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[size=0.8465em]Nat Commun. 2015 Apr 8;6:6553. doi: 10.1038/ncomms7553.
Mammalian adaptation of influenza A(H7N9) virus is limited by a narrow genetic bottleneck.Abstract

Human infection with avian influenza A(H7N9) virus is associated mainly with the exposure to infected poultry. The factors that allow interspecies transmission but limit human-to-human transmission are unknown. Here we show that A/Anhui/1/2013(H7N9) influenza virus infection of chickens (natural hosts) is asymptomatic and that it generates a high genetic diversity. In contrast, diversity is tightly restricted in infected ferrets, limiting further adaptation to a fully transmissible form. Airborne transmission in ferrets is accompanied by the mutations in PB1, NP and NA genes that reduce viral polymerase and neuraminidase activity. Therefore, while A(H7N9) virus can infect mammals, further adaptation appears to incur a fitness cost. Our results reveal that a tight genetic bottleneck during avian-to-mammalian transmission is a limiting factor in A(H7N9) influenza virus adaptation to mammals. This previously unrecognized biological mechanism limiting species jumps provides a measure of adaptive potential and may serve as a risk assessment tool for pandemic preparedness.

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陈华兰团队JV文章
J Virol. 2015 Apr 8. pii: JVI.00017-15. [Epub ahead of print]
Genetics, receptor binding, and virulence in mice of H10N8 influenza viruses isolated from ducks and chickens in live poultry markets in China.
Deng G1, Shi J1, Wang J1, Kong H1, Cui P1, Zhang F1, Tan D1, Suzuki Y2, Liu L1, Jiang Y1, Guan Y1, Chen H3.
Author information
Abstract
We analyzed eight H10N8 viruses isolated from ducks and chickens in live poultry markets from 2009 to 2013 in China. These viruses showed distinct genetic diversity and formed five genotypes: the four duck isolates formed four different genotypes, whereas the four chicken viruses belong to a single genotype. The viruses bound to both human- and avian-type receptors, and four of the viruses caused 12.7% - 22.5% body weight loss in mice.

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2015 Apr 8. pii: JVI.00319-15. [Epub ahead of print]
Influenza A virus protein PA-X contributes to viral growth and suppression of the host antiviral and immune responses.

Hayashi T1, MacDonald LA1, Takimoto T2.
Author information

• 1Department of Microbiology and Immunology, University of Rochester Medical Center, Box 672, 601 Elmwood Avenue, Rochester, NY 14642, USA.
• 2Department of Microbiology and Immunology, University of Rochester Medical Center, Box 672, 601 Elmwood Avenue, Rochester, NY 14642, USA toru_takimoto@urmc.rochester.edu.
  

Abstract

Influenza virus infection causes global inhibition of host protein synthesis in infected cells. This host shutoff is thought to allow viruses to escape from the host antiviral response, which restricts virus replication and spread. Although the mechanism of host shutoff is unclear, a novel viral protein expressed by ribosomal frameshifting PA-X, was found to play a major role in influenza virus-induced host shutoff. However, little is known about the impact of PA-X expression on currently circulating influenza A virus pathogenicity and the host antiviral response.

In this study, we rescued a recombinant influenza A virus A/California/04/09 (H1N1, Cal) containing mutations at the frameshift motif in the PA gene (Cal PA-XFS). Cal PA-XFS expressed significantly less PA-X than Cal wild type (WT). Cal WT, but not Cal PA-XFS, induced degradation of host β-actin mRNA and suppressed host protein synthesis, supporting the idea that PA-X induces host shutoff via mRNA decay. Moreover, Cal WT inhibited IFN-β expression and replicated more rapidly than Cal PA-XFS in human respiratory cells. Mice infected with Cal PA-XFS had significantly lower levels of virus growth and enhanced expression of IFN-β mRNA in their lungs than mice infected with Cal WT. Importantly, more anti-hemagglutinin and neutralizing antibodies were produced in Cal PA-XFS-infected mice than Cal WT-infected mice, despite the lower level of virus replication in the lungs. Our data indicate that PA-X of the pandemic H1N1 virus has a strong impact on viral growth and the host innate and acquired immune response to influenza virus.

IMPORTANCE:

Virus-induced host protein shutoff is considered to be a major factor to allow viruses to evade innate and acquired immune recognition. We provide evidence that the 2009 H1N1 influenza A virus protein PA-X plays a role in virus replication and inhibition of host antiviral response by means of its host protein synthesis shutoff activity both in vitro and in vivo. We also demonstrated that while growth of Cal PA-XFS was attenuated in the lungs of infected animals, this mutant induced a stronger humoral response than Cal WT. Our findings clearly highlight the importance of PA-X in counteracting the host innate and acquired immune response to influenza virus, an important global pathogen. This work demonstrates that inhibition of PA-X expression in influenza virus vaccine strains may provide a novel way of safely attenuating viral growth while inducing a more robust immune response.

全文链接：http://jvi.asm.org/content/early/2015/04/02/JVI.00319-15.long

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Clin Microbiol Infect. 2015 Apr 13. pii: S1198-743X(15)00373-0. doi: 10.1016/j.cmi.2015.03.009. [Epub ahead of print]
Epidemiological study of influenza B in Shanghai during the 2009-2014 seasons: implications for influenzavaccination strategy.
Zhao B1, Qin S2, Teng Z3, Chen J3, Yu X3, Gao Y3, Shen J3, Cui X3, Zeng M4, Zhang X5.
Author information
1Bio-X Institutes, Shanghai Jiao Tong University, Shanghai, China; Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
2Bio-X Institutes, Shanghai Jiao Tong University, Shanghai, China.
3Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
4Department of Infectious Diseases, Children's Hospital of Fudan University, Shanghai, China. Electronic address: zengmeigao@aliyun.com.
5Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China. Electronic address: Zhangxi@scdc.sh.cn.

Abstract
A new quadrivalent influenza vaccine has been available for influenza B, which can pose a significant global health burden. Shanghai has the highest GDP and largest metropolitan population in China. To understand the impact of influenza B in Shanghai in terms of age-related incidence and relative prevalence compared with other subtypes, we conducted this retrospective epidemiological study of influenza B in the 2009-2014 seasons. A total of 71 354 outpatients with influenza-like illness were included, and both lineages of influenza B and subtypes of influenza A were identified using real-time RT-PCR. The antigenic characteristics of influenza B isolates were analysed by sequencing and reciprocal haemagglutinin inhibition assay. On average, 33.45% of influenza strains were influenza B, and 40.20% of strains isolated from children were influenza B. The incidence of influenza B was highest (12.52 per 100 people with influenza-like illness) in children ages 6-17 years and usually peaked in this age group at the early stage of aninfluenza B epidemic. Overall, both matched and mismatched influenza B strains co-circulated in Shanghai annually, and 44.57% of the circulatinginfluenza B belonged to the opposite lineage of the vaccine strains. We concluded that influenza B has caused a substantial impact in Shanghai and that school-aged children play a key role in the transmission of influenza B. Hence, it may be beneficial to prioritize influenza vaccination for school-aged children to mitigate the outbreaks of influenza B.

年 度	WHO推荐的疫苗组分（北半球）
2013-2014	A/California/7/2009 (H1N1)pdm09-like virusa; A(H3N2) virus antigenically like the cell-propagated prototype virus A/Victoria/361/2011b*; B/Massachusetts/2/2012-like virus. B/Brisbane/60/2008-like virus
2012-2013	A/California/7/2009 (H1N1)pdm09-like virus; A/Victoria/361/2011 (H3N2)-like virus; B/Wisconsin/1/2010-like virus.
2011-2012	A/California/7/2009 (H1N1)-like virus; A/Perth/16/2009 (H3N2)-like virus; B/Brisbane/60/2008-like virus.
2010-2011	A/California/7/2009 (H1N1)-like virus; A/Perth/16/2009 (H3N2)-like virus;* B/Brisbane/60/2008-like virus.
2009-2010	A/Brisbane/59/2007 (H1N1)-like virus*; A/Brisbane/10/2007 (H3N2)-like virus**; B/Brisbane/60/2008-like virus

自1983年以来，有两种B型抗原性和遗传性不同的B型流感病毒B/Victoria/2/87-样（Victoria系）和B/Yamagata/16/88-样（Yamagata系）同时在全球流行，然而当前季节性流感疫苗只包含一种B型毒株，该研究发现，在上海两种谱系的病毒同时在人群流行，分离到毒株与疫苗所用毒株不同的比例高达44.57%

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Biotechnol Res Int. 2015;2015:402628. doi: 10.1155/2015/402628. Epub 2015 Mar 30.
Establishment of MDCK Stable Cell Lines Expressing TMPRSS2 and MSPL and Their Applications in Propagating Influenza Vaccine Viruses in Absence of Exogenous Trypsin.
Wen Z1, Wu C1, Chen W1, Zeng X1, Shi J1, Ge J1, Chen H1, Bu Z1.
Author information
1State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 427 Maduan Street, Harbin 150001, China.
Abstract
We established two Madin-Darby canine kidney (MDCK) cell lines stably expressing human airway transmembrane protease: transmembrane protease, serine 2 (TMPRSS2) and mosaic serine protease large form (MSPL) which support multicycle growth of two H5 highly pathogenic avian influenza viruses (HPAIV) recombinant vaccines (Re-5 and Re-6) and an H9 avian influenza virus (AIV) recombinant vaccine (Re-9) in the absence of trypsin. Data showed that the cell lines stably expressed TMPRSS2 and MSPL after 20 serial passages. Both MDCK-TMPRSS2 and MDCK-MSPL could proteolytically cleave the HA of Re-5, Re-6, and Re-9 and supported high-titer growth of the vaccine without exogenous trypsin. Re-5, Re-6, and Re-9 efficiently infected and replicated within MDCK-TMPRSS2 and MDCK-MSPL cells and viral titer were comparable to the virus grown in MDCK cells with TPCK-trypsin. Thus, our results indicate a potential application for these cell lines in cell-based influenza vaccine production and may serve as a useful tool for HA proteolytic cleavage-related studies.

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[size=0.8465em]Virus Res. 2015 Apr 24. pii: S0168-1702(15)00168-9. doi: 10.1016/j.virusres.2015.03.017. [Epub ahead of print]

Influenza virus polymerase: functions on host range, inhibition of cellular response to infection and pathogenicity.
[size=0.923em]Rodriguez-Frandsen A[size=0.8461em]1, Alfonso R[size=0.8461em]2, Nieto A[size=0.8461em]3.

Author information

Abstract

The viral polymerase is an essential complex for the influenza virus life cycle as it performs the viral RNA transcription and replication processes. To that end, the polymerase carries out a wide array of functions and associates to a large number of cellular proteins. Due to its importance, recent studies have found numerous mutations in all three polymerase protein subunits contributing to virus host range and pathogenicity. In this review, we will point out viral polymerase polymorphisms that have been associated with virus adaptation to mammalian hosts, increased viral polymerase activity and virulence. Furthermore, we will summarize the current knowledge regarding the new set of proteins expressed from the viral polymerase genes and their contribution to infection. In addition, the mechanisms used by the virus to counteract the cellular immune response in which the viral polymerase complex or its subunits are involved will be highlighted. Finally, the degradative process induced by the viral polymerase on the cellular transcription machinery and its repercussions on virus pathogenicity will be of particular interest.

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J Med Virol. 2015 May 12. doi: 10.1002/jmv.24231. [Epub ahead of print]
Human infection with an avian influenza A (H9N2) virus in the middle region of China.
Huang Y1, Li X2, Zhang H1, Chen B3, Jiang Y3, Yang L2, Zhu W2, Hu S1, Zhou S1, Tang Y3, Xiang X1, Li F1, Li W1, Gao L1.
Author information
1Hunan Provincial Center for Disease Control and Prevention, Changsha, China.
2National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
3Yongzhou City Center for Disease Control and Prevention, Yongzhou, China.

Abstract
During the epidemic period of the novel H7N9 viruses, an influenza A (H9N2) virus was isolated from a 7-year-old boy with influenza-like illness in Yongzhou city of Hunan province in November 2013. To identify the possible source of infection, environmental specimens collected from local live poultry markets epidemiologically linked to the human case in Yongzhou city were tested for influenza type A and its subtypes H5, H7, and H9 using real-time RT-PCR methods as well as virus isolation, and four other H9N2 viruses were isolated. The real-time RT-PCR results showed that the environment was highly contaminated with avian influenza H9 subtype viruses (18.0%). Sequencing analyses revealed that the virus isolated from the patient, which was highly similar (98.5-99.8%) to one of isolates from environment in complete genome sequences, was of avian origin. Based on phylogenetic and antigenic analyses, it belonged to genotype S and Y280 lineage. In addition, the virus exhibited high homology (95.7-99.5%) of all six internal gene lineages with the novel H7N9 and H10N8 viruses which caused epidemic and endemic in China. Meanwhile, it carried several mammalian adapted molecular residues including Q226L in HA protein, L13P in PB1 protein, K356R, S409N in PA protein, V15I in M1 protein, I28V, L55F in M2 protein, and E227K in NS protein. These findings reinforce the significance of continuous surveillance of H9N2 influenza viruses. J. Med. Virol. 9999: 1-8, 2015. © 2015 Wiley Periodicals, Inc.


原文链接：http://www.ncbi.nlm.nih.gov/pubmed/25965534