#Influenza A (#H3) #Outbreak at a #Hurricane #Harvey #Megashelter in Harris County, #Texas: Successes and Challenges in Disease Identification and Control Measure Implementation (Disaster Med Public Health Prep., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Disaster Med Public Health Prep. 2019 Feb;13(1):97-101. doi: 10.1017/dmp.2018.159.

Influenza A (H3) Outbreak at a Hurricane Harvey Megashelter in Harris County, Texas: Successes and Challenges in Disease Identification and Control Measure Implementation.

Liu L1, Haynie A1, Jin S1, Zangeneh A1, Bakota E1, Hornstein BD1, Beckham D1, Reed BC1, Kiger J1, McClendon M1, Perez E1, Schaffer M1, Becker L1, Shah UA1.

Author information: 1 Harris County Public Health,Houston, Texas (Dr. Aisha Haynie is no longer affiliated with the agency).

 

Abstract

When Hurricane Harvey landed along the Texas coast on August 25, 2017, it caused massive flooding and damage and displaced tens of thousands of residents of Harris County, Texas. Between August 29 and September 23, Harris County, along with community partners, operated a megashelter at NRG Center, which housed 3365 residents at its peak. Harris County Public Health conducted comprehensive public health surveillance and response at NRG, which comprised disease identification through daily medical record reviews, nightly “cot-to-cot” resident health surveys, and epidemiological consultations; messaging and communications; and implementation of control measures including stringent isolation and hygiene practices, vaccinations, and treatment. Despite the lengthy operation at the densely populated shelter, an early seasonal influenza A (H3) outbreak of 20 cases was quickly identified and confined. Influenza outbreaks in large evacuation shelters after a disaster pose a significant threat to populations already experiencing severe stressors. A holistic surveillance and response model, which consists of coordinated partnerships with onsite agencies, in-time epidemiological consultations, predesigned survey tools, trained staff, enhanced isolation and hygiene practices, and sufficient vaccines, is essential for effective disease identification and control. The lessons learned and successes achieved from this outbreak may serve for future disaster response settings. (Disaster Med Public Health Preparedness. 2019;13:97-101).

KEYWORDS: Hurricane Harvey; influenza outbreak; shelter surveillance and response

PMID: 30841952 DOI: 10.1017/dmp.2018.159 [Indexed for MEDLINE]

Keywords: Seasonal Influenza; H3N2; Disaster preparedness; Hurricanes; USA; Texas.

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#Virological #Surveillance of #Influenza in the eight #epidemic seasons after the 2009 #pandemic in Emilia-Romagna (Northern #Italy) (Acta Biomed., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Acta Biomed. 2019 Sep 13;90(9-S):35-44. doi: 10.23750/abm.v90i9-S.8722.

Virological Surveillance of Influenza in the eight epidemic seasons after the 2009 pandemic in Emilia-Romagna (Northern Italy).

Affanni P1, Colucci ME, Bracchi MT, Capobianco E, Zoni R, Caruso L, Castrucci MR, Puzelli S, Cantarelli A, Veronesi L.

Author information: 1 Department of Medicine and Surgery, University of Parma, Italy. paola.affanni@unipr.it.

 

Abstract

BACKGROUND AND AIM OF THE WORK:

Influenza virological surveillance is essential for monitoring the evolution of influenza viruses (IVs) as well as for annual updating of the vaccine composition. The aim of this study is to analyse IVs circulation in Emilia-Romagna during the eight epidemic seasons after the 2009 pandemic and to evaluate their match with seasonal vaccine strains.

METHODS:

A total of 7882 respiratory specimens from patients with influenza-like illness (ILI), were collected by regional sentinel practitioners and hospital physicians. Viral investigations were conducted by rRT-PCR assay. Genetic characterization was performed for a spatial-temporal representative number of influenza laboratory-confirmed specimens.

RESULTS:

Influenza-positive samples per season ranged between 28.9% (2013-2014) and 66.8% (2012-2013). Co-circulation of IVs type A and type B was observed in all seasons, although with a different intensity. In all seasons, the highest number of positive samples was recorded in younger patients aged 5-14 years with relative frequencies ranging from 40% in the 2013-2014 season and 78% in the 2012-2013 season. Since the 2009 pandemic, A/H1N1pdm09 IVs circulating were closely related to the vaccine strain A/California/7/2009. Antigenic mismatch between vaccine strain and A/H3N2 IVs was observed in the 2011-2012 and 2014-2015 seasons. During 2015-2016, 2016-2017 and 2017-2018 seasons a complete or nearly complete mismatch between the predominant influenza B lineage of IVs type B circulating and vaccine B lineage occurred.

CONCLUSIONS:

This analysis confirms the importance of the virological surveillance and highlights the need of a continuous monitoring of IVs circulation, to improve the most appropriate vaccination strategies. (www.actabiomedica.it).

PMID: 31517888 DOI: 10.23750/abm.v90i9-S.8722

Keywords: Seasonal Influenza; H1N1pdm09; H3N2; Influenza B; Italy.

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#Growth activation of #influenza virus by #trypsin and effect of T-705 (#favipiravir) on trypsin-optimized growth condition (Acta Virol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Acta Virol. 2019;63(3):309-315. doi: 10.4149/av_2019_311.

Growth activation of influenza virus by trypsin and effect of T-705 (favipiravir) on trypsin-optimized growth condition.

Daikoku T, Okuda T, Kawai M, Morita N, Tanaka T, Takemoto M, Fukuda Y, Takahashi K, Nomura N, Shiraki K.

 

Abstract

Influenza virus is activated by proteolytic cleavage of hemagglutinin by trypsin. After determining the optimal trypsin concentration, intracellular and extracellular influenza A/PR/8/34 (H1N1) and A/Victoria/361/2011 (H3N2) virus productions were compared in cultures treated with T-705 (favipiravir) and GS 4071 (an active form of oseltamivir). Although both drugs efficiently inhibited extracellular viral RNA release in a dose-dependent manner, T-705 inhibited it to the level of the inoculum without trypsin treatment, while GS 4071 inhibited it to a final level 10 times higher than that without trypsin. T-705 inhibited intracellular viral RNA production to the level of input virus in both trypsin-treated and untreated cells. In contrast, GS 4071 dose-dependently inhibited intracellular viral RNA production in cells treated with trypsin but allowed viral RNA synthesis. The level of maximum inhibition by GS 4071 was 10 times higher than that of cells without trypsin and 1,000 times greater than the inoculum titer in cells without trypsin. T-705 inhibited both intracellular and extracellular virus production 1,000 and 10 times more strongly, respectively, than GS 4071. T-705 has powerful anti-influenza activity in the absence of trypsin and even in the trypsin-optimized growth condition, suggesting the therapeutic advantage in treatment of influenza complicated with bacterial pneumonia.

Keywords: influenza; T-705; Tamiflu; trypsin; bacterial trypsin-like protease.

PMID: 31507197 DOI: 10.4149/av_2019_311

Keywords: Influenza A; H1N1; H3N2; Antivirals; Favipiravir; Oseltamivir.

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#Influenza Viruses in #Mice: Deep #Sequencing Analysis of Serial Passage and Effects of #Sialic Acid Structural #Variation (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

Influenza Viruses in Mice: Deep Sequencing Analysis of Serial Passage and Effects of Sialic Acid Structural Variation

Brian R. Wasik, Ian E.H. Voorhees, Karen N. Barnard, Brynn K. Alford-Lawrence, Wendy S. Weichert, Grace Hood, Aitor Nogales, Luis Martínez-Sobrido, Edward C. Holmes, Colin R. Parrish

DOI: 10.1128/JVI.01039-19

 

ABSTRACT

Influenza A viruses have regularly jumped to new host species to cause epidemics or pandemics, an evolutionary process that involves variation in the viral traits necessary to overcome host barriers and facilitate transmission. Mice are not a natural host for influenza virus, but are frequently used as models in studies of pathogenesis, often after multiple passages to achieve higher viral titers that result in clinical disease such as weight loss or death. Here we examine the processes of influenza A virus infection and evolution in mice by comparing single nucleotide variation of a human H1N1 pandemic virus, a seasonal H3N2 virus, and a H3N2 canine influenza virus during experimental passage. We also compared replication and sequence variation in wild-type mice expressing N-glycolylneuraminic acid (Neu5Gc) with that seen in mice expressing only N-acetylneuraminic acid (Neu5Ac). Viruses derived from plasmids were propagated in MDCK cells and then passaged in mice up to four times. Full genome deep sequencing of the plasmids, cultured viruses, and viruses from mice at various passages revealed only small numbers of mutational changes. The H3N2 canine influenza virus showed increases in frequency of sporadic mutations in the PB2, PA, and NA segments. The H1N1 pandemic virus grew well in mice, and while it exhibited the maintenance of some minority mutations, there was no clear evidence for adaptive evolution. The H3N2 seasonal virus did not establish in the mice. Finally, there were no clear sequence differences associated with the presence or absence of Neu5Gc.

 

SIGNIFICANCE

Mice are commonly used as a model to study the growth and virulence of influenza A viruses in mammals, but are not a natural host and have distinct sialic acid receptor profiles compared to humans. Using experimental infections with different subtypes of influenza A virus derived from different hosts we found that evolution of influenza A virus in mice did not necessarily proceed through the linear accumulation of host-adaptive mutations, that there was variation in the patterns of mutations detected in each repetition, and the mutation dynamics depended on the virus examined. In addition, variation in the viral receptor, sialic acid, did not affect influenza evolution in this model. Overall, our results show that while mice provide a useful animal model for influenza pathology, host passage evolution will vary depending on the specific virus tested.

Copyright © 2019 American Society for Microbiology. All Rights Reserved.

Keywords: Influenza A; H1N1pdm09; H3N2; Animal models.

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#Vaccination With Viral Vectors Expressing Chimeric #Hemagglutinin, NP and M1 #Antigens Protects Ferrets Against #Influenza Virus Challenge (Front Immunol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Front Immunol. 2019 Aug 21;10:2005. doi: 10.3389/fimmu.2019.02005. eCollection 2019.

Vaccination With Viral Vectors Expressing Chimeric Hemagglutinin, NP and M1 Antigens Protects Ferrets Against Influenza Virus Challenge.

McMahon M1, Asthagiri Arunkumar G1,2, Liu WC1,3, Stadlbauer D1,4, Albrecht RA1,3, Pavot V5, Aramouni M5, Lambe T5, Gilbert SC5, Krammer F1.

Author information: 1 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 2 Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 3 Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States. 4 Department of Biotechnology, University of Natural Resources and Life Sciences, Vienna, Austria. 5 The Jenner Institute, University of Oxford, Oxford, United Kingdom.

 

Abstract

Seasonal influenza viruses cause significant morbidity and mortality in the global population every year. Although seasonal vaccination limits disease, mismatches between the circulating strain and the vaccine strain can severely impair vaccine effectiveness. Because of this, there is an urgent need for a universal vaccine that induces broad protection against drifted seasonal and emerging pandemic influenza viruses. Targeting the conserved stalk region of the influenza virus hemagglutinin (HA), the major glycoprotein on the surface of the virus, results in the production of broadly protective antibody responses. Furthermore, replication deficient viral vectors based on Chimpanzee Adenovirus Oxford 1 (ChAdOx1) and modified vaccinia Ankara (MVA) virus expressing the influenza virus internal antigens, the nucleoprotein (NP) and matrix 1 (M1) protein, can induce strong heterosubtypic influenza virus-specific T cell responses in vaccinated individuals. Here, we combine these two platforms to evaluate the efficacy of a viral vectored vaccination regimen in protecting ferrets from H3N2 influenza virus infection. We observed that viral vectored vaccines expressing both stalk-targeting, chimeric HA constructs, and the NP+M1 fusion protein, in a prime-boost regimen resulted in the production of antibodies toward group 2 HAs, the HA stalk, NP and M1, as well as in induction of influenza virus-specific-IFNγ responses. The immune response induced by this vaccination regime ultimately reduced viral titers in the respiratory tract of influenza virus infected ferrets. Overall, these results improve our understanding of vaccination platforms capable of harnessing both cellular and humoral immunity with the goal of developing a universal influenza virus vaccine.

KEYWORDS: CD8 T-cells; influenza; stalk antibodies; universal influenza virus vaccine; vectored vaccine

PMID: 31497029 PMCID: PMC6712942 DOI: 10.3389/fimmu.2019.02005

Keywords: Influenza A; Vaccines; Animal models.

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#H3N2 #avian #influenza viruses detected in live #poultry #markets in #China bind to #human-type #receptors and transmit in guinea pigs and ferrets (Emerg Microbes Infect., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Emerg Microbes Infect. 2019;8(1):1280-1290. doi: 10.1080/22221751.2019.1660590.

H3N2 avian influenza viruses detected in live poultry markets in China bind to human-type receptors and transmit in guinea pigs and ferrets.

Guan L1, Shi J1, Kong X1, Ma S1, Zhang Y1, Yin X1, He X1, Liu L1, Suzuki Y2, Li C1, Deng G1, Chen H1.

Author information: 1 State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, CAAS , Harbin , People’s Republic of China. 2 College of Life and Health Sciences, Chubu University , Aichi , Japan.

 

Abstract

The H3N2 influenza viruses became widespread in humans during the 1968 H3N2 pandemic and have been a major cause of influenza epidemics ever since. Different lineages of H3N2 influenza viruses are also commonly found in animals. If a different lineage of H3N2 virus jumps to humans, a human influenza pandemic could occur with devastating consequences. Here, we studied the genetics, receptor-binding properties, and replication and transmission in mammals of 15 H3N2 avian influenza viruses detected in live poultry markets in China. We found that the H3N2 avian influenza viruses are complicated reassortants with distinct replication phenotypes in mice. Five viruses replicated efficiently in mice and bound to both human-type and avian-type receptors. These viruses transmitted efficiently to direct-contact guinea pigs, and three of them also transmitted among guinea pigs and ferrets via respiratory droplets. Moreover, ferret antiserum induced by human H3N2 viruses did not react with any of the H3N2 avian influenza viruses. Our study demonstrates that the H3N2 avian influenza viruses pose a clear threat to human health and emphasizes the need for continued surveillance and evaluation of the H3N2 influenza viruses circulating in nature.

KEYWORDS: Avian influenza virus; H3N2; ferret; guinea pig; transmission

PMID: 31495283 DOI: 10.1080/22221751.2019.1660590

Keywords: Avian Influenza; H3N2; Reassortant strain; Poultry; Live poultry markets; China.

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#Antigenic #pressure on #H3N2 #influenza #drift strains imposes constraints on binding to sialylated receptors, but not phosphorylated glycans (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

Antigenic pressure on H3N2 influenza drift strains imposes constraints on binding to sialylated receptors, but not phosphorylated glycans

Lauren Byrd-Leotis, Chao Gao, Nan Jia, Akul Mehta, Jessica Trost, Sandra F. Cummings, Jamie Heimburg-Molinaro, Richard D. Cummings, David A. Steinhauer

DOI: 10.1128/JVI.01178-19

 

ABSTRACT

H3N2 strains of influenza A virus emerged in humans in 1968 and have continued to circulate, evolving in response to human immune pressure. During this process of “antigenic drift,” viruses have progressively lost the ability to agglutinate erythrocytes of various species and to replicate efficiently under the established conditions for amplifying clinical isolates and generating vaccine candidates. We have determined the glycome profiles of chicken and guinea pig erythrocytes to gain insights into reduced agglutination properties displayed by drifted strains and show that both contain complex sialylated N-glycans, but they differ with respect to the extent of branching, core fucosylation, and the abundance of poly-N-acetyllactosamine (PL) [-3Galβ1-4GlcNAcβ1-]n structures. We also examined binding of the H3N2 viruses using three different glycan microarrays: the synthetic Consortium for Functional Glycomics array, the defined N-glycan array designed to reveal contributions to binding based on sialic acid linkage type, branched structures, and core modifications, and the human lung shotgun glycan microarray. The results demonstrate that H3N2 viruses have progressively lost their capacity to bind nearly all canonical sialylated receptors other than a selection of bi-antennary structures and PL structures with or without sialic acid. Significantly, all viruses displayed robust binding to non-sialylated high mannose phosphorylated glycans, even as the recognition of sialylated structures is decreased through antigenic drift.

 

Importance

Influenza H3N2 subtype viruses have circulated in humans for over 50 years, continuing to cause annual epidemics. Such viruses have undergone antigenic drift in response to immune pressure, reducing the protective effects of pre-existing immunity to previously circulating H3N2 strains. The changes in HA affiliated with drift have implications for the receptor binding properties of these viruses, affecting virus replication in culture systems commonly used to generate and amplify vaccine strains. Therefore, the antigenic properties of the vaccines may not directly reflect those of the circulating strains from which they were derived, compromising vaccine efficacy. In order to reproducibly provide effective vaccines, it will be critical to understand the interrelationships between binding, antigenicity, and replication properties in different growth substrates.

Copyright © 2019 Byrd-Leotis et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

Keywords: Seasonal Influenza; H3N2.

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