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  1 / 18118 MEDLINE  
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PMID:28855247
Autor:Brooke CB
Dirección:Department of Microbiology and Carl R. Woese Institute for Genomic Biology, University of Illinois, Urbana, Illinois, USA cbrooke@illinois.edu.
Título:Population Diversity and Collective Interactions during Influenza Virus Infection.
Fuente:J Virol; 91(22), 2017 Nov 15.
ISSN:1098-5514
País de publicación:United States
Idioma:eng
Resumen:Influenza A virus (IAV) continues to pose an enormous and unpredictable global public health threat, largely due to the continual evolution of escape from preexisting immunity and the potential for zoonotic emergence. Understanding how the unique genetic makeup and structure of IAV populations influences their transmission and evolution is essential for developing more-effective vaccines, therapeutics, and surveillance capabilities. Owing to their mutation-prone replicase and unique genome organization, IAV populations exhibit enormous amounts of diversity both in terms of sequence and functional gene content. Here, I review what is currently known about the genetic and genomic diversity present within IAV populations and how this diversity may shape the replicative and evolutionary dynamics of these viruses.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (Influenza Vaccines)


  2 / 18118 MEDLINE  
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PMID:28478526
Autor:Ghafouri SA; GhalyanchiLangeroudi A; Maghsoudloo H; Kh Farahani R; Abdollahi H; Tehrani F; Fallah MH
Dirección:Iranian Veterinary Organization, Tehran, Iran.
Título:Clade 2.3.4.4 avian influenza A (H5N8) outbreak in commercial poultry, Iran, 2016: the first report and update data.
Fuente:Trop Anim Health Prod; 49(5):1089-1093, 2017 Jun.
ISSN:1573-7438
País de publicación:United States
Idioma:eng
Resumen:In 2010, H5N8 highly pathogenic avian influenza (HPAI) viruses of the A/Goose/Guangdong/1/1996 lineage dramatically affected poultry and wild birds in Asia, Europe, and North America. In November 2016, HPAI H5N8 was detected in a commercial layer farm in Tehran province. The diagnosis was based on real-time reverse transcriptase PCR (RRT-PCR) and sequencing of haemaglutinin (HA) and neuraminidase (NA) genes from suspected samples. Genetic and phylogenetic analysis of the HA gene demonstrated that the Iranian HPAI H5N8 viruses belong to the HPAI H5 virus clade 2.3.4.4 and cluster within group B (Gochang-like). In particular, the highest similarity was found with the sequences of the HPAI H5N8 identified in Russia in 2016. To our knowledge, this clade has not been previously detected in Iran. Previous HPAI A (H5) epidemic in Iran occurred in 2015 and involved exclusively viruses of clade 2.3.2.1c. These findings indicate that Iran is at high risk of introduction of HPAI H5 of the A/Goose/Guangdong/1/1996 lineage from East Asia and highlight the need to maintain adequate monitoring activities in target wild and domestic bird species for HPAI early detection. This study is useful for better understanding the genetic and antigenic evolution of H5 HPAI viruses in the region and the world.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Hemagglutinins, Viral); EC 3.2.1.18 (Neuraminidase)


  3 / 18118 MEDLINE  
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PMID:28864473
Autor:Desai P; Abboud G; Stanfield J; Thomas PG; Song J; Ware CF; Croft M; Salek-Ardakani S
Dirección:Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32603.
Título:HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity.
Fuente:J Immunol; 199(8):2968-2975, 2017 Oct 15.
ISSN:1550-6606
País de publicación:United States
Idioma:eng
Resumen:Mucosal immunity to reinfection with a highly virulent virus requires the accumulation and persistence of memory CD8 T cells at the site of primary infection. These cells may derive from memory precursor effector cells (MPECs), which are distinct from short-lived effector cells that provide acute protection but are often destined to die. Using respiratory virus infection, we show that herpes virus entry mediator (HVEM; TNFRSF14), a member of the TNF receptor superfamily, provides key signals for MPEC persistence. HVEM-deficient CD8 T cells expanded normally but were skewed away from MPECs with resultant poor development of circulating and lung-resident memory cells. HVEM was selectively expressed on MPECs whereas MPECs deficient in HVEM failed to survive in adoptive transfer recipients. As a consequence, HVEM-deficient recipients failed to afford protection against respiratory reinfection with influenza virus. HVEM therefore represents a critical signal for MPECs and development of protective mucosal CD8 T cell memory.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Tnfrsf14 protein, mouse)


  4 / 18118 MEDLINE  
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PMID:28396461
Autor:Deeg CM; Hassan E; Mutz P; Rheinemann L; Götz V; Magar L; Schilling M; Kallfass C; Nürnberger C; Soubies S; Kochs G; Haller O; Schwemmle M; Staeheli P
Dirección:Institute of Virology, Medical Center University of Freiburg, 79106 Freiburg, Germany.
Título:In vivo evasion of MxA by avian influenza viruses requires human signature in the viral nucleoprotein.
Fuente:J Exp Med; 214(5):1239-1248, 2017 May 01.
ISSN:1540-9538
País de publicación:United States
Idioma:eng
Resumen:Zoonotic transmission of influenza A viruses can give rise to devastating pandemics, but currently it is impossible to predict the pandemic potential of circulating avian influenza viruses. Here, we describe a new mouse model suitable for such risk assessment, based on the observation that the innate restriction factor MxA represents an effective species barrier that must be overcome by zoonotic viruses. Our mouse lacks functional endogenous genes but instead carries the human locus as a transgene. Such transgenic mice were largely resistant to highly pathogenic avian H5 and H7 influenza A viruses, but were almost as susceptible to infection with influenza viruses of human origin as nontransgenic littermates. Influenza A viruses that successfully established stable lineages in humans have acquired adaptive mutations which allow partial MxA escape. Accordingly, an engineered avian H7N7 influenza virus carrying a nucleoprotein with signature mutations typically found in human virus isolates was more virulent in transgenic mice than parental virus, demonstrating that a few amino acid changes in the viral target protein can mediate escape from MxA restriction in vivo. Similar mutations probably need to be acquired by emerging influenza A viruses before they can spread in the human population.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (MX1 protein, human); 0 (Myxovirus Resistance Proteins); 0 (Nucleoproteins)


  5 / 18118 MEDLINE  
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PMID:29020100
Autor:Barauskas O; Xing W; Aguayo E; Willkom M; Sapre A; Clarke M; Birkus G; Schultz BE; Sakowicz R; Kwon H; Feng JY
Dirección:Gilead Sciences, Inc., Foster City, California, United States of America.
Título:Biochemical characterization of recombinant influenza A polymerase heterotrimer complex: Polymerase activity and mechanisms of action of nucleotide analogs.
Fuente:PLoS One; 12(10):e0185998, 2017.
ISSN:1932-6203
País de publicación:United States
Idioma:eng
Resumen:Influenza polymerase is a heterotrimer protein with both endonuclease and RNA-dependent RNA polymerase (RdRp) activity. It plays a critical role in viral RNA replication and transcription and has been targeted for antiviral drug development. In this study, we characterized the activity of recombinant RdRp purified at 1:1:1 ratio in both ApG-primed RNA replication and mRNA-initiated RNA transcription. The heterotrimer complex showed comparable activity profiles to that of viral particle derived crude replication complex, and in contrast to the crude replication complex, was suitable for detailed mechanistic studies of nucleotide incorporation. The recombinant RdRp was further used to examine distinct modes of inhibition observed with five different nucleotide analog inhibitors, and the apparent steady-state binding affinity Kapp was measured for selected analogs to correlate antiviral activity and enzymatic inhibition with substrate efficiency.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Antiviral Agents); 0 (Nucleotides); 0 (Recombinant Proteins); EC 2.7.7.6 (DNA-Directed RNA Polymerases)


  6 / 18118 MEDLINE  
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PMID:28575086
Autor:VanLeuven JT; Ridenhour BJ; Gonzalez AJ; Miller CR; Miura TA
Dirección:Center for Modeling Complex Interactions, University of Idaho, Moscow, Idaho, United States of America.
Título:Lung epithelial cells have virus-specific and shared gene expression responses to infection by diverse respiratory viruses.
Fuente:PLoS One; 12(6):e0178408, 2017.
ISSN:1932-6203
País de publicación:United States
Idioma:eng
Resumen:The severity of respiratory viral infections is partially determined by the cellular response mounted by infected lung epithelial cells. Disease prevention and treatment is dependent on our understanding of the shared and unique responses elicited by diverse viruses, yet few studies compare host responses to viruses from different families while controlling other experimental parameters. Murine models are commonly used to study the pathogenesis of respiratory viral infections, and in vitro studies using murine cells provide mechanistic insight into the pathogenesis observed in vivo. We used microarray analysis to compare changes in gene expression of murine lung epithelial cells infected individually by three respiratory viruses causing mild (rhinovirus, RV1B), moderate (coronavirus, MHV-1), and severe (influenza A virus, PR8) disease in mice. RV1B infection caused numerous gene expression changes, but the differential effect peaked at 12 hours post-infection. PR8 altered an intermediate number of genes whose expression continued to change through 24 hours. MHV-1 had comparatively few effects on host gene expression. The viruses elicited highly overlapping responses in antiviral genes, though MHV-1 induced a lower type I interferon response than the other two viruses. Signature genes were identified for each virus and included host defense genes for PR8, tissue remodeling genes for RV1B, and transcription factors for MHV-1. Our comparative approach identified universal and specific transcriptional signatures of virus infection that can be used to distinguish shared and virus-specific mechanisms of pathogenesis in the respiratory tract.
Tipo de publicación:JOURNAL ARTICLE


  7 / 18118 MEDLINE  
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PMID:28433538
Autor:Panthu B; Terrier O; Carron C; Traversier A; Corbin A; Balvay L; Lina B; Rosa-Calatrava M; Ohlmann T
Dirección:CIRI, International Center for Infectiology Research, Université de Lyon, 69364 Lyon, France; Inserm, U1111, 69364 Lyon, France; Ecole Normale Supérieure de Lyon, 69364 Lyon, France; Université Lyon 1, Centre International de Recherche en Infectiologie, 69364 Lyon, France; CNRS, UMR5308, 69364 Lyon,
Título:The NS1 Protein from Influenza Virus Stimulates Translation Initiation by Enhancing Ribosome Recruitment to mRNAs.
Fuente:J Mol Biol; 429(21):3334-3352, 2017 Oct 27.
ISSN:1089-8638
País de publicación:England
Idioma:eng
Resumen:The non-structural protein NS1 of influenza A viruses exerts pleiotropic functions during infection. Among these functions, NS1 was shown to be involved in the control of both viral and cellular translation; however, the mechanism by which this occurs remains to be determined. Thus, we have revisited the role of NS1 in translation by using a combination of influenza infection, mRNA reporter transfection, and in vitro functional and biochemical assays. Our data show that the NS1 protein is able to enhance the translation of virtually all tested mRNAs with the exception of constructs bearing the Dicistroviruses Internal ribosome entry segment (IRESes) (DCV and CrPV), suggesting a role at the level of translation initiation. The domain of NS1 required for translation stimulation was mapped to the RNA binding amino-terminal motif of the protein with residues R38 and K41 being critical for activity. Although we show that NS1 can bind directly to mRNAs, it does not correlate with its ability to stimulate translation. This activity rather relies on the property of NS1 to associate with ribosomes and to recruit them to target mRNAs.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (INS1 protein, influenza virus); 0 (RNA, Messenger); 0 (RNA, Viral); 0 (Viral Nonstructural Proteins)


  8 / 18118 MEDLINE  
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PMID:28321029
Autor:Shimoda H; VAN Nguyen D; Yonemitsu K; Minami S; Nagata N; Hara N; Kuwata R; Murakami S; Kodera Y; Takeda T; Yoshikawa Y; Horimoto T; Maeda K
Dirección:Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
Título:Influenza A virus infection in Japanese wild boars (Sus scrofa leucomystax).
Fuente:J Vet Med Sci; 79(5):848-851, 2017 May 03.
ISSN:1347-7439
País de publicación:Japan
Idioma:eng
Resumen:Serum samples were collected from 385 wild boars between 2010 and 2013 to examine the seroprevalence of influenza A virus (IAV) in Japan. Antibodies against IAV were identified using a commercial kit in 13 wild boars (3.4%). To identify the serotypes, positive sera were examined by virus-neutralization test using representative serotypes and strains. Three wild boars in Yamaguchi and four in Tochigi showed the highest antibody titers against the pandemic H1N1 2009 virus and classical swine H1N1 virus strains, respectively. These data indicate that wild boars may have close contact with humans and domestic pigs and therefore that there is potential for IAVs to reassort in wild boars as they have been shown to do in pigs.
Tipo de publicación:JOURNAL ARTICLE


  9 / 18118 MEDLINE  
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PMID:28770344
Autor:Root JJ; Shriner SA; Ellis JW; VanDalen KK; Sullivan HJ
Dirección:United States Department of Agriculture, National Wildlife Research Center, 4101 La Porte Avenue, Fort Collins, CO, 80521, USA. Jeff.root@aphis.usda.gov.
Título:Low viral doses are sufficient to infect cottontail rabbits with avian influenza A virus.
Fuente:Arch Virol; 162(11):3381-3388, 2017 Nov.
ISSN:1432-8798
País de publicación:Austria
Idioma:eng
Resumen:Influenza A viruses (IAVs) have been reported in wild lagomorphs in environments where they share resources with waterfowl. Recent studies have conclusively shown that a North American lagomorph, cottontail rabbits (Sylvilagus sp.), become infected following exposure to IAVs and can shed significant quantities of virus. However, the minimum infectious dose and the efficiency of various routes of infection have not been evaluated. Thirty-six cottontail rabbits were used in a dose response study assessing both the oral and nasal routes of infection. The nasal route of infection proved to be the most efficient, as all cottontail rabbits shed viral RNA following inoculation with doses as low as 10 EID . The oral route of infection was less efficient, but still produced infection rates of ≥ 50% at relatively low doses (i.e., 10 and 10 EID ). These results suggest that cottontail rabbits are highly susceptible to IAVs at low exposure doses that have been routinely observed in environments contaminated by waterfowl. Furthermore, this study supports earlier observations that cottontail rabbits may pose a biosecurity risk to poultry operations, as a virus-contaminated water source or contaminated environment, even at low viral titers, could be sufficient to initiate viral replication in cottontail rabbits.
Tipo de publicación:JOURNAL ARTICLE


  10 / 18118 MEDLINE  
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PMID:28736803
Autor:Lee IH; Jin SY; Seo SH
Dirección:Laboratory of Influenza Research, College of Veterinary Medicine, Chungnam National University, Daejeon, 34134, Republic of Korea.
Título:Genetic and pathogenic analysis of a novel reassortant H5N6 influenza virus isolated from waterfowl in South Korea in 2016.
Fuente:Arch Virol; 162(11):3507-3510, 2017 Nov.
ISSN:1432-8798
País de publicación:Austria
Idioma:eng
Resumen:A novel reassortant highly pathogenic H5N6 influenza virus was isolated from waterfowl in South Korea in 2016. Seven genes of this virus originated from an H5N6 virus from China, whereas the remaining gene, PB1, was from an unknown virus. This virus productively infected pigs, which showed viral shedding through their noses and developed severe interstitial pneumonia.
Tipo de publicación:JOURNAL ARTICLE



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