scholarly journals Chicken interferon alpha pretreatment reduces virus replication of pandemic H1N1 and H5N9 avian influenza viruses in lung cell cultures from different avian species

2011 ◽  
Vol 8 (1) ◽  
pp. 447 ◽  
Author(s):  
Haijun Jiang ◽  
Hanchun Yang ◽  
Darrell R Kapczynski
Keyword(s):  
Avian Influenza ◽  
Virus Replication ◽  
Interferon Alpha ◽  
Cell Cultures ◽  
Influenza Viruses ◽  
Avian Species ◽  
Pandemic H1n1 ◽  
Avian Influenza Viruses ◽  
Lung Cell Cultures

scholarly journals Swine ANP32A Supports Avian Influenza Virus Polymerase

2020 ◽  
Vol 94 (12) ◽  
Author(s):  
Thomas P. Peacock ◽  
Olivia C. Swann ◽  
Hamish A. Salvesen ◽  
Ecco Staller ◽  
P. Brian Leung ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Virus Replication ◽  
Mammalian Species ◽  
Gene Mutations ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
2009 H1n1 ◽  
Mixing Vessels

ABSTRACT Avian influenza viruses occasionally infect and adapt to mammals, including humans. Swine are often described as “mixing vessels,” being susceptible to both avian- and human-origin viruses, which allows the emergence of novel reassortants, such as the precursor to the 2009 H1N1 pandemic. ANP32 proteins are host factors that act as influenza virus polymerase cofactors. In this study, we describe how swine ANP32A, uniquely among the mammalian ANP32 proteins tested, supports the activity of avian-origin influenza virus polymerases and avian influenza virus replication. We further show that after the swine-origin influenza virus emerged in humans and caused the 2009 pandemic, it evolved polymerase gene mutations that enabled it to more efficiently use human ANP32 proteins. We map the enhanced proviral activity of swine ANP32A to a pair of amino acids, 106 and 156, in the leucine-rich repeat and central domains and show these mutations enhance binding to influenza virus trimeric polymerase. These findings help elucidate the molecular basis for the mixing vessel trait of swine and further our understanding of the evolution and ecology of viruses in this host. IMPORTANCE Avian influenza viruses can jump from wild birds and poultry into mammalian species such as humans or swine, but they only continue to transmit if they accumulate mammalian adapting mutations. Pigs appear uniquely susceptible to both avian and human strains of influenza and are often described as virus “mixing vessels.” In this study, we describe how a host factor responsible for regulating virus replication, ANP32A, is different between swine and humans. Swine ANP32A allows a greater range of influenza viruses, specifically those from birds, to replicate. It does this by binding the virus polymerase more tightly than the human version of the protein. This work helps to explain the unique properties of swine as mixing vessels.

scholarly journals Avian influenza viruses in humans: lessons from past outbreaks

2019 ◽  
Vol 132 (1) ◽  
pp. 81-95 ◽  
Author(s):  
Yao-Tsun Li ◽  
Martin Linster ◽  
Ian H Mendenhall ◽  
Yvonne C F Su ◽  
Gavin J D Smith
Keyword(s):  
Risk Factors ◽  
Avian Influenza ◽  
Virus Transmission ◽  
Human Infection ◽  
Influenza Viruses ◽  
Avian Species ◽  
Avian Influenza Viruses ◽  
Virus Surveillance ◽  
Changing Patterns ◽  
Human Infections

Abstract Background Human infections with avian influenza viruses (AIV) represent a persistent public health threat. The principal risk factor governing human infection with AIV is from direct contact with infected poultry and is primarily observed in Asia and Egypt where live-bird markets are common. Areas of agreement Changing patterns of virus transmission and a lack of obvious disease manifestations in avian species hampers early detection and efficient control of potentially zoonotic AIV. Areas of controversy Despite extensive studies on biological and environmental risk factors, the exact conditions required for cross-species transmission from avian species to humans remain largely unknown. Growing points The development of a universal (‘across-subtype’) influenza vaccine and effective antiviral therapeutics are a priority. Areas timely for developing research Sustained virus surveillance and collection of ecological and physiological parameters from birds in different environments is required to better understand influenza virus ecology and identify risk factors for human infection.

Reassortment ability of the 2009 pandemic H1N1 influenza virus with circulating human and avian influenza viruses: Public health risk implications

2013 ◽  
Vol 175 (2) ◽  
pp. 151-154 ◽  
Author(s):  
Maria Stincarelli ◽  
Rosaria Arvia ◽  
Maria Alessandra De Marco ◽  
Valeria Clausi ◽  
Fabiana Corcioli ◽  
...  
Keyword(s):  
Public Health ◽  
Influenza Virus ◽  
Avian Influenza ◽  
Health Risk ◽  
H1n1 Influenza ◽  
Influenza Viruses ◽  
Pandemic H1n1 ◽  
H1n1 Influenza Virus ◽  
Avian Influenza Viruses ◽  
Pandemic H1n1 Influenza

Susceptibility of Avian Species to North American H13 Low Pathogenic Avian Influenza Viruses

2012 ◽  
Vol 56 (4s1) ◽  
pp. 969-975 ◽  
Author(s):  
Justin Brown ◽  
Rebecca Poulson ◽  
Deborah Carter ◽  
Camille Lebarbenchon ◽  
Mary Pantin-Jackwood ◽  
...  
Keyword(s):  
Avian Influenza ◽  
North American ◽  
Influenza Viruses ◽  
Avian Species ◽  
Avian Influenza Viruses ◽  
Pathogenic Avian Influenza ◽  
Low Pathogenic Avian Influenza

scholarly journals Low Polymerase Activity Attributed to PA Drives the Acquisition of the PB2 E627K Mutation of H7N9 Avian Influenza Virus in Mammals

mBio ◽  
2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Libin Liang ◽  
Li Jiang ◽  
Junping Li ◽  
Qingqing Zhao ◽  
Jinguang Wang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Avian Influenza ◽  
Virus Replication ◽  
Driving Force ◽  
Polymerase Activity ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
Viral Polymerase ◽  
Adaptive Mutations ◽  
Highly Sensitive

ABSTRACTAvian influenza viruses (AIVs) must acquire mammalian-adaptive mutations before they can efficiently replicate in and transmit among humans. The PB2 E627K mutation is known to play a prominent role in the mammalian adaptation of AIVs. The H7N9 AIVs that emerged in 2013 in China easily acquired the PB2 E627K mutation upon replication in humans. Here, we generate a series of reassortant or mutant H7N9 AIVs and test them in mice. We show that the low polymerase activity attributed to the viral PA protein is the intrinsic driving force behind the emergence of PB2 E627K during H7N9 AIV replication in mice. Four residues in the N-terminal region of PA are critical in mediating the PB2 E627K acquisition. Notably, due to the identity of viral PA protein, the polymerase activity and growth of H7N9 AIV are highly sensitive to changes in expression levels of human ANP32A protein. Furthermore, the impaired viral polymerase activity of H7N9 AIV caused by the depletion of ANP32A led to reduced virus replication inAnp32a−/−mice, abolishing the acquisition of the PB2 E627K mutation and instead driving the virus to acquire the alternative PB2 D701N mutation. Taken together, our findings show that the emergence of the PB2 E627K mutation of H7N9 AIV is driven by the intrinsic low polymerase activity conferred by the viral PA protein, which also involves the engagement of mammalian ANP32A.IMPORTANCEThe emergence of the PB2 E627K substitution is critical in the mammalian adaptation and pathogenesis of AIV. H7N9 AIVs that emerged in 2013 possess a prominent ability in gaining the PB2 E627K mutation in humans. Here, we demonstrate that the acquisition of the H7N9 PB2 E627K mutation is driven by the low polymerase activity conferred by the viral PA protein in human cells, and four PA residues are collectively involved in this process. Notably, the H7N9 PA protein leads to significant dependence of viral polymerase function on human ANP32A protein, andAnp32aknockout abolishes PB2 E627K acquisition in mice. These findings reveal that viral PA and host ANP32A are crucial for the emergence of PB2 E627K during adaptation of H7N9 AIVs to humans.

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