Infectious #cDNA #clones of two #strains of #Mayaro virus for studies on viral #pathogenesis and #vaccine development (Virology, abstract)

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

Virology. 2019 Jul 14;535:227-231. doi: 10.1016/j.virol.2019.07.013. [Epub ahead of print]

Infectious cDNA clones of two strains of Mayaro virus for studies on viral pathogenesis and vaccine development.

Chuong C1, Bates TA1, Weger-Lucarelli J2.

Author information: 1 Department of Biomedical Sciences and Pathobiology, Virginia Tech, VA-MD Regional College of Veterinary Medicine, Blacksburg, VA, USA. 2 Department of Biomedical Sciences and Pathobiology, Virginia Tech, VA-MD Regional College of Veterinary Medicine, Blacksburg, VA, USA. Electronic address: weger@vt.edu.

 

Abstract

Mayaro virus (MAYV; family Togaviridae, genus Alphavirus) is an emerging global threat that can cause severe clinical manifestations similar to Zika, dengue, and chikungunya viruses. Currently, there is a lack of molecular tools to enable a better understanding of the transmission and pathogenesis of MAYV. Here, we detail the development and characterization of infectious clones of two strains of MAYV that produce infectious virus and replicate in mammalian and mosquito cells similarly to wild-type virus. Additionally, clone-derived viruses produced identical infection rates and phenotypes in CD-1 mice compared to the parental strains. This infectious clone system will provide a resource to the research community to analyze MAYV genetic determinants of virulence, determine vector competence, and develop vaccines.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS: Alphavirus; Infectious clones; Mayaro virus

PMID: 31325837 DOI: 10.1016/j.virol.2019.07.013

Keywords: Alphavirus; Togavirus; Mayaro virus; Viral pathogenesis.

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The #PB2 and M genes of #genotype S #H9N2 virus contribute to the enhanced #fitness of #H5Nx and #H7N9 #avian #influenza viruses in chickens (Virology, abstract)

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

Virology. 2019 Jul 8;535:218-226. doi: 10.1016/j.virol.2019.07.001. [Epub ahead of print]

The PB2 and M genes of genotype S H9N2 virus contribute to the enhanced fitness of H5Nx and H7N9 avian influenza viruses in chickens.

Hao X1, Wang X1, Hu J1, Gu M1, Wang J1, Deng Y1, Jiang D1, He D1, Xu H1, Yang Y1, Hu Z1, Chen S1, Hu S1, Liu X1, Shang S1, Peng D1, Jiao X2, Liu X3.

Author information: 1 Animal Infectious Disease Laboratory, School of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, Yangzhou University, Yangzhou, Jiangsu, China; Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agri-food Safety and Quality, Ministry of Agriculture of China, Yangzhou University, Yangzhou, Jiangsu, China. 2 Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, Yangzhou University, Yangzhou, Jiangsu, China; Jiangsu Key Laboratory of Zoonosis, Yangzhou University, Yangzhou, Jiangsu, China; Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agri-food Safety and Quality, Ministry of Agriculture of China, Yangzhou University, Yangzhou, Jiangsu, China. 3 Animal Infectious Disease Laboratory, School of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, Yangzhou University, Yangzhou, Jiangsu, China; Jiangsu Key Laboratory of Zoonosis, Yangzhou University, Yangzhou, Jiangsu, China; Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agri-food Safety and Quality, Ministry of Agriculture of China, Yangzhou University, Yangzhou, Jiangsu, China. Electronic address: xfliu@yzu.edu.cn.

 

Abstract

Genotype S H9N2 viruses frequently donate their internal genes to facilitate the generation of novel influenza viruses, e.g., H5N6, H7N9, and H10N8, which have caused human infection. Genotype S was originated from the replacement of F/98-like M and PB2 genes of the genotype H with those from G1-like lineage. However, whether this gene substitution will influence the viral fitness of emerging influenza viruses remains unclear. We found that H5Nx and H7N9 viruses with G1-like PB2 or M gene exhibited higher virulence and replication than those with F/98-like PB2 or M in chickens. We also determined the functional significance of G1-like PB2 in conferring increased polymerase activity and improved nucleus transportation efficiency, and facilitated RNP nuclear export by G1-like M. Our results suggest that G1-like PB2 and M genes optimize viral fitness, and thus play a crucial role in the genesis of emerging influenza viruses that cause rising prevalence in chickens.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS: Avian influenza virus; Chickens; G1-like PB2 and M; H5Nx; H7N9; Viral fitness

PMID: 31325836  DOI: 10.1016/j.virol.2019.07.001

Keywords: Avian Influenza; H9N2; H5N6; H10N8; H7N9; Reassortant strain; Poultry.

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Identification of key #hemagglutinin #residues responsible for #cleavage, acid stability, and #virulence of fifth-wave highly pathogenic #avian #influenza A(#H7N9) viruses (Virology, abstract)

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

Virology. 2019 Jul 12;535:232-240. doi: 10.1016/j.virol.2019.07.012. [Epub ahead of print]

Identification of key hemagglutinin residues responsible for cleavage, acid stability, and virulence of fifth-wave highly pathogenic avian influenza A(H7N9) viruses.

Sun X1, Belser JA1, Yang H1, Pulit-Penaloza JA1, Pappas C1, Brock N2, Zeng H1, Creager HM1, Stevens J1, Maines TR3.

Author information: 1 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. 2 CNI Advantage LLC, Norman, OK, USA. 3 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. Electronic address: tmaines@cdc.gov.

 

Abstract

We previously demonstrated that despite no airborne transmissibility increase compared to low pathogenic avian influenza viruses, select human isolates of highly pathogenic avian influenza A(H7N9) virus exhibit greater virulence in animal models and a lower threshold pH for fusion. In the current study, we utilized both in vitro and in vivo approaches to identify key residues responsible for hemagglutinin (HA) intracellular cleavage, acid stability, and virulence in mice. We found that the four amino acid insertion (-KRTA-) at the HA cleavage site of A/Taiwan/1/2017 virus is essential for HA intracellular cleavage and contributes to disease in mice. Furthermore, a lysine to glutamic acid mutation at position HA2-64 increased the threshold pH for HA activation, reduced virus stability, and replication in mice. Identification of a key residue responsible for enhanced acid stability of A(H7N9) viruses is of great significance for future surveillance activities and improvements in vaccine stability.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS: A(H7N9); Acid stability; Fusion; Hemagglutinin cleavage; Influenza virus; Mice; Virulence

PMID: 31325838 DOI: 10.1016/j.virol.2019.07.012

Keywords: Avian Influenza; H7N9; Viral pathogenesis; Animal models.

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#Recombinant subunit #vaccines protect guinea pigs from lethal #Ebola virus challenge (Vaccine, abstract)

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

Vaccine. 2019 Jul 16. pii: S0264-410X(19)30797-2. doi: 10.1016/j.vaccine.2019.06.035. [Epub ahead of print]

Recombinant subunit vaccines protect guinea pigs from lethal Ebola virus challenge.

Lehrer AT1, Wong TS2, Lieberman MM3, Johns L2, Medina L3, Feldmann F4, Feldmann H5, Marzi A6.

Author information: 1 PanThera Biopharma, LLC, Aiea, HI 96701, United States; University of Hawaii at Manoa, John A. Burns School of Medicine, Honolulu, HI 96813, United States. Electronic address: lehrer@hawaii.edu. 2 PanThera Biopharma, LLC, Aiea, HI 96701, United States; University of Hawaii at Manoa, John A. Burns School of Medicine, Honolulu, HI 96813, United States. 3 University of Hawaii at Manoa, John A. Burns School of Medicine, Honolulu, HI 96813, United States. 4 Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, United States. 5 Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, United States. 6 Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, United States. Electronic address: marzia@niaid.nih.gov.

 

Abstract

Ebola virus (EBOV) is among the deadliest pathogens known to man causing infrequent outbreaks of hemorrhagic disease. In humans, the case fatality rates in the outbreaks can reach 90%. During the West African epidemic almost 30,000 people were infected and of these over 11,000 fatalities were reported. Currently, we are facing an uncontained larger outbreak in the Democratic Republic of the Congo. Even though EBOV was discovered in 1976, extensive efforts to develop countermeasures, particularly therapeutics and vaccines, started late and there is still no FDA-approved product available. Nevertheless, one candidate vaccine, the rVSV-ZEBOV, is being used in clinical trials during the current outbreak with the hope of ending the human transmission chains. However, adverse reactions to administration of some EBOV vaccines have been reported; therefore, we have developed a safe and efficacious formulation of insect-cell derived adjuvanted protein vaccines. Vaccine candidates containing the EBOV glycoprotein with or without matrix proteins VP24 and VP40 formulated with one of three different adjuvants were tested in guinea pigs for immunogenicity and efficacy against lethal EBOV challenge. The results demonstrated that these vaccine candidates engendered high titers of antigen-specific antibodies in immunized animals and two of these vaccine candidates afforded complete or nearly complete protection against lethal challenge. Interestingly, we found a sex bias in partially protected immunized groups with male guinea pigs succumbing to disease and females surviving. In summary, we developed a safe and immunogenic adjuvanted subunit vaccine uniformly protective against EBOV disease in guinea pigs.

Copyright © 2019 Elsevier Ltd. All rights reserved.

KEYWORDS: Glycoprotein; Recombinant protein; VP24; VP40; Zaire ebolavirus

PMID: 31324500 DOI: 10.1016/j.vaccine.2019.06.035

Keywords: Ebola; ZEBOV; Vaccines; Animal models.

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The Long-Lasting #Influenza: The #Impact of #Fetal #Stress During the 1918 Influenza #Pandemic on #Socioeconomic Attainment and Health in #Sweden, 1968-2012 (Demography, abstract)

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

Demography. 2019 Jul 19. doi: 10.1007/s13524-019-00799-x. [Epub ahead of print]

The Long-Lasting Influenza: The Impact of Fetal Stress During the 1918 Influenza Pandemic on Socioeconomic Attainment and Health in Sweden, 1968-2012.

Helgertz J1,2, Bengtsson T3,4,5.

Author information: 1 Centre for Economic Demography (CED) and Department of Economic History, Lund University, Box 7083, 220 07, Lund, Sweden. Jonas.Helgertz@ekh.lu.se. 2 Minnesota Population Center, University of Minnesota, 50 Willey Hall, 225 19th Avenue South, Minneapolis, MN, 55455, USA. Jonas.Helgertz@ekh.lu.se. 3 Centre for Economic Demography (CED) and Department of Economic History, Lund University, Box 7083, 220 07, Lund, Sweden. 4 IZA, Institute of Labor Economics, Schaumburg-Lippe-Strasse 5-9, 53113, Bonn, Germany. 5 CEPR, Centre for Economic Policy Research, 33 Great Sutton Street, London, EC1V 0DX, UK.

 

Abstract

The 1918 influenza pandemic had not only a massive instant death toll but also lasting effects on its survivors. Several studies have shown that children born in 1919, and thus exposed to the H1N1 virus in utero, experienced worse health and socioeconomic outcomes in older ages than surrounding birth cohorts. This study combines several sources of contemporary statistics with full-population individual-level data for Sweden during 1968-2012 to examine the influence of fetal exposure to the Spanish flu on health, adulthood income, and occupational attainment. For both men and women, fetal exposure resulted in higher morbidity in ages 54-87, as measured by hospitalization. For males, exposure during the second trimester also affected mortality in cancer and heart disease. Overall, the effects on all-cause mortality were modest, with about three months shorter remaining life expectancy for the cohorts exposed during the second trimester. For socioeconomic outcomes, results fail to provide consistent evidence supporting any long-term consequences of fetal exposure. We conclude that although the immediate health effects of exposure to the 1918 pandemic were huge, the long-term effects were modest in size.

KEYWORDS: Fetal origins; Health and socioeconomic outcomes; Longitudinal data; Spanish influenza pandemic; Sweden

PMID: 31325150 DOI: 10.1007/s13524-019-00799-x

Keywords: Pandemic Influenza; Spanish Flu; Sweden; Society.

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Attack on Spanish Treasure Galleys, Portugal, Hendrick Cornelisz Vroom (1602)

Annotazione 2019-07-20 185928

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Attack on Spanish Treasure Galleys, Portugal
Hendrick Cornelisz Vroom
Date: 1602
Style: Baroque
Genre: battle painting

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Permissions: Public Domain.

Source: WikiArt, full page: https://www.wikiart.org/en/hendrick-cornelisz-vroom/attack-on-spanish-treasure-galleys-portugal-1602

 

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