenxi Wang, Chong Li, Junda Zhu, Jingwei Song, Haoran Sun, Zhimin Jiang, Litao Liu, Xin Zhang, Kai Wei, Dongjun Hou, Juan Pu, Yipeng Sun, Qi Tong, Yuhai Bi, Kin-Chow Chang, Sidang Liu, George F. Gao, Jinhua Liu. Prevalent Eurasian avian-like H1N1 swine influenza virus with 2009 pandemic viral genes facilitating human infection. Proceedings of the National Academy of Sciences. 2020; 117 (29):17204-17210.

Chicago/Turabian Style

Honglei Sun; Yihong Xiao; Jiyu Liu; Dayan Wang; Fangtao Li; Chenxi Wang; Chong Li; Junda Zhu; Jingwei Song; Haoran Sun; Zhimin Jiang; Litao Liu; Xin Zhang; Kai Wei; Dongjun Hou; Juan Pu; Yipeng Sun; Qi Tong; Yuhai Bi; Kin-Chow Chang; Sidang Liu; George F. Gao; Jinhua Liu. 2020. "Prevalent Eurasian avian-like H1N1 swine influenza virus with 2009 pandemic viral genes facilitating human infection." Proceedings of the National Academy of Sciences 117, no. 29: 17204-17210.

Journal article
Published: 01 September 2019 in Journal of General Virology
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Adaptation of PB2 protein is important for the establishment of avian influenza viruses in mammalian hosts. Here, we identify I292V as the prevalent mutation in PB2 of circulating avian H9N2 and pandemic H1N1 viruses. The same dominant PB2 mutation is also found in most human isolates of emergent avian H7N9 and H10N8 viruses. In human cells, PB2-292V in H9N2 virus has the combined ability of conferring higher viral polymerase activity and stronger attenuation of IFN-β induction than that of its predecessor PB2-292I. IFN-β attenuation is accompanied by higher binding affinity of PB2-292V for host mitochondrial antiviral signalling protein, an important intermediary protein in the induction of IFN-β. In the mouse in vivo model, PB2-292V mutation increases H9N2 virus replication with ensuing increase in disease severity. Collectively, PB2-292V is a new mammalian adaptive marker that promotes H9N2 virus replication in mammalian hosts with the potential to improve transmission from birds to humans.

ACS Style

Weihua Gao; Zhipeng Zu; Jiyu Liu; Jingwei Song; Xinyu Wang; Chenxi Wang; Litao Liu; Qi Tong; Mingyang Wang; Honglei Sun; Yipeng Sun; Jinhua Liu; Kin-Chow Chang; Juan Pu. Prevailing I292V PB2 mutation in avian influenza H9N2 virus increases viral polymerase function and attenuates IFN-β induction in human cells. Journal of General Virology 2019, 100, 1273 -1281.

AMA Style

Weihua Gao, Zhipeng Zu, Jiyu Liu, Jingwei Song, Xinyu Wang, Chenxi Wang, Litao Liu, Qi Tong, Mingyang Wang, Honglei Sun, Yipeng Sun, Jinhua Liu, Kin-Chow Chang, Juan Pu. Prevailing I292V PB2 mutation in avian influenza H9N2 virus increases viral polymerase function and attenuates IFN-β induction in human cells. Journal of General Virology. 2019; 100 (9):1273-1281.

Chicago/Turabian Style

Weihua Gao; Zhipeng Zu; Jiyu Liu; Jingwei Song; Xinyu Wang; Chenxi Wang; Litao Liu; Qi Tong; Mingyang Wang; Honglei Sun; Yipeng Sun; Jinhua Liu; Kin-Chow Chang; Juan Pu. 2019. "Prevailing I292V PB2 mutation in avian influenza H9N2 virus increases viral polymerase function and attenuates IFN-β induction in human cells." Journal of General Virology 100, no. 9: 1273-1281.

Journal article
Published: 10 April 2018 in Virology Journal
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With the recent discovery of novel H17N10 and H18N11 influenza viral RNA in bats and report on high frequency of avian H9 seroconversion in a species of free ranging bats, an important issue to address is the extent bats are susceptible to conventional avian and human influenza A viruses. To this end, three bat species (Eidolon helvum, Carollia perspicillata and Tadarida brasiliensis) of lung epithelial cells were separately infected with two avian and two human influenza viruses to determine their relative host innate immune resistance to infection. All three species of bat cells were more resistant than positive control Madin-Darby canine kidney (MDCK) cells to all four influenza viruses. TB1-Lu cells lacked sialic acid α2,6-Gal receptors and were most resistant among the three bat species. Interestingly, avian viruses were relatively more replication permissive in all three bat species of cells than with the use of human viruses which suggest that bats could potentially play a role in the ecology of avian influenza viruses. Chemical inhibition of the JAK-STAT pathway in bat cells had no effect on virus production suggesting that type I interferon signalling is not a major factor in resisting influenza virus infection. Although all three species of bat cells are relatively more resistant to influenza virus infection than control MDCK cells, they are more permissive to avian than human viruses which suggest that bats could have a contributory role in the ecology of avian influenza viruses.

ACS Style

Tessa Slater; Isabella Eckerle; Kin-Chow Chang. Bat lung epithelial cells show greater host species-specific innate resistance than MDCK cells to human and avian influenza viruses. Virology Journal 2018, 15, 68 .

AMA Style

Tessa Slater, Isabella Eckerle, Kin-Chow Chang. Bat lung epithelial cells show greater host species-specific innate resistance than MDCK cells to human and avian influenza viruses. Virology Journal. 2018; 15 (1):68.

Chicago/Turabian Style

Tessa Slater; Isabella Eckerle; Kin-Chow Chang. 2018. "Bat lung epithelial cells show greater host species-specific innate resistance than MDCK cells to human and avian influenza viruses." Virology Journal 15, no. 1: 68.

Journal article
Published: 01 June 2017 in Journal of General Virology
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The H10 subtype of avian influenza viruses (AIVs) circulates globally in wild birds and poultry, and this subtype has been shown to be increasingly prevalent in China. Among the various H10 viruses, H10N7 AIVs have caused repeated mammal and human infections. To investigate their genetic adaptation in mammals, we generated a mouse-adapted avian H10N7 variant (A/mallard/Beijing/27/2011-MA; BJ27-MA) which exhibited increased virulence in mice compared to wild-type virus and acquired neurotropism. Sequencing showed the absence of the widely recognized mammalian adaptation markers of E627K and D701N in PB2 in the mouse-adapted strain; instead, five amino acid mutations were identified: E158G and M631L in PB2; G218E in haemagglutinin (H3 numbering); and K110E and S453I in neuraminidase (NA). The neurovirulence of the BJ27-MA virus necessitated the combined presence of the PB2 and NA mutations. Mutations M631L and E158G of PB2 and K110E of NA were required to mediate increased virus replication and severity of infection in mice and mammalian cells. PB2-M631L was functionally the most dominant mutation in that it strongly upregulated viral polymerase activity and played a critical role in the enhancement of virus replication and disease severity in mice. K110E mutation in NA, on the other hand, significantly promoted NA enzymatic activity. These results indicate that the novel mutations in PB2 and NA genes are critical for the adaptation of H10N7 AIV in mice, and they could serve as molecular signatures of virus transmission to mammalian hosts, including humans.

ACS Style

Xuxiao Zhang; GuanLong Xu; Chenxi Wang; Ming Jiang; Weihua Gao; Mingyang Wang; Honglei Sun; Yipeng Sun; Kin-Chow Chang; Jinhua Liu; Juan Pu. Enhanced pathogenicity and neurotropism of mouse-adapted H10N7 influenza virus are mediated by novel PB2 and NA mutations. Journal of General Virology 2017, 98, 1185 -1195.

AMA Style

Xuxiao Zhang, GuanLong Xu, Chenxi Wang, Ming Jiang, Weihua Gao, Mingyang Wang, Honglei Sun, Yipeng Sun, Kin-Chow Chang, Jinhua Liu, Juan Pu. Enhanced pathogenicity and neurotropism of mouse-adapted H10N7 influenza virus are mediated by novel PB2 and NA mutations. Journal of General Virology. 2017; 98 (6):1185-1195.

Chicago/Turabian Style

Xuxiao Zhang; GuanLong Xu; Chenxi Wang; Ming Jiang; Weihua Gao; Mingyang Wang; Honglei Sun; Yipeng Sun; Kin-Chow Chang; Jinhua Liu; Juan Pu. 2017. "Enhanced pathogenicity and neurotropism of mouse-adapted H10N7 influenza virus are mediated by novel PB2 and NA mutations." Journal of General Virology 98, no. 6: 1185-1195.

Journal article
Published: 15 April 2017 in Journal of Virology
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Segment reassortment and base mutagenesis of influenza A viruses are the primary routes to the rapid evolution of high-fitness virus genotypes. We recently described a predominant G57 genotype of avian H9N2 viruses that caused countrywide outbreaks in chickens in China during 2010 to 2013, which led to the zoonotic emergence of H7N9 viruses. One of the key features of the G57 genotype is the replacement of the earlier A/chicken/Beijing/1/1994 (BJ/94)-like M gene with the A/quail/Hong Kong/G1/1997 (G1)-like M gene of quail origin. We report here the functional significance of the G1-like M gene in H9N2 viruses in conferring increased infection severity and infectivity in primary chicken embryonic fibroblasts and chickens. H9N2 virus housing the G1-like M gene, in place of the BJ/94-like M gene, showed an early surge in viral mRNA and viral RNA (vRNA) transcription that was associated with enhanced viral protein production and with an early elevated release of progeny virus comprising largely spherical rather than filamentous virions. Importantly, H9N2 virus with the G1-like M gene conferred extrapulmonary virus spread in chickens. Five highly represented signature amino acid residues (37A, 95K, 224N, and 242N in the M1 protein and 21G in the M2 protein) encoded by the prevalent G1-like M gene were demonstrated to be prime contributors to enhanced infectivity. Therefore, the genetic evolution of the M gene in H9N2 virus increases reproductive virus fitness, indicating its contribution to the rising virus prevalence in chickens in China. IMPORTANCE We recently described the circulation of a dominant genotype (genotype G57) of H9N2 viruses in countrywide outbreaks in chickens in China, which was responsible, through reassortment, for the emergence of H7N9 viruses that cause severe human infections. A key feature of the genotype G57 H9N2 virus is the presence of the quail-origin G1-like M gene, which had replaced the earlier BJ/94-like M gene. We found that H9N2 virus with the G1-like M gene, but not the BJ/94-like M gene, showed an early surge in progeny virus production and more severe pathology and extrapulmonary virus spread in chickens. Five highly represented amino acid residues in the M1 and M2 proteins derived from the G1-like M gene were shown to mediate enhanced virus infectivity. These observations enhance what we currently know about the roles of reassortment and mutations in virus fitness and have implications for assessing the potential of variant influenza viruses that can cause a rising prevalence in chickens.

ACS Style

Juan Pu; Honglei Sun; Yi Qu; Chenxi Wang; Weihua Gao; Junda Zhu; Yipeng Sun; Yuhai Bi; Yinhua Huang; Kin-Chow Chang; Jie Cui; Jinhua Liu. M Gene Reassortment in H9N2 Influenza Virus Promotes Early Infection and Replication: Contribution to Rising Virus Prevalence in Chickens in China. Journal of Virology 2017, 91, e02055-16 .

AMA Style

Juan Pu, Honglei Sun, Yi Qu, Chenxi Wang, Weihua Gao, Junda Zhu, Yipeng Sun, Yuhai Bi, Yinhua Huang, Kin-Chow Chang, Jie Cui, Jinhua Liu. M Gene Reassortment in H9N2 Influenza Virus Promotes Early Infection and Replication: Contribution to Rising Virus Prevalence in Chickens in China. Journal of Virology. 2017; 91 (8):e02055-16.

Chicago/Turabian Style

Juan Pu; Honglei Sun; Yi Qu; Chenxi Wang; Weihua Gao; Junda Zhu; Yipeng Sun; Yuhai Bi; Yinhua Huang; Kin-Chow Chang; Jie Cui; Jinhua Liu. 2017. "M Gene Reassortment in H9N2 Influenza Virus Promotes Early Infection and Replication: Contribution to Rising Virus Prevalence in Chickens in China." Journal of Virology 91, no. 8: e02055-16.

Journal article
Published: 15 September 2016 in Journal of Virology
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Adaptation of the viral polymerase complex comprising PB1, PB2, and PA is necessary for efficient influenza A virus replication in new host species. We found that PA mutation K356R (PA-K356R) has become predominant since 2014 in avian H9N2 viruses in China as with seasonal human H1N1 viruses. The same mutation is also found in most human isolates of emergent avian H7N9 and H10N8 viruses whose six internal gene segments are derived from the H9N2 virus. We further demonstrated the mammalian adaptive functionality of the PA-K356R mutation. Avian H9N2 virus with the PA-K356R mutation in human A549 cells showed increased nuclear accumulation of PA and increased viral polymerase activity that resulted in elevated levels of viral transcription and virus output. The same mutant virus in mice also enhanced virus replication and caused lethal infection. In addition, combined mutation of PA-K356R and PB2-E627K, a well-known mammalian adaptive marker, in the H9N2 virus showed further cooperative increases in virus production and severity of infection in vitro and in vivo . In summary, PA-K356R behaves as a novel mammalian tropism mutation, which, along with other mutations such as PB2-E627K, might render avian H9N2 viruses adapted for human infection. IMPORTANCE Mutations of the polymerase complex (PB1, PB2, and PA) of influenza A virus are necessary for viral adaptation to new hosts. This study reports a novel and predominant mammalian adaptive mutation, PA-K356R, in avian H9N2 viruses and human isolates of emergent H7N9 and H10N8 viruses. We found that PA-356R in H9N2 viruses causes significant increases in virus replication and severity of infection in human cells and mice and that PA-K356R cooperates with the PB2-E627K mutation, a well-characterized human adaptive marker, to exacerbate mammalian infection in vitro and in vivo . Therefore, the PA-K356R mutation is a significant adaptation in H9N2 viruses and related H7N9 and H10N8 reassortants toward human infectivity.

ACS Style

GuanLong Xu; Xuxiao Zhang; Weihua Gao; Chenxi Wang; Jinliang Wang; Honglei Sun; Yipeng Sun; Lu Guo; Rui Zhang; Kin-Chow Chang; Jinhua Liu; Juan Pu. Prevailing PA Mutation K356R in Avian Influenza H9N2 Virus Increases Mammalian Replication and Pathogenicity. Journal of Virology 2016, 90, 8105 -8114.

AMA Style

GuanLong Xu, Xuxiao Zhang, Weihua Gao, Chenxi Wang, Jinliang Wang, Honglei Sun, Yipeng Sun, Lu Guo, Rui Zhang, Kin-Chow Chang, Jinhua Liu, Juan Pu. Prevailing PA Mutation K356R in Avian Influenza H9N2 Virus Increases Mammalian Replication and Pathogenicity. Journal of Virology. 2016; 90 (18):8105-8114.

Chicago/Turabian Style

GuanLong Xu; Xuxiao Zhang; Weihua Gao; Chenxi Wang; Jinliang Wang; Honglei Sun; Yipeng Sun; Lu Guo; Rui Zhang; Kin-Chow Chang; Jinhua Liu; Juan Pu. 2016. "Prevailing PA Mutation K356R in Avian Influenza H9N2 Virus Increases Mammalian Replication and Pathogenicity." Journal of Virology 90, no. 18: 8105-8114.

Comparative study
Published: 15 July 2016 in Journal of Virology
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Since May 2014, highly pathogenic avian influenza H5N6 virus has been reported to cause six severe human infections three of which were fatal. The biological properties of this subtype, in particular its relative pathogenicity and transmissibility in mammals, are not known. We characterized the virus receptor-binding affinity, pathogenicity, and transmissibility in mice and ferrets of four H5N6 isolates derived from waterfowl in China from 2013-2014. All four H5N6 viruses have acquired a binding affinity for human-like SAα2,6Gal-linked receptor to be able to attach to human tracheal epithelial and alveolar cells. The emergent H5N6 viruses, which share high sequence similarity with the human isolate A/Guangzhou/39715/2014 (H5N6), were fully infective and highly transmissible by direct contact in ferrets but showed less-severe pathogenicity than the parental H5N1 virus. The present results highlight the threat of emergent H5N6 viruses to poultry and human health and the need to closely track their continual adaptation in humans. IMPORTANCE Extended epizootics and panzootics of H5N1 viruses have led to the emergence of the novel 2.3.4.4 clade of H5 virus subtypes, including H5N2, H5N6, and H5N8 reassortants. Avian H5N6 viruses from this clade have caused three fatalities out of six severe human infections in China since the first case in 2014. However, the biological properties of this subtype, especially the pathogenicity and transmission in mammals, are not known. Here, we found that natural avian H5N6 viruses have acquired a high affinity for human-type virus receptor. Compared to the parental clade 2.3.4 H5N1 virus, emergent H5N6 isolates showed less severe pathogenicity in mice and ferrets but acquired efficient in-contact transmission in ferrets. These findings suggest that the threat of avian H5N6 viruses to humans should not be ignored.

ACS Style

Honglei Sun; Juan Pu; YanDi Wei; Yipeng Sun; Jiao Hu; Litao Liu; GuanLong Xu; Weihua Gao; Chong Li; Xuxiao Zhang; Yinhua Huang; Kin-Chow Chang; Xiufan Liu; Jinhua Liu. Highly Pathogenic Avian Influenza H5N6 Viruses Exhibit Enhanced Affinity for Human Type Sialic Acid Receptor and In-Contact Transmission in Model Ferrets. Journal of Virology 2016, 90, 6235 -6243.

AMA Style

Honglei Sun, Juan Pu, YanDi Wei, Yipeng Sun, Jiao Hu, Litao Liu, GuanLong Xu, Weihua Gao, Chong Li, Xuxiao Zhang, Yinhua Huang, Kin-Chow Chang, Xiufan Liu, Jinhua Liu. Highly Pathogenic Avian Influenza H5N6 Viruses Exhibit Enhanced Affinity for Human Type Sialic Acid Receptor and In-Contact Transmission in Model Ferrets. Journal of Virology. 2016; 90 (14):6235-6243.

Chicago/Turabian Style

Honglei Sun; Juan Pu; YanDi Wei; Yipeng Sun; Jiao Hu; Litao Liu; GuanLong Xu; Weihua Gao; Chong Li; Xuxiao Zhang; Yinhua Huang; Kin-Chow Chang; Xiufan Liu; Jinhua Liu. 2016. "Highly Pathogenic Avian Influenza H5N6 Viruses Exhibit Enhanced Affinity for Human Type Sialic Acid Receptor and In-Contact Transmission in Model Ferrets." Journal of Virology 90, no. 14: 6235-6243.

Journal article
Published: 02 June 2016 in Scientific Reports
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Given the present extensive co-circulation in pigs of Eurasian avian-like (EA) swine H1N1 and 2009 pandemic (pdm/09) H1N1 viruses, reassortment between them is highly plausible but largely uncharacterized. Here, experimentally co-infected pigs with a representative EA virus and a pdm/09 virus yielded 55 novel reassortant viruses that could be categorized into 17 genotypes from Gt1 to Gt17 based on segment segregation. Majority of novel reassortants were isolated from the lower respiratory tract. Most of reassortant viruses were more pathogenic and contagious than the parental EA viruses in mice and guinea pigs. The most transmissible reassortant genotypes demonstrated in guinea pigs (Gt2, Gt3, Gt7, Gt10 and Gt13) were also the most lethal in mice. Notably, nearly all these highly virulent reassortants (all except Gt13) were characterized with possession of EA H1 and full complement of pdm/09 ribonucleoprotein genes. Compositionally, we demonstrated that EA H1-222G contributed to virulence by its ability to bind avian-type sialic acid receptors, and that pdm/09 RNP conferred the most robust polymerase activity to reassortants. The present study revealed high reassortment compatibility between EA and pdm/09 viruses in pigs, which could give rise to progeny reassortant viruses with enhanced virulence and transmissibility in mice and guinea pig models.

ACS Style

Weili Kong; Qinfang Liu; Yipeng Sun; Yu Wang; Huijie Gao; Lirong Liu; Zhihua Qin; Qiming He; Honglei Sun; Juan Pu; Dayan Wang; Xin Guo; Hanchun Yang; Kin-Chow Chang; Yuelong Shu; Jinhua Liu. Transmission and pathogenicity of novel reassortants derived from Eurasian avian-like and 2009 pandemic H1N1 influenza viruses in mice and guinea pigs. Scientific Reports 2016, 6, 27067 .

AMA Style

Weili Kong, Qinfang Liu, Yipeng Sun, Yu Wang, Huijie Gao, Lirong Liu, Zhihua Qin, Qiming He, Honglei Sun, Juan Pu, Dayan Wang, Xin Guo, Hanchun Yang, Kin-Chow Chang, Yuelong Shu, Jinhua Liu. Transmission and pathogenicity of novel reassortants derived from Eurasian avian-like and 2009 pandemic H1N1 influenza viruses in mice and guinea pigs. Scientific Reports. 2016; 6 (1):27067.

Chicago/Turabian Style

Weili Kong; Qinfang Liu; Yipeng Sun; Yu Wang; Huijie Gao; Lirong Liu; Zhihua Qin; Qiming He; Honglei Sun; Juan Pu; Dayan Wang; Xin Guo; Hanchun Yang; Kin-Chow Chang; Yuelong Shu; Jinhua Liu. 2016. "Transmission and pathogenicity of novel reassortants derived from Eurasian avian-like and 2009 pandemic H1N1 influenza viruses in mice and guinea pigs." Scientific Reports 6, no. 1: 27067.

Journal article
Published: 08 December 2015 in Scientific Reports
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Pigs are evidently more resistant to avian than swine influenza A viruses, mediated in part through frontline epithelial cells and alveolar macrophages (AM). Although porcine AM (PAM) are crucial in influenza virus control, their mode of control is unclear. To gain insight into the possible role of PAM in the mediation of avian influenza virus resistance, we compared the host effects and replication of two avian (H2N3 and H6N1) and three mammalian (swine H1N1, human H1N1 and pandemic H1N1) influenza viruses in PAM. We found that PAM were readily susceptible to initial infection with all five avian and mammalian influenza viruses but only avian viruses caused early and extensive apoptosis (by 6 h of infection) resulting in reduced virus progeny and moderated pro-inflammation. Full length viral PB1-F2 present only in avian influenza viruses is a virulence factor that targets AM for mitochondrial-associated apoptotic cell death. With the use of reverse genetics on an avian H5N1 virus, we found that full length PB1-F2 contributed to increased apoptosis and pro-inflammation but not to reduced virus replication. Taken together, we propose that early apoptosis of PAM limits the spread of avian influenza viruses and that PB1-F2 could play a contributory role in the process.

ACS Style

Pengxiang Chang; Suresh Kuchipudi; Kenneth Mellits; Sujith Sebastian; Joe James; Jinhua Liu; Holly Shelton; Kin-Chow Chang. Early apoptosis of porcine alveolar macrophages limits avian influenza virus replication and pro-inflammatory dysregulation. Scientific Reports 2015, 5, 17999 .

AMA Style

Pengxiang Chang, Suresh Kuchipudi, Kenneth Mellits, Sujith Sebastian, Joe James, Jinhua Liu, Holly Shelton, Kin-Chow Chang. Early apoptosis of porcine alveolar macrophages limits avian influenza virus replication and pro-inflammatory dysregulation. Scientific Reports. 2015; 5 (1):17999.

Chicago/Turabian Style

Pengxiang Chang; Suresh Kuchipudi; Kenneth Mellits; Sujith Sebastian; Joe James; Jinhua Liu; Holly Shelton; Kin-Chow Chang. 2015. "Early apoptosis of porcine alveolar macrophages limits avian influenza virus replication and pro-inflammatory dysregulation." Scientific Reports 5, no. 1: 17999.

Evaluation study
Published: 17 September 2015 in BMC Cell Biology
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Issued under a CC-BY 4.0 licence (http://creativecommons.org/licenses/by/4.0/).BACKGROUND. The traditional problems of performing skeletal muscle cell cultures derived from mammalian or avian species are limited myotube differentiation, and transient myotube persistence which greatly restricts the ability of myotubes to undergo phenotypic maturation. We report here on a major technical breakthrough in the establishment of a simple and effective method of extended porcine myotube cultures (beyond 50 days) in two-dimension (2D) that recapitulates key features of postnatal fibre types. RESULTS. Primary porcine muscle satellite cells (myoblasts) were isolated from the longissimus dorsi of 4 to 6 weeks old\ud pigs for 2D cultures to optimise myotube formation, improve surface adherence and characterise myotube maturation. Over 95% of isolated cells were myoblasts as evidenced by the expression of Pax3 and Pax7. Our relatively simple approach, based on modifications of existing surface coating reagents (Maxgel), and of proliferation and differentiation (Ultroser G) media, typically achieved by 5 days of differentiation fusion index of around 80 % manifested in an abundance of discrete myosin heavy chain (MyHC) slow and fast myotubes. There was little deterioration in myotube viability over 50 days, and the efficiency of myotube formation was maintained over seven myoblast passages. Regular spontaneous contractions of myotubes were frequently observed throughout culture. Myotubes in extended cultures were able to undergo phenotypic adaptation in response to different culture media, including the adoption of a dominant postnatal phenotype of fast-glycolytic MyHC 2x and 2b expression by about day 20 of differentiation. Furthermore, fast-glycolytic myotubes coincided with enhanced expression of the putative porcine long intergenic non-coding RNA (linc-MYH), which has recently been shown to be a key coordinator of MyHC 2b expression in vivo. CONCLUSIONS. Our revised culture protocol allows the efficient differentiation and fusion of porcine myoblasts into myotubes and their prolonged adherence to the culture surface. Furthermore, we are able to recapitulate in 2D the maturation process of myotubes to resemble postnatal fibre types which represent a major technical advance in opening access to the in vitro study of coordinated postnatal muscle gene expression

ACS Style

Sujith Sebastian; Leah Goulding; Suresh V. Kuchipudi; Kin-Chow Chang. Extended 2D myotube culture recapitulates postnatal fibre type plasticity. BMC Cell Biology 2015, 16, 23 .

AMA Style

Sujith Sebastian, Leah Goulding, Suresh V. Kuchipudi, Kin-Chow Chang. Extended 2D myotube culture recapitulates postnatal fibre type plasticity. BMC Cell Biology. 2015; 16 (1):23.

Chicago/Turabian Style

Sujith Sebastian; Leah Goulding; Suresh V. Kuchipudi; Kin-Chow Chang. 2015. "Extended 2D myotube culture recapitulates postnatal fibre type plasticity." BMC Cell Biology 16, no. 1: 23.

Journal article
Published: 01 September 2015 in Journal of General Virology
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H9N2 influenza viruses have been circulating worldwide in multiple avian species and regularly infect pigs and humans. Recently, a novel protein PA-X, produced from ribosomal frame-shift during PA translation, is demonstrated to be an anti-virulence factor in that it moderated infection severity in pandemic 2009 H1N1, highly pathogenic avian H5N1 and 1918 H1N1 viruses. However, a similar role of PA-X in the prevalent H9N2 avian influenza viruses has not been established. In this study, we compared the virulence and cytopathogenicity H9N2 wild type virus and H9N2 PA-X deficient virus. Loss of PA-X in H9N2 virus reduced apoptosis and had marginal effect on progeny virus output in human pulmonary adenocarcinoma (A549) cells. Without PA-X, PA was less able to suppress co-expressed green fluorescence protein (GFP) in human 293T cells. Furthermore, absence of PA-X in H9N2 virus attenuated viral pathogenicity in mice which showed no mortality, reduced progeny virus production, mild to normal lung histopathology, and dampened proinflammatory cytokine and chemokine response. Therefore, unlike previously reported H1N1 and H5N1 viruses, we show that PA-X protein in H9N2 virus is a pro-virulence factor in facilitating viral pathogenicity, and that the pro- or anti-virulence role of PA-X in influenza viruses is virus-strain dependent.

ACS Style

Huijie Gao; GuanLong Xu; Yipeng Sun; Lu Qi; Jinliang Wang; Weili Kong; Honglei Sun; Juan Pu; Kin-Chow Chang; Jinhua Liu. PA-X is a virulence factor in avian H9N2 influenza virus. Journal of General Virology 2015, 96, 2587 -2594.

AMA Style

Huijie Gao, GuanLong Xu, Yipeng Sun, Lu Qi, Jinliang Wang, Weili Kong, Honglei Sun, Juan Pu, Kin-Chow Chang, Jinhua Liu. PA-X is a virulence factor in avian H9N2 influenza virus. Journal of General Virology. 2015; 96 (9):2587-2594.

Chicago/Turabian Style

Huijie Gao; GuanLong Xu; Yipeng Sun; Lu Qi; Jinliang Wang; Weili Kong; Honglei Sun; Juan Pu; Kin-Chow Chang; Jinhua Liu. 2015. "PA-X is a virulence factor in avian H9N2 influenza virus." Journal of General Virology 96, no. 9: 2587-2594.

Journal article
Published: 01 August 2015 in Journal of General Virology
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The PA-X protein, arising from ribosomal frameshift during PA translation, was recently discovered in influenza A virus (IAV). The C-terminal domain ‘X’ of PA-X proteins in IAVs can be classified as full-length (61 aa) or truncated (41 aa). In the main, avian influenza viruses express full-length PA-X proteins, whilst 2009 pandemic H1N1 (pH1N1) influenza viruses harbour truncated PA proteins. The truncated form lacks aa 232–252 of the full-length PA-X protein. The significance of PA-X length in virus function remains unclear. To address this issue, we constructed a set of contemporary influenza viruses (pH1N1, avian H5N1 and H9N2) with full and truncated PA-X by reverse genetics to compare their replication and host pathogenicity. All full-length PA-X viruses in human A549 cells conferred 10- to 100-fold increase in viral replication and 5–8 % increase in apoptosis relative to corresponding truncated PA-X viruses. Full-length PA-X viruses were more virulent and caused more severe inflammatory responses in mice. Furthermore, aa 233–252 at the C terminus of PA-X strongly suppressed co-transfected gene expression by ∼50 %, suggesting that these terminal 20 aa could play a role in enhancing viral replication and contribute to virulence.

ACS Style

Huijie Gao; Honglei Sun; Jiao Hu; Lu Qi; Jinliang Wang; Xin Xiong; Yu Wang; Qiming He; Yang Lin; Weili Kong; Lai-Giea Seng; Juan Pu; Kin-Chow Chang; Xiufan Liu; Jinhua Liu; Yipeng Sun. Twenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity. Journal of General Virology 2015, 96, 2036 -2049.

AMA Style

Huijie Gao, Honglei Sun, Jiao Hu, Lu Qi, Jinliang Wang, Xin Xiong, Yu Wang, Qiming He, Yang Lin, Weili Kong, Lai-Giea Seng, Juan Pu, Kin-Chow Chang, Xiufan Liu, Jinhua Liu, Yipeng Sun. Twenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity. Journal of General Virology. 2015; 96 (8):2036-2049.

Chicago/Turabian Style

Huijie Gao; Honglei Sun; Jiao Hu; Lu Qi; Jinliang Wang; Xin Xiong; Yu Wang; Qiming He; Yang Lin; Weili Kong; Lai-Giea Seng; Juan Pu; Kin-Chow Chang; Xiufan Liu; Jinhua Liu; Yipeng Sun. 2015. "Twenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity." Journal of General Virology 96, no. 8: 2036-2049.

Brief communication
Published: 01 April 2015 in Acta Veterinaria Scandinavica
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The use of the generic term "meat and animal derivatives" in declared ingredient lists of pet foods in the European Union is virtually universal. In the wake of the 2013 "horse meat scandal" in the human food chain, we examined the presence and authenticity of animal sources (cow, chicken, pig and horse) of proteins in a range of popular wet pet foods in the United Kingdom. Seventeen leading dog and cat foods were sampled for the relative presence of DNA from each of the four animal species by quantitative real-time polymerase chain reaction. No horse DNA was detected. However, there was detection at substantial levels of unspecified animal species in most products tested. In 14 out of 17 samples, bovine, porcine and chicken DNA were found in various proportions and combinations but were not explicitly identified on the product labels. Of the 7 products with prominent headline descriptions containing the term "with beef", only 2 were found to contain more bovine DNA (>50%) than pig and chicken DNA combined. There is a need for the pet food industry to show greater transparency to customers in the disclosure of the types of animal proteins (animal species and tissue types) in their products. Full disclosure of animal contents will (a) allow more informed choices to be made on purchases which are particularly important for pets with food allergies, (b) reduce the risk of product misinterpretation by shoppers, and

ACS Style

Isabella R Maine; Robert Atterbury; Kin-Chow Chang. Investigation into the animal species contents of popular wet pet foods. Acta Veterinaria Scandinavica 2015, 57, 7 .

AMA Style

Isabella R Maine, Robert Atterbury, Kin-Chow Chang. Investigation into the animal species contents of popular wet pet foods. Acta Veterinaria Scandinavica. 2015; 57 (1):7.

Chicago/Turabian Style

Isabella R Maine; Robert Atterbury; Kin-Chow Chang. 2015. "Investigation into the animal species contents of popular wet pet foods." Acta Veterinaria Scandinavica 57, no. 1: 7.

Short communication
Published: 20 March 2015 in Genomics Data
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The data described in this article pertain to the article by Kuchipudi et al. (2014) titled “Highly Pathogenic Avian Influenza Virus Infection in Chickens But Not Ducks Is Associated with Elevated Host Immune and Pro-inflammatory Responses” [1]. While infection of chickens with highly pathogenic avian influenza (HPAI) H5N1 virus subtypes often leads to 100% mortality within 1 to 2 days, infection of ducks in contrast causes mild or no clinical signs. The rapid onset of fatal disease in chickens, but with no evidence of severe clinical symptoms in ducks, suggests underlying differences in their innate immune mechanisms. We used Chicken Genechip microarrays (Affymetrix) to analyse the gene expression profiles of primary chicken and duck lung cells infected with a low pathogenic avian influenza (LPAI) H2N3 virus and two HPAI H5N1 virus subtypes to understand the molecular basis of host susceptibility and resistance in chickens and ducks. Here, we described the experimental design, quality control and analysis that were performed on the data set. The data are publicly available through the Gene Expression Omnibus (GEO)database with accession number GSE33389, and the analysis and interpretation of these data are included in Kuchipudi et al. (2014) [1].

ACS Style

Suresh V. Kuchipudi; Stephen P. Dunham; Kin-Chow Chang. DNA microarray global gene expression analysis of influenza virus-infected chicken and duck cells. Genomics Data 2015, 4, 60 -64.

AMA Style

Suresh V. Kuchipudi, Stephen P. Dunham, Kin-Chow Chang. DNA microarray global gene expression analysis of influenza virus-infected chicken and duck cells. Genomics Data. 2015; 4 ():60-64.

Chicago/Turabian Style

Suresh V. Kuchipudi; Stephen P. Dunham; Kin-Chow Chang. 2015. "DNA microarray global gene expression analysis of influenza virus-infected chicken and duck cells." Genomics Data 4, no. : 60-64.

Journal article
Published: 05 February 2015 in Scientific Reports
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PA-X is a novel protein encoded by PA mRNA and is found to decrease the pathogenicity of pandemic 1918 H1N1 virus in mice. However, the importance of PA-X proteins in current epidemiologically important influenza A virus strains is not known. In this study, we report on the pathogenicity and pathological effects of PA-X deficient 2009 pandemic H1N1 (pH1N1) and highly pathogenic avian influenza H5N1 viruses. We found that loss of PA-X expression in pH1N1 and H5N1 viruses increased viral replication and apoptosis in A549 cells and increased virulence and host inflammatory response in mice. In addition, PA-X deficient pH1N1 and H5N1 viruses up-regulated PA mRNA and protein synthesis and increased viral polymerase activity. Loss of PA-X was also accompanied by accelerated nuclear accumulation of PA protein and reduced suppression of PA on non-viral protein expression. Our study highlights the effects of PA-X on the moderation of viral pathogenesis and pathogenicity.

ACS Style

Huijie Gao; Yipeng Sun; Jiao Hu; Lu Qi; Jinliang Wang; Xin Xiong; Yu Wang; Qiming He; Yang Lin; Weili Kong; Lai-Giea Seng; Honglei Sun; Juan Pu; Kin-Chow Chang; Xiufan Liu; Jinhua Liu. The contribution of PA-X to the virulence of pandemic 2009 H1N1 and highly pathogenic H5N1 avian influenza viruses. Scientific Reports 2015, 5, 8262 .

AMA Style

Huijie Gao, Yipeng Sun, Jiao Hu, Lu Qi, Jinliang Wang, Xin Xiong, Yu Wang, Qiming He, Yang Lin, Weili Kong, Lai-Giea Seng, Honglei Sun, Juan Pu, Kin-Chow Chang, Xiufan Liu, Jinhua Liu. The contribution of PA-X to the virulence of pandemic 2009 H1N1 and highly pathogenic H5N1 avian influenza viruses. Scientific Reports. 2015; 5 (1):8262.

Chicago/Turabian Style

Huijie Gao; Yipeng Sun; Jiao Hu; Lu Qi; Jinliang Wang; Xin Xiong; Yu Wang; Qiming He; Yang Lin; Weili Kong; Lai-Giea Seng; Honglei Sun; Juan Pu; Kin-Chow Chang; Xiufan Liu; Jinhua Liu. 2015. "The contribution of PA-X to the virulence of pandemic 2009 H1N1 and highly pathogenic H5N1 avian influenza viruses." Scientific Reports 5, no. 1: 8262.