Response Modifiers: Tweaking the Immune Response Against Influenza A Virus

被引:13
作者
Elbahesh, Husni [1 ]
Gerlach, Thomas [1 ]
Saletti, Giulietta [1 ]
Rimmelzwaan, Guus F. [1 ]
机构
[1] Univ Vet Med TiHo, Res Ctr Emerging Infect & Zoonoses, Hannover, Germany
来源
FRONTIERS IN IMMUNOLOGY | 2019年 / 10卷
关键词
influenza; treatment; response modifiers; antiviral; immune response; immunomodulators; ACTIVATED PROTEIN-KINASE; FOCAL ADHESION KINASE; PANDEMIC INFLUENZA; TREATING INFLUENZA; ANTIVIRAL ACTIVITY; INNATE IMMUNITY; H7N9; VIRUS; IN-VITRO; C-JUN; INFECTION;
D O I
10.3389/fimmu.2019.00809
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Despite causing pandemics and yearly epidemics that result in significant morbidity and mortality, our arsenal of options to treat influenza A virus (IAV) infections remains limited and is challenged by the virus itself. While vaccination is the preferred intervention strategy against influenza, its efficacy is reduced in the elderly and infants who are most susceptible to severe and/or fatal infections. In addition, antigenic variation of IAV complicates the production of efficacious vaccines. Similarly, effectiveness of currently used antiviral drugs is jeopardized by the development of resistance to these drugs. Like many viruses, IAV is reliant on host factors and signaling-pathways for its replication, which could potentially offer alternative options to treat infections. While host-factors have long been recognized as attractive therapeutic candidates against other viruses, only recently they have been targeted for development as IAV antivirals. Future strategies to combat IAV infections will most likely include approaches that alter host-virus interactions on the one hand or dampen harmful host immune responses on the other, with the use of biological response modifiers (BRMs). In principle, BRMs are biologically active agents including antibodies, small peptides, and/or other (small) molecules that can influence the immune response. BRMs are already being used in the clinic to treat malignancies and autoimmune diseases. Repurposing such agents would allow for accelerated use against severe and potentially fatal IAV infections. In this review, we will address the potential therapeutic use of different BRM classes to modulate the immune response induced after IAV infections.
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页数:8
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  • [1] Network-Guided Discovery of Influenza Virus Replication Host Factors
    Ackerman, Emily E.
    Kawakami, Eiryo
    Katoh, Manami
    Watanabe, Tokiko
    Watanabe, Shinji
    Tomita, Yuriko
    Lopes, Tiago J.
    Matsuoka, Yukiko
    Kitano, Hiroaki
    Shoemaker, Jason E.
    Kawaoka, Yoshihiro
    [J]. MBIO, 2018, 9 (06): : 1 - 14
  • [2] Albericio F, 2012, FUTURE MED CHEM, V4, P1527, DOI [10.4155/FMC.12.94, 10.4155/fmc.12.94]
  • [3] TNF/iNOS-producing dendritic cells are the necessary evil of lethal influenza virus infection
    Aldridge, Jerry R., Jr.
    Moseley, Carson E.
    Boltz, David A.
    Negovetich, Nicholas J.
    Reynolds, Cory
    Franks, John
    Brown, Scott A.
    Doherty, Peter C.
    Webster, Robert G.
    Thomas, Paul G.
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (13) : 5306 - 5311
  • [4] Antiviral Activity and Increased Host Defense against Influenza Infection Elicited by the Human Cathelicidin LL-37
    Barlow, Peter G.
    Svoboda, Pavel
    Mackellar, Annie
    Nash, Anthony A.
    York, Ian A.
    Pohl, Jan
    Davidson, Donald J.
    Donis, Ruben O.
    [J]. PLOS ONE, 2011, 6 (10):
  • [5] Intracellular Toll-like Receptors
    Blasius, Amanda L.
    Beutler, Bruce
    [J]. IMMUNITY, 2010, 32 (03) : 305 - 315
  • [6] Inhibition of p38 Mitogen-activated Protein Kinase Impairs Influenza Virus-induced Primary and Secondary Host Gene Responses and Protects Mice from Lethal H5N1 Infection
    Boergeling, Yvonne
    Schmolke, Mirco
    Viemann, Dorothee
    Nordhoff, Carolin
    Roth, Johannes
    Ludwig, Stephan
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2014, 289 (01) : 13 - 27
  • [7] The IFITM Proteins Mediate Cellular Resistance to Influenza A H1N1 Virus, West Nile Virus, and Dengue Virus
    Brass, Abraham L.
    Huang, I-Chueh
    Benita, Yair
    John, Sinu P.
    Krishnan, Manoj N.
    Feeley, Eric M.
    Ryan, Bethany J.
    Weyer, Jessica L.
    van der Weyden, Louise
    Fikrig, Erol
    Adams, David J.
    Xavier, Ramnik J.
    Farzan, Michael
    Elledge, Stephen J.
    [J]. CELL, 2009, 139 (07) : 1243 - 1254
  • [8] CD8 T cells utilize TRAIL to control influenza virus infection
    Brincks, Erik L.
    Katewa, Arna
    Kucaba, Tamara A.
    Griffith, Thomas S.
    Legge, Kevin L.
    [J]. JOURNAL OF IMMUNOLOGY, 2008, 181 (07) : 4918 - 4925
  • [9] The Magnitude of the T Cell Response to a Clinically Significant Dose of Influenza Virus Is Regulated by TRAIL
    Brincks, Erik L.
    Gurung, Prajwal
    Langlois, Ryan A.
    Hemann, Emily A.
    Legge, Kevin L.
    Griffith, Thomas S.
    [J]. JOURNAL OF IMMUNOLOGY, 2011, 187 (09) : 4581 - 4588
  • [10] Increased survival after gemfibrozil treatment of severe mouse influenza
    Budd, Alison
    Alleva, Lisa
    Alsharifi, Mohammed
    Koskinen, Aulikki
    Smythe, Victoria
    Mullbacher, Arno
    Wood, Jeff
    Clark, Ian
    [J]. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 2007, 51 (08) : 2965 - 2968