A novel strategy for dengue viruses to escape host immune surveillance and disseminate infection

2018 ◽  
Vol 102 ◽  
pp. 200-201
Author(s):  
Nuntaya Pornmun ◽  
Somchai Thiemmeca ◽  
Hunsa Praneejit ◽  
Adisak Songjang ◽  
Kasima Wasuworawong ◽  
...  
Keyword(s):  
Immune Surveillance ◽  
Dengue Viruses ◽  
Novel Strategy ◽  
Host Immune Surveillance

scholarly journals Gamma Interferon Blocks Gammaherpesvirus Reactivation from Latency

2006 ◽  
Vol 80 (1) ◽  
pp. 192-200 ◽  
Author(s):  
Ashley L. Steed ◽  
Erik S. Barton ◽  
Scott A. Tibbetts ◽  
Daniel L. Popkin ◽  
Mary L. Lutzke ◽  
...  
Keyword(s):  
Immune Surveillance ◽  
Viral Gene Expression ◽  
Gamma Interferon ◽  
Viral Gene ◽  
Herpesvirus Infection ◽  
Murine Gammaherpesvirus ◽  
Ifn Γ ◽  
Gammaherpesvirus 68 ◽  
Novel Strategy

ABSTRACT Establishment of latent infection and reactivation from latency are critical aspects of herpesvirus infection and pathogenesis. Interfering with either of these steps in the herpesvirus life cycle may offer a novel strategy for controlling herpesvirus infection and associated disease pathogenesis. Prior studies show that mice deficient in gamma interferon (IFN-γ) or the IFN-γ receptor have elevated numbers of cells reactivating from murine gammaherpesvirus 68 (γHV68) latency, produce infectious virus after the establishment of latency, and develop large-vessel vasculitis. Here, we demonstrate that IFN-γ is a powerful inhibitor of reactivation of γHV68 from latency in tissue culture. In vivo, IFN-γ controls viral gene expression during latency. Importantly, depletion of IFN-γ in latently infected mice results in an increased frequency of cells reactivating virus. This demonstrates that IFN-γ is important for immune surveillance that limits reactivation of γHV68 from latency.

scholarly journals The Impact of Interferon Gamma Receptor Expression on the Mechanism of Escape From Host Immune Surveillance in Hepatocellular Carcinoma

Hepatology ◽  
2000 ◽  
Vol 32 (3) ◽  
pp. 491-500 ◽  
Author(s):  
Mitsuo Nagao ◽  
Yoshiyuki Nakajima ◽  
Hiromichi Kanehiro ◽  
Michiyoshi Hisanaga ◽  
Yukio Aomatsu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Interferon Gamma ◽  
Immune Surveillance ◽  
Receptor Expression ◽  
Gamma Receptor ◽  
The Impact ◽  
Host Immune Surveillance

scholarly journals Biochemical mechanisms implemented by human acute myeloid leukemia cells to suppress host immune surveillance

2018 ◽  
Vol 15 (11) ◽  
pp. 989-991 ◽  
Author(s):  
Inna M. Yasinska ◽  
Isabel Gonçalves Silva ◽  
Svetlana Sakhnevych ◽  
Bernhard F. Gibbs ◽  
Ulrike Raap ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Immune Surveillance ◽  
Leukemia Cells ◽  
Human Acute Myeloid Leukemia ◽  
Acute Myeloid Leukemia Cells ◽  
Biochemical Mechanisms ◽  
Host Immune Surveillance ◽  
Acute Myeloid

scholarly journals Tumor PD-L1 Induction by Resveratrol/Piceatannol May Function as a Search, Enhance, and Engage (“SEE”) Signal to Facilitate the Elimination of “Cold, Non-Responsive” Low PD-L1-Expressing Tumors by PD-L1 Blockade

2019 ◽  
Vol 20 (23) ◽  
pp. 5969 ◽  
Author(s):  
Tze-Chen Hsieh ◽  
Joseph M. Wu
Keyword(s):  
Cell Death ◽  
Antitumor Activity ◽  
Programmed Cell Death ◽  
Selection Criteria ◽  
Regulatory Protein ◽  
Immune Surveillance ◽  
Tumor Escape ◽  
Free Response ◽  
High Level ◽  
Host Immune Surveillance

Programmed cell death ligand 1 (PD-L1) is an immune regulatory protein that facilitates tumor escape from host immune surveillance. In the clinic, tumors with high level of PD-L1 have been used to identify patients who might respond favorably to treatment by anti-PD-L1 antibodies (PD-L1 blockade, PLB). Typically, a progression-free response of 9–20% to PLB has been observed, the basis for the low success rate is largely unknown. Recently, we show upregulation of PD-L1 in cancer cells by ≥IC50 supra-pharmacological dose of grape polyphenol resveratrol and piceatannol, alone and combined. Herein, we summarize recent published studies on the regulation of tumor PD-L1 by flavonoids and grape polyphenols. We hypothesize that the induced tumor PD-L1 by resveratrol and/or piceatannol may serve as a Search, Enhance, and Engage (“SEE”) signal to sensitize and augment the recognition and detection of low PD-L1-expressing “cold, non-responsive” tumors. The “SEE” strategy enhances the “visibility” of previously unidentified tumor cells for targeting and eventual eradication by the host antitumor activity. This strategy expands the selection criteria for patients with improved sensitivity and potential responsiveness when used in combination with PLB. The modulation of tumor PD-L1 by flavonoids or polyphenols is proposed to improve the response to PLB in low PD-L1 tumors.

scholarly journals New Insights on Human Polyomavirus JC and Pathogenesis of Progressive Multifocal Leukoencephalopathy

2013 ◽  
Vol 2013 ◽  
pp. 1-17 ◽  
Author(s):  
Anna Bellizzi ◽  
Elena Anzivino ◽  
Donatella Maria Rodio ◽  
Anna Teresa Palamara ◽  
Lucia Nencioni ◽  
...  
Keyword(s):  
Progressive Multifocal Leukoencephalopathy ◽  
Immune Surveillance ◽  
Viral Reactivation ◽  
Human Polyomavirus ◽  
Predisposing Factor ◽  
New Findings ◽  
Immunodeficiency Virus ◽  
Review Current ◽  
Host Immune Surveillance

John Cunningham virus (JCV) is a member of thePolyomaviridaefamily. It was first isolated from the brain of a patient with Hodgkin disease in 1971, and since then the etiological agent of the progressive multifocal leukoencephalopathy (PML) was considered. Until the human immunodeficiency virus (HIV) pandemic, PML was rare: in fact HIV-induced immunodeficiency is the most common predisposing factor accounting for 85% of all instances of PML. This data led to intense research on JCV infection and resulted in better understanding of epidemiology and clinic-pathologic spectrum. Recently, cases of PML have been observed after the introduction of monoclonal antibodies, such as natalizumab, rituximab, efalizumab, and infliximab, in the treatment of autoimmune disease, underlining the important role of host immunity in PML pathogenesis. In this review current understanding of the JCV infection and the new findings relating to the pathogenesis of PML has been comprehensively revised, focusing our attention on the interaction between the cellular and viral molecular pathways implicated in the JCV infection and the modulating role of host immune surveillance in the viral reactivation from a latent state.

scholarly journals Deregulation of DNA Damage Signal Transduction by Herpesvirus Latency-Associated M2

2006 ◽  
Vol 80 (12) ◽  
pp. 5862-5874 ◽  
Author(s):  
Xiaozhen Liang ◽  
Mary T. Pickering ◽  
Nam-Hyuk Cho ◽  
Heesoon Chang ◽  
Michael R. Volkert ◽  
...  
Keyword(s):  
Dna Damage ◽  
Immune Surveillance ◽  
Atm Kinase ◽  
Kinase Activation ◽  
Cycle Arrest ◽  
Damage Response ◽  
Gamma Herpesvirus ◽  
Infected Cells ◽  
Induced Apoptosis ◽  
Host Immune Surveillance

ABSTRACT Infected cells recognize viral replication as a DNA damage stress and elicit a DNA damage response that ultimately induces apoptosis as part of host immune surveillance. Here, we demonstrate a novel mechanism where the murine gamma herpesvirus 68 (γHV68) latency-associated, anti-interferon M2 protein inhibits DNA damage-induced apoptosis by interacting with the DDB1/COP9/cullin repair complex and the ATM DNA damage signal transducer. M2 expression constitutively induced DDB1 nuclear localization and ATM kinase activation in the absence of DNA damage. Activated ATM subsequently induced Chk activation and p53 phosphorylation and stabilization without eliciting H2AX phosphorylation and MRN recruitment to foci upon DNA damage. Consequently, M2 expression inhibited DNA repair, rendered cells resistant to DNA damage-induced apoptosis, and induced a G1 cell cycle arrest. Our results suggest that γHV68 M2 blocks apoptosis-mediated intracellular innate immunity, which might ultimately contribute to its role in latent infection.

scholarly journals Pharmacophore-based peptide biologics neutralize SARS-CoV-2 S1 and deter S1-ACE2 interaction in vitro

2020 ◽  
Author(s):  
Masaud Shah ◽  
Sung Ung Moon ◽  
Hyun Goo Woo
Keyword(s):  
Cell Attachment ◽  
Immune Surveillance ◽  
Cell Entry ◽  
Viral Fusion ◽  
Receptor Binding Domain ◽  
Spontaneous Movement ◽  
Viral Receptor ◽  
Dose Dependent ◽  
Host Immune Surveillance

AbstractEffective therapeutics and stable vaccine are the urgent need of the day to combat COVID-19 pandemic. SARS-CoV-2 spike protein has a pivotal role in cell-entry and host immune response, thus regarded as potential drug- and vaccine-target. As the virus utilizes the S1 domain of spike to initiate cell-attachment and S2 domain for membrane fusion, several attempts have been made to design viral-receptor and viral-fusion blockers. Here, by deploying interactive structure-based design and pharmacophore-based approaches, we designed short and stable peptide-biologics i.e. CoV-spike-neutralizing peptides (CSNPs) including CSNP1, CSNP2, CSNP3, CSNP4. We could demonstrate in cell culture experiments that CSNP2 binds to S1 at submicromolar concentration and abrogates the S1-hACE2 interaction. CSNP3, a modified and downsized form of CSNP2, could neither interfere with the S1-hACE2 interaction nor bind to S1. CSNP4 exhibited dose-dependent binding to both S1 and hACE2 and abolished the S1-hACE2 interaction in vitro. CSNP4 possibly enhance the mAb-based S1 neutralization by limiting the spontaneous movement of spike receptor-binding domain (RBD), whereas CSNP2 allowed RBD-mAb binding without any steric hindrance. Taken together, we suggest that CSNP2 and CSNP4 are potent and stable candidate peptides that can neutralize the SARS-CoV-2 spike and possibly pose the virus to host immune surveillance.

scholarly journals Helicobacter pyloriOuter Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γSignaling

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Yuqun Shan ◽  
Xingxiao Lu ◽  
Yingnan Han ◽  
Xinpeng Li ◽  
Xiao Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Type Strain ◽  
Wild Type Strain ◽  
Outer Membrane Proteins ◽  
Immune Surveillance ◽  
Survival Rates ◽  
Wild Type ◽  
Qrt Pcr ◽  
H Pylori ◽  
Host Immune Surveillance

Outer membrane proteins (OMPs) can induce an immune response. Omp18 (HP1125) ofH. pyloriis a powerful antigen that can induce significant interferon-γ(IFN-γ) levels. Previous studies have suggested that IFN-γplays an important role inH. pyloriclearance. However,H. pylorihas multiple mechanisms to avoid host immune surveillance for persistent colonization. We generated anomp18mutant (H. pylori26695 andH. pyloriSS1) strain to examine whether Omp18 interacts with IFN-γand is involved inH. pyloricolonization. qRT-PCR revealed that IFN-γinduced Omp18 expression. qRT-PCR and western blot analysis revealed reduced expressions of virulence factors CagA and NapA inH. pylori26695 with IFN-γtreatment, but they were induced in the Δomp18strain. In C57BL/6 mice infected withH. pyloriSS1 and the Δomp18strain, the Δomp18strain conferred defective colonization and activated a stronger inflammatory response. Signal transducer phosphorylation and transcription 1 (STAT1) activator was downregulated by the wild-type strain but not the Δomp18strain in IFN-γ-treated macrophages. Furthermore, Δomp18strain survival rates were poor in macrophages compared to the wild-type strain. We concluded thatH. pyloriOmp18 has an important function influencing IFN-γ-mediated immune response to participate in persistent colonization.

scholarly journals Cancer metastasis as a non-healing wound

2021 ◽  
Author(s):  
Matthew Deyell ◽  
Christopher S. Garris ◽  
Ashley M. Laughney
Keyword(s):  
Wound Healing ◽  
Cancer Metastasis ◽  
Cell Function ◽  
Primary Tumour ◽  
Immune Surveillance ◽  
Tumour Cells ◽  
Healing Wound ◽  
Disseminated Tumour Cells ◽  
Novel Strategy ◽  
The 19Th Century

AbstractMost cancer deaths are caused by metastasis: recurrence of disease by disseminated tumour cells at sites distant from the primary tumour. Large numbers of disseminated tumour cells are released from the primary tumour, even during the early stages of tumour growth. However, only a minority survive as potential seeds for future metastatic outgrowths. These cells must adapt to a relatively inhospitable microenvironment, evade immune surveillance and progress from the micro- to macro-metastatic stage to generate a secondary tumour. A pervasive driver of this transition is chronic inflammatory signalling emanating from tumour cells themselves. These signals can promote migration and engagement of stem and progenitor cell function, events that are also central to a wound healing response. In this review, we revisit the concept of cancer as a non-healing wound, first introduced by Virchow in the 19th century, with a new tumour cell-intrinsic perspective on inflammation and focus on metastasis. Cellular responses to inflammation in both wound healing and metastasis are tightly regulated by crosstalk with the surrounding microenvironment. Targeting or restoring canonical responses to inflammation could represent a novel strategy to prevent the lethal spread of cancer.

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