scholarly journals Specific Nucleoprotein Residues Affect Influenza Virus Morphology

2013 ◽  
Vol 88 (4) ◽  
pp. 2227-2234 ◽  
Author(s):  
K. M. Bialas ◽  
K. A. Bussey ◽  
R. L. Stone ◽  
T. Takimoto
Keyword(s):  
Influenza Virus ◽  
Virus Morphology

scholarly journals Repurposing Papaverine as an Antiviral Agent against Influenza Viruses and Paramyxoviruses

2020 ◽  
Vol 94 (6) ◽  
Author(s):  
Megha Aggarwal ◽  
George P. Leser ◽  
Robert A. Lamb
Keyword(s):  
Influenza Virus ◽  
Life Cycle ◽  
Nuclear Export ◽  
Antiviral Agent ◽  
Influenza Viruses ◽  
Parainfluenza Virus ◽  
Potential Candidate ◽  
Effective Inhibitor ◽  
Virus Life Cycle ◽  
Virus Morphology

ABSTRACT Influenza viruses are highly infectious and are the leading cause of human respiratory diseases and may trigger severe epidemics and occasional pandemics. Although antiviral drugs against influenza viruses have been developed, there is an urgent need to design new strategies to develop influenza virus inhibitors due to the increasing resistance of viruses toward currently available drugs. In this study, we examined the antiviral activity of natural compounds against the following influenza virus strains: A/WSN/33 (H1N1), A/Udorn/72 (H3N2), and B/Lee/40. Papaverine (a nonnarcotic alkaloid that has been used for the treatment of heart disease, impotency, and psychosis) was found to be an effective inhibitor of multiple strains of influenza virus. Kinetic studies demonstrated that papaverine inhibited influenza virus infection at a late stage in the virus life cycle. An alteration in influenza virus morphology and viral ribonucleoprotein (vRNP) localization was observed as an effect of papaverine treatment. Papaverine is a well-known phosphodiesterase inhibitor and also modifies the mitogen-activated protein kinase (MAPK) pathway by downregulating the phosphorylation of MEK and extracellular signal-regulated kinase (ERK). Thus, the modulation of host cell signaling pathways by papaverine may be associated with the nuclear retention of vRNPs and the reduction of influenza virus titers. Interestingly, papaverine also inhibited paramyxoviruses parainfluenza virus 5 (PIV5), human parainfluenza virus 3 (HPIV3), and respiratory syncytial virus (RSV) infections. We propose that papaverine can be a potential candidate to be used as an antiviral agent against a broad range of influenza viruses and paramyxoviruses. IMPORTANCE Influenza viruses are important human pathogens that are the causative agents of epidemics and pandemics. Despite the availability of an annual vaccine, a large number of cases occur every year globally. Here, we report that papaverine, a vasodilator, shows inhibitory action against various strains of influenza virus as well as the paramyxoviruses PIV5, HPIV3, and RSV. A significant effect of papaverine on the influenza virus morphology was observed. Papaverine treatment of influenza-virus-infected cells resulted in the inhibition of virus at a later time in the virus life cycle through the suppression of nuclear export of vRNP and also interfered with the host cellular cAMP and MEK/ERK cascade pathways. This study explores the use of papaverine as an effective inhibitor of both influenza viruses as well as paramyxoviruses.

Influenza virus-induced expression of CCL5 in monocyte/T-cell co-cultures is reduced in COPD

2019 ◽  
Author(s):  
L Betke ◽  
S Yanik ◽  
K Jamal Jameel ◽  
E Bülthoff ◽  
P Bürger ◽  
...  
Keyword(s):  
Influenza Virus ◽  
T Cell ◽  
Induced Expression

Protein expression changes in cells inoculated with Equine Influenza Virus: antibody microarray analysis

2013 ◽  
Vol 16 (4) ◽  
pp. 663-669
Author(s):  
W. Rozek ◽  
M. Kwasnik ◽  
J.F. Zmudzinski
Keyword(s):  
Influenza Virus ◽  
Protein Quality ◽  
Biological Properties ◽  
Regulation Of Transcription ◽  
Equine Influenza Virus ◽  
Virus Antibody ◽  
Antibody Microarray ◽  
Equine Influenza ◽  
Microarray Technique ◽  
In Cells

AbstractChanges in the level of cellular proteins in cells inoculated with equine influenza virus H7N7 and H3N8 were studied with microarray technique. H3N8 induced pro-apoptotic proteins while H7N7 induced both pro- as well as anti-apoptotic factors. The higher level of some cytoskeleton components and proteins involved in the protein quality control was recorded. Relatively high number of proteins involved in the regulation of transcription was down-regulated. The pattern of changes observed for H7N7 and H3N8 may reflect differences in the biological properties of both serotypes.

PLASMACYTOID DENDRITIC CELLS FUNCTION IN HIV INFECTION

2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Hiv Infection ◽  
Gene Transcription ◽  
Sendai Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Type I Interferons ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.

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