scholarly journals Identification of a Putative Coreceptor on Vero Cells That Participates in Dengue 4 Virus Infection

2001 ◽  
Vol 75 (17) ◽  
pp. 7818-7827 ◽  
Author(s):  
José de Jesús Martı́nez-Barragán ◽  
Rosa M. del Angel
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Vero Cells ◽  
Host Cells ◽  
Cell Surface Receptor ◽  
Target Cells ◽  
Virus Binding ◽  
Dengue Virus Infection ◽  
Surface Receptor ◽  
A Cell

ABSTRACT Dengue virus infects target cells by attaching to a cell surface receptor through the envelope (E) glycoprotein, located on the surface of the viral membrane. On Vero and BHK cells, heparan sulfate (HS) moieties of proteoglycans are the receptors for dengue virus; however, additional proteins have also been described as putative dengue virus receptors on C6/36, HL60, and BM cells. HS can also act as a receptor for other types of viruses or as an attachment molecule for viruses that require additional host cell molecules to allow viral penetration. In this study we searched for molecules other than HS that could participate in dengue virus infection of Vero cells. Labeled dengue 4 virus bound with high affinity to two molecules of 74 and 44 kDa. Binding of dengue virus to the 74-kDa molecule was susceptible to protease and sodium periodate treatment and resistant to heparinase treatments. Lectins such as concanavalin A and wheat germ agglutinin prevented dengue virus binding to both the 74- and the 44-kDa protein in overlay assays, while phytohemagglutinin P did not affect binding, suggesting that carbohydrate residues (α-mannose orN-acetylglucosamine) are important in virus binding to host cells. Protease susceptibility, biotin labeling, and immunofluorescence with a polyclonal antibody raised against the 74-kDa protein consistently identified the protein on the surfaces of Vero cells. Moreover, the antibody against the 74-kDa protein was able to inhibit dengue virus infection. These data suggest that HS might serve as a primary receptor, probably concentrating virus particles on the surfaces of Vero cells, and then other molecules, such as the 74-kDa protein, might participate as coreceptors in viral penetration. The 74-kDa protein possibly constitutes part of a putative receptor complex for dengue virus infection of Vero cells.

SARS-CoV-2 Entry inhibitors targeting virus-ACE2 or virus-TMPRSS2 interactions

2021 ◽  
Vol 28 ◽  
Author(s):  
Hao Lin ◽  
Srinivasulu Cherukupalli ◽  
Da Feng ◽  
Shenghua Gao ◽  
Dongwei Kang ◽  
...  
Keyword(s):  
Life Cycle ◽  
Host Cells ◽  
Cell Surface Receptor ◽  
Target Cells ◽  
S Protein ◽  
Angiotensin Converting Enzyme 2 ◽  
Entry Inhibitors ◽  
Concise Report ◽  
Surface Receptor ◽  
Transmembrane Serine Protease

: COVID-19 is an infectious disease caused by SARS-CoV-2. The life cycle of SARS-CoV-2 includes the entry into the target cells, replicase translation, replicating and transcribing genomes, translating structural proteins, assembling and releasing new virions. Entering host cells is a crucial stage in the early life cycle of the virus, and blocking this stage can effectively prevent virus infection. SARS enters the target cells mediated by the interaction between the viral S protein and the target cell surface receptor angiotensin-converting enzyme 2 (ACE2), as well as the cleavage effect of type-II transmembrane serine protease (TMPRSS2) on the S protein. Therefore, the ACE2 receptor and TMPRSS2 are important targets for SARS-CoV-2 entry inhibitors. Herein, we provide a concise report/information on drugs with potential therapeutic value targeting virus-ACE2 or virus-TMPRSS2 interactions, to provide a reference for the design and discovery of potential entry inhibitors against SARS-CoV-2.

scholarly journals Identification of a Receptor-Binding Domain of Bordetella Dermonecrotic Toxin

2002 ◽  
Vol 70 (7) ◽  
pp. 3427-3432 ◽  
Author(s):  
Takeshi Matsuzawa ◽  
Takashige Kashimoto ◽  
Jun Katahira ◽  
Yasuhiko Horiguchi
Keyword(s):  
Amino Acids ◽  
Receptor Binding ◽  
Focal Adhesions ◽  
Small Gtpase ◽  
Binding Domain ◽  
Cell Surface Receptor ◽  
Target Cells ◽  
Dermonecrotic Toxin ◽  
Surface Receptor ◽  
A Cell

ABSTRACT Bordetella dermonecrotic toxin (DNT) stimulates the assembly of actin stress fibers and focal adhesions by deamidating or polyaminating Gln63 of the small GTPase Rho. DNT is an A-B toxin which is composed of an N-terminal receptor-binding (B) domain and a C-terminal enzymatically active (A) domain. In this study, to analyze the functional and structural organization of DNT, we prepared 10 clones of hybridoma producing anti-DNT monoclonal antibodies. One of these antibodies, 2B3, neutralized the effects of DNT on target cells when mixed with the toxin. When microinjected into cells, however, 2B3 did not inhibit the intoxication by DNT. Western blot analysis revealed that 2B3 recognized the N-terminal region of DNT. To delineate the DNT-binding domain, we examined a series of truncated DNT mutants for the ability to competitively inhibit the intoxication of cells by the full-length DNT and found that a fragment consisting of the N-terminal 54 amino acids (DNT1-54) was the smallest inhibitory fragment. The radioiodinated DNT1-54 actually bound to target cells, which was inhibited by 2B3. These results suggest that the N-terminal 54 amino acids of DNT are responsible for the binding to target cells. DNT1-54 bound to none of the DNT-resistant cells, implying the presence of a cell surface receptor specific to DNT-sensitive cells.

scholarly journals The Dual-Specific Binding of Dengue Virus and Target Cells for the Antibody-Dependent Enhancement of Dengue Virus Infection

2006 ◽  
Vol 176 (5) ◽  
pp. 2825-2832 ◽  
Author(s):  
Kao-Jean Huang ◽  
Yu-Ching Yang ◽  
Yee-Shin Lin ◽  
Jyh-Hsiung Huang ◽  
Hsiao-Sheng Liu ◽  
...  
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Specific Binding ◽  
Target Cells ◽  
Dengue Virus Infection ◽  
Antibody Dependent Enhancement

scholarly journals Cyclin-Dependent Kinases 8 and 19 Regulate Host Cell Metabolism during Dengue Virus Serotype 2 Infection

Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 654
Author(s):  
Molly Butler ◽  
Nunya Chotiwan ◽  
Connie D. Brewster ◽  
James E. DiLisio ◽  
David F. Ackart ◽  
...  
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Viral Genome ◽  
Metabolic Changes ◽  
Target Cells ◽  
Genome Replication ◽  
Dengue Virus Infection ◽  
Infectious Particle ◽  
Virus Serotype ◽  
Viral Genome Replication

Dengue virus infection is associated with the upregulation of metabolic pathways within infected cells. This effect is common to infection by a broad array of viruses. These metabolic changes, including increased glucose metabolism, oxidative phosphorylation and autophagy, support the demands of viral genome replication and infectious particle formation. The mechanisms by which these changes occur are known to be, in part, directed by viral nonstructural proteins that contact and control cellular structures and metabolic enzymes. We investigated the roles of host proteins with overarching control of metabolic processes, the transcriptional regulators, cyclin-dependent kinase 8 (CDK8) and its paralog, CDK19, as mediators of virally induced metabolic changes. Here, we show that expression of CDK8, but not CDK19, is increased during dengue virus infection in Huh7 human hepatocellular carcinoma cells, although both are required for efficient viral replication. Chemical inhibition of CDK8 and CDK19 with Senexin A during infection blocks virus-induced expression of select metabolic and autophagic genes, hexokinase 2 (HK2) and microtubule-associated protein 1 light chain 3 (LC3), and reduces viral genome replication and infectious particle production. The results further define the dependence of virus replication on increased metabolic capacity in target cells and identify CDK8 and CDK19 as master regulators of key metabolic genes. The common inhibition of CDK8 and CDK19 offers a host-directed therapeutic intervention that is unlikely to be overcome by viral evolution.

scholarly journals Release of Vasoactive Cytokines by Antibody-Enhanced Dengue Virus Infection of a Human Mast Cell/Basophil Line

2000 ◽  
Vol 74 (15) ◽  
pp. 7146-7150 ◽  
Author(s):  
Christine A. King ◽  
Jean S. Marshall ◽  
Hashem Alshurafa ◽  
Robert Anderson
Keyword(s):  
Mast Cell ◽  
Virus Infection ◽  
Dengue Virus ◽  
Human Mast Cell ◽  
Dengue Virus Infection ◽  
Ku812 Cells ◽  
A Cell ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

ABSTRACT We report here the first demonstration of dengue virus infection and vasoactive cytokine response of a cell of the mast cell/basophil lineage. Infection of KU812 cells was dependent on dengue-specific antibody and gave rise to infectious virions. This antibody-enhanced dengue virus infection triggered a four- to fivefold increase in the release of interleukin-1β (IL-1β) and a modest increase for IL-6 but not for an alternate cytokine, granulocyte-macrophage colony-stimulating factor. The results suggest a potential role for mast cells/basophils in the pathogenesis of dengue virus-induced disease.

scholarly journals Effect of dengue virus infection on the permeability of vero cells line

2016 ◽  
Author(s):  
Nur Kaliwantoro ◽  
Marsetyawan Hne Soesatyo ◽  
Indarto ◽  
Mohammad Juffrie ◽  
Rini Dharmastiti
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Vero Cells ◽  
Dengue Virus Infection

scholarly journals Bystander Target Cell Lysis and Cytokine Production by Dengue Virus-Specific Human CD4+ Cytotoxic T-Lymphocyte Clones

1999 ◽  
Vol 73 (5) ◽  
pp. 3623-3629 ◽  
Author(s):  
Susan J. Gagnon ◽  
Francis A. Ennis ◽  
Alan L. Rothman
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
T Lymphocyte ◽  
Hepg2 Cells ◽  
Fas Ligand ◽  
Cytokine Production ◽  
Cytotoxic T Lymphocyte ◽  
Target Cells ◽  
Dengue Virus Infection ◽  
Antigen Presenting

ABSTRACT Dengue hemorrhagic fever, the severe form of dengue virus infection, is believed to be an immunopathological response to a secondary infection with a heterologous serotype of dengue virus. Dengue virus capsid protein-specific CD4+ cytotoxic T-lymphocyte (CTL) clones were shown to be capable of mediating bystander lysis of non-antigen-presenting target cells. After activation by anti-CD3 or in the presence of unlabeled antigen-presenting target cells, these clones could lyse both Jurkat cells and HepG2 cells as bystander targets. Lysis of HepG2 cells suggests a potential role for CD4+ CTL in the liver involvement observed during dengue virus infection. Three CD4+ CTL clones were demonstrated to lyse cognate, antigen-presenting target cells by a mechanism that primarily involves perforin, while bystander lysis occurred through Fas/Fas ligand interactions. In contrast, one clone used a Fas/Fas ligand mechanism to lyse both cognate and bystander targets. Cytokine production by the CTL clones was also examined. In response to stimulation with D2 antigen, CD4+ T-cell clones produced gamma interferon, tumor necrosis factor alpha (TNF-α) and TNF-β. The data suggest that CD4+ CTL clones may contribute to the immunopathology observed upon secondary dengue virus infections through direct cytolysis and/or cytokine production.

scholarly journals Dengue Virus Infection: A Tale of Viral Exploitations and Host Responses

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1967
Author(s):  
Nikita Nanaware ◽  
Anwesha Banerjee ◽  
Satarupa Mullick Bagchi ◽  
Parikshit Bagchi ◽  
Anupam Mukherjee
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Genetic Material ◽  
Viral Disease ◽  
Host Cells ◽  
Severe Dengue ◽  
Mammalian Host ◽  
Infection Cycle ◽  
Dengue Virus Infection ◽  
Enveloped Virus

Dengue is a mosquito-borne viral disease (arboviral) caused by the Dengue virus. It is one of the prominent public health problems in tropical and subtropical regions with no effective vaccines. Every year around 400 million people get infected by the Dengue virus, with a mortality rate of about 20% among the patients with severe dengue. The Dengue virus belongs to the Flaviviridae family, and it is an enveloped virus with positive-sense single-stranded RNA as the genetic material. Studies of the infection cycle of this virus revealed potential host targets important for the virus replication cycle. Here in this review article, we will be discussing different stages of the Dengue virus infection cycle inside mammalian host cells and how host proteins are exploited by the virus in the course of infection as well as how the host counteracts the virus by eliciting different antiviral responses.

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