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

BMC Infectious Diseases ◽

10.1186/s12879-019-4405-5 ◽

2019 ◽

Vol 19 (1) ◽

Author(s):

Xiaorong Guo ◽

Dong Yang ◽

Ruchun Liu ◽

Yaman Li ◽

Qingqing Hu ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Surveillance System ◽

Large City ◽

Influenza Viruses ◽

Influenza Surveillance ◽

Surveillance Systems ◽

Incident Cases ◽

Death Cases

Abstract Background Detecting avian influenza virus has become an important public health strategy for controlling the emerging infectious disease. Methods The HIS (hospital information system) modified influenza surveillance system (ISS) and a newly built pneumonia surveillance system (PSS) were used to monitor the influenza viruses in Changsha City, China. The ISS was used to monitor outpatients in two sentinel hospitals and to detect mild influenza and avian influenza cases, and PSS was used to monitor inpatients in 49 hospitals and to detect severe and death influenza cases. Results From 2005 to 2016, there were 3,551,917 outpatients monitored by the ISS system, among whom 126,076 were influenza-like illness (ILI) cases, with the ILI proportion (ILI%) of 3.55%. After the HIS was used, the reported incident cases of ILI and ILI% were increased significantly. From March, 2009 to September, 2016, there were 5,491,560 inpatient cases monitored by the PSS system, among which 362,743 were pneumonia cases, with a proportion of 6.61%. Among pneumonia cases, about 10.55% (38,260/362,743) of cases were severe or death cases. The pneumonia incidence increased each year in the city. Among 15 avian influenza cases reported from January, 2005 to September, 2016, there were 26.7% (4/15) mild cases detected by the HIS-modified 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. Conclusions The HIS was able to improve the efficiency of the ISS for monitoring ILI and emerging avian influenza virus. However, the efficiency of the system needs to be verified in a wider area for a longer time span in China.

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Avian Influenza Virus PB1 Gene in H3N2 Viruses Evolved in Humans To Reduce Interferon Inhibition by Skewing Codon Usage toward Interferon-Altered tRNA Pools

mBio ◽

10.1128/mbio.01222-18 ◽

2018 ◽

Vol 9 (4) ◽

Cited By ~ 14

Author(s):

Bartram L. Smith ◽

Guifang Chen ◽

Claus O. Wilke ◽

Robert M. Krug

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Codon Usage ◽

Avian Influenza Virus ◽

Influenza A ◽

Human Cells ◽

Influenza Viruses ◽

Human Adaptation ◽

Influenza A Viruses ◽

Avian Influenza Viruses

ABSTRACTInfluenza A viruses cause an annual contagious respiratory disease in humans and are responsible for periodic high-mortality human pandemics. Pandemic influenza A viruses usually result from the reassortment of gene segments between human and avian influenza viruses. These avian influenza virus gene segments need to adapt to humans. Here we focus on the human adaptation of the synonymous codons of the avian influenza virus PB1 gene of the 1968 H3N2 pandemic virus. We generated recombinant H3N2 viruses differing only in codon usage of PB1 mRNA and demonstrated that codon usage of the PB1 mRNA of recent H3N2 virus isolates enhances replication in interferon (IFN)-treated human cells without affecting replication in untreated cells, thereby partially alleviating the interferon-induced antiviral state. High-throughput sequencing of tRNA pools explains the reduced inhibition of replication by interferon: the levels of some tRNAs differ between interferon-treated and untreated human cells, and evolution of the codon usage of H3N2 PB1 mRNA is skewed toward interferon-altered human tRNA pools. Consequently, the avian influenza virus-derived PB1 mRNAs of modern H3N2 viruses have acquired codon usages that better reflect tRNA availabilities in IFN-treated cells. Our results indicate that the change in tRNA availabilities resulting from interferon treatment is a previously unknown aspect of the antiviral action of interferon, which has been partially overcome by human-adapted H3N2 viruses.IMPORTANCEPandemic influenza A viruses that cause high human mortality usually result from reassortment of gene segments between human and avian influenza viruses. These avian influenza virus gene segments need to adapt to humans. Here we focus on the human adaptation of the avian influenza virus PB1 gene that was incorporated into the 1968 H3N2 pandemic virus. We demonstrate that the coding sequence of the PB1 mRNA of modern H3N2 viruses enhances replication in human cells in which interferon has activated a potent antiviral state. Reduced interferon inhibition results from evolution of PB1 mRNA codons skewed toward the pools of tRNAs in interferon-treated human cells, which, as shown here, differ significantly from the tRNA pools in untreated human cells. Consequently, avian influenza virus-derived PB1 mRNAs of modern H3N2 viruses have acquired codon usages that better reflect tRNA availabilities in IFN-treated cells and are translated more efficiently.

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

10.21203/rs.2.1751/v3 ◽

2019 ◽

Author(s):

Xiaorong Guo ◽

Dong Yang ◽

Ruchun Liu ◽

Yaman Li ◽

Qingqing Hu ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Surveillance System ◽

Large City ◽

Influenza Viruses ◽

Influenza Surveillance ◽

Surveillance Systems ◽

Incident Cases ◽

Death Cases

Abstract BACKGROUND: Detecting avian influenza virus has become an important public health strategy for controlling the emerging infectious disease. METHODS: The HIS (hospital information system) modified influenza surveillance system (ISS) and a newly built pneumonia surveillance system (PSS) were used to monitor the influenza viruses in Changsha City, China. The ISS was used to monitor outpatients in two sentinel hospitals and to detect mild influenza and avian influenza cases, and PSS was used to monitor inpatients in 49 hospitals and to detect severe and death influenza cases. RESULTS: From 2005 to 2016, there were 3,551,917 outpatients monitored by the ISS system, among whom 126,076 were influenza-like illness (ILI) cases, with the ILI proportion (ILI%) of 3.55%. After the HIS was used, the reported incident cases of ILI and ILI% were increased significantly. From March, 2009 to September, 2016, there were 5,491,560 inpatient cases monitored by the PSS system, among which 362,743 were pneumonia cases, with a proportion of 6.61%. Among pneumonia cases, about 10.55% (38,260/362,743) of cases were severe or death cases. The pneumonia incidence increased each year in the city. Among 15 avian influenza cases reported from January, 2005 to September, 2016, there were 26.7% (4/15) mild cases detected by the HIS-modified 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. CONCLUSIONS: The HIS was able to improve the efficiency of the ISS for monitoring ILI and emerging avian influenza virus. However, the efficiency of the system needs to be verified in a wider area for a longer time span in China.

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Protecting Mice from H7 Avian Influenza Virus by Immunisation with a Recombinant Adenovirus Encoding Influenza A Virus Conserved Antigens

BIOpreparations Prevention Diagnosis Treatment ◽

10.30895/2221-996x-2020-20-1-60-67 ◽

2020 ◽

Vol 20 (1) ◽

pp. 60-67

Author(s):

E. S. Sedova ◽

L. V. Verkhovskaya ◽

E. A. Artemova ◽

D. N. Shcherbinin ◽

A. A. Lysenko ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Influenza A ◽

Recombinant Adenovirus ◽

Lethal Dose ◽

Influenza Viruses ◽

Avian Influenza Viruses ◽

Protective Properties ◽

Virus Subtype

Influenza is a highly contagious disease that causes annual epidemics and occasional pandemics. Birds are believed to be the source of newly emerging pandemic strains, including highly pathogenic avian influenza viruses of the subtype H7. The aim of the study: to evaluate the ability of the recombinant human adenovirus, serotype 5, which expresses genes of influenza A highly conserved antigens (ion channel M2 and nucleoprotein NP), to provide protection to laboratory mice against infection with a lethal dose of avian influenza virus, subtype H7. To achieve this goal, it was necessary to adapt influenza A virus, subtype H7 for reproduction in the lungs of mice, to characterise it, and to use it for evaluation of the protective properties of the recombinant adenovirus. Materials and methods: avian influenza virus A/Chicken/NJ/294508-12/2004 (H7N2) was adapted for reproduction in the lungs of mice by repeated passages. The adapted strain was sequenced and assessed using hemagglutination test, EID50 and LD50 for laboratory mice. BALB/c mice were immunised once with Ad5-tet-M2NP adenovirus intranasally, and 21 days after the immunisation they were infected with a lethal dose (5 LD50) of influenza virus A/Chicken/NJ/294508-12/2004 (H7N2) in order to assess the protective properties of the recombinant adenovirus. The level of viral shedding from the lungs of the infected mice was evaluated by titration of the lung homogenates in MDCK cell culture on days 3 and 6 after infection. The level of specific antibodies to H7 avian influenza virus was determined by indirect enzyme immunoassay. Results: the use of Ad5-tet-M2NP adenovirus for immunisation of the mice ensured 100% survival of the animals that had disease symptoms (weight loss) after their infection with the lethal dose (5 LD50) of H7 avian influenza virus. The study demonstrated a high post-vaccination level of humoral immune response to H7 avian influenza virus. The virus titer decreased significantly by day 6 in the lungs of mice that had been immunised with Ad5-tet-M2NP compared to the control group. Conclusion: the Ad5-tetM2NP recombinant adenovirus can be used to create a candidate pandemic influenza vaccine that would protect against avian influenza viruses, subtype H7, in particular.

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Contemporary Avian Influenza A Virus Subtype H1, H6, H7, H10, and H15 Hemagglutinin Genes Encode a Mammalian Virulence Factor Similar to the 1918 Pandemic Virus H1 Hemagglutinin

mBio ◽

10.1128/mbio.02116-14 ◽

2014 ◽

Vol 5 (6) ◽

Cited By ~ 16

Author(s):

Li Qi ◽

Lindsey M. Pujanauski ◽

A. Sally Davis ◽

Louis M. Schwartzman ◽

Daniel S. Chertow ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Virulence Factor ◽

Pandemic Influenza ◽

Influenza A ◽

Influenza Viruses ◽

Avian Influenza Viruses ◽

Zoonotic Infections ◽

Human Lung Cells

ABSTRACTZoonotic avian influenza virus infections may lead to epidemics or pandemics. The 1918 pandemic influenza virus has an avian influenza virus-like genome, and its H1 hemagglutinin was identified as a key mammalian virulence factor. A chimeric 1918 virus expressing a contemporary avian H1 hemagglutinin, however, displayed murine pathogenicity indistinguishable from that of the 1918 virus. Here, isogenic chimeric avian influenza viruses were constructed on an avian influenza virus backbone, differing only by hemagglutinin subtype expressed. Viruses expressing the avian H1, H6, H7, H10, and H15 subtypes were pathogenic in mice and cytopathic in normal human bronchial epithelial cells, in contrast to H2-, H3-, H5-, H9-, H11-, H13-, H14-, and H16-expressing viruses. Mouse pathogenicity was associated with pulmonary macrophage and neutrophil recruitment. These data suggest that avian influenza virus hemagglutinins H1, H6, H7, H10, and H15 contain inherent mammalian virulence factors and likely share a key virulence property of the 1918 virus. Consequently, zoonotic infections with avian influenza viruses bearing one of these hemagglutinins may cause enhanced disease in mammals.IMPORTANCEInfluenza viruses from birds can cause outbreaks in humans and may contribute to the development of pandemics. The 1918 pandemic influenza virus has an avian influenza virus-like genome, and its main surface protein, an H1 subtype hemagglutinin, was identified as a key mammalian virulence factor. In a previous study, a 1918 virus expressing an avian H1 gene was as virulent in mice as the reconstructed 1918 virus. Here, a set of avian influenza viruses was constructed, differing only by hemagglutinin subtype. Viruses with the avian H1, H6, H7, H10, and H15 subtypes caused severe disease in mice and damaged human lung cells. Consequently, infections with avian influenza viruses bearing one of these hemagglutinins may cause enhanced disease in mammals, and therefore surveillance for human infections with these subtypes may be important in controlling future outbreaks.

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

10.21203/rs.2.1751/v4 ◽

2019 ◽

Author(s):

Xiaorong Guo ◽

Dong Yang ◽

Ruchun Liu ◽

Yaman Li ◽

Qingqing Hu ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Surveillance System ◽

Large City ◽

Influenza Viruses ◽

Influenza Surveillance ◽

Surveillance Systems ◽

Incident Cases ◽

Death Cases

Abstract BACKGROUND: Detecting avian influenza virus has become an important public health strategy for controlling the emerging infectious disease. METHODS: The HIS (hospital information system) modified influenza surveillance system (ISS) and a newly built pneumonia surveillance system (PSS) were used to monitor the influenza viruses in Changsha City, China. The ISS was used to monitor outpatients in two sentinel hospitals and to detect mild influenza and avian influenza cases, and PSS was used to monitor inpatients in 49 hospitals and to detect severe and death influenza cases. RESULTS: From 2005 to 2016, there were 3,551,917 outpatients monitored by the ISS system, among whom 126,076 were influenza-like illness (ILI) cases, with the ILI proportion (ILI%) of 3.55%. After the HIS was used, the reported incident cases of ILI and ILI% were increased significantly. From March, 2009 to September, 2016, there were 5,491,560 inpatient cases monitored by the PSS system, among which 362,743 were pneumonia cases, with a proportion of 6.61%. Among pneumonia cases, about 10.55% (38,260/362,743) of cases were severe or death cases. The pneumonia incidence increased each year in the city. Among 15 avian influenza cases reported from January, 2005 to September, 2016, there were 26.7% (4/15) mild cases detected by the HIS-modified 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. CONCLUSIONS: The HIS was able to improve the efficiency of the ISS for monitoring ILI and emerging avian influenza virus. However, the efficiency of the system needs to be verified in a wider area for a longer time span in China.

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Swine ANP32A Supports Avian Influenza Virus Polymerase

Journal of Virology ◽

10.1128/jvi.00132-20 ◽

2020 ◽

Vol 94 (12) ◽

Cited By ~ 2

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.

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A review of H5Nx avian influenza viruses

Therapeutic Advances in Vaccines and Immunotherapy ◽

10.1177/2515135518821625 ◽

2019 ◽

Vol 7 ◽

pp. 251513551882162 ◽

Cited By ~ 9

Author(s):

Ivette A. Nuñez ◽

Ted M. Ross

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Highly Pathogenic Avian Influenza ◽

Influenza Viruses ◽

Avian Influenza Viruses ◽

Highly Pathogenic ◽

Bird Populations ◽

Pathogenic Avian Influenza ◽

Pathogenic Avian Influenza Virus

Highly pathogenic avian influenza viruses (HPAIVs), originating from the A/goose/Guangdong/1/1996 H5 subtype, naturally circulate in wild-bird populations, particularly waterfowl, and often spill over to infect domestic poultry. Occasionally, humans are infected with HPAVI H5N1 resulting in high mortality, but no sustained human-to-human transmission. In this review, the replication cycle, pathogenicity, evolution, spread, and transmission of HPAIVs of H5Nx subtypes, along with the host immune responses to Highly Pathogenic Avian Influenza Virus (HPAIV) infection and potential vaccination, are discussed. In addition, the potential mechanisms for Highly Pathogenic Avian Influenza Virus (HPAIV) H5 Reassorted Viruses H5N1, H5N2, H5N6, H5N8 (H5Nx) viruses to transmit, infect, and adapt to the human host are reviewed.

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The PA Subunit of the Influenza Virus Polymerase Complex Affects Replication and Airborne Transmission of the H9N2 Subtype Avian Influenza Virus

Viruses ◽

10.3390/v11010040 ◽

2019 ◽

Vol 11 (1) ◽

pp. 40 ◽

Cited By ~ 1

Author(s):

Mengchan Hao ◽

Shaojie Han ◽

Dan Meng ◽

Rong Li ◽

Jing Lin ◽

...

Keyword(s):

Influenza Virus ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Guinea Pigs ◽

Influenza A ◽

Reverse Genetics ◽

Species Barrier ◽

Airborne Transmission ◽

H9n2 Subtype ◽

Influenza A H1n1

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.

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Distinct Pathogenesis of Hong Kong-Origin H5N1 Viruses in Mice Compared to That of Other Highly Pathogenic H5 Avian Influenza Viruses

Journal of Virology ◽

10.1128/jvi.74.3.1443-1450.2000 ◽

2000 ◽

Vol 74 (3) ◽

pp. 1443-1450 ◽

Cited By ~ 97

Author(s):

Jody K. Dybing ◽

Stacey Schultz-Cherry ◽

David E. Swayne ◽

David L. Suarez ◽

Michael L. Perdue

Keyword(s):

Influenza Virus ◽

Hong Kong ◽

Avian Influenza ◽

Avian Influenza Virus ◽

Transforming Growth Factor ◽

Clinical Signs ◽

Influenza Viruses ◽

Rapid Weight Loss ◽

Avian Influenza Viruses ◽

Highly Pathogenic

ABSTRACT In 1997, an outbreak of virulent H5N1 avian influenza virus occurred in poultry in Hong Kong (HK) and was linked to a direct transmission to humans. The factors associated with transmission of avian influenza virus to mammals are not fully understood, and the potential risk of other highly virulent avian influenza A viruses infecting and causing disease in mammals is not known. In this study, two avian and one human HK-origin H5N1 virus along with four additional highly pathogenic H5 avian influenza viruses were analyzed for their pathogenicity in 6- to 8-week-old BALB/c mice. Both the avian and human HK H5 influenza virus isolates caused severe disease in mice, characterized by induced hypothermia, clinical signs, rapid weight loss, and 75 to 100% mortality by 6 to 8 days postinfection. Three of the non-HK-origin isolates caused no detectable clinical signs. One isolate, A/tk/England/91 (H5N1), induced measurable disease, and all but one of the animals recovered. Infections resulted in mild to severe lesions in both the upper and lower respiratory tracts. Most consistently, the viruses caused necrosis in respiratory epithelium of the nasal cavity, trachea, bronchi, and bronchioles with accompanying inflammation. The most severe and widespread lesions were observed in the lungs of HK avian influenza virus-infected mice, while no lesions or only mild lesions were evident with A/ck/Scotland/59 (H5N1) and A/ck/Queretaro/95 (H5N2). The A/ck/Italy/97 (H5N2) and the A/tk/England/91 (H5N1) viruses exhibited intermediate pathogenicity, producing mild to moderate respiratory tract lesions. In addition, infection by the different isolates could be further distinguished by the mouse immune response. The non-HK-origin isolates all induced production of increased levels of active transforming growth factor β following infection, while the HK-origin isolates did not.

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