Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Inhibition of autophagy in EBV-positive Burkitt’s lymphoma cells enhances EBV lytic genes expression and replication

3 Sept 2015

Abstract excerpt

Autophagy, an important degradation system involved in maintaining cellular homeostasis, serves also to eliminate pathogens and process their fragments for presentation to the immune system. Several viruses have been shown to interact with the host autophagic machinery to suppress or make use of this cellular catabolic pathway to enhance their survival and replication. Epstein Barr virus (EBV) is a γ-herpes virus...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Cytomegalovirus and herpesvirus research
Share to Viral-associated cancers and disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26335716
DOI: 10.1038/cddis.2015.156

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inhibition of autophagy in EBV-positive Burkitt’s lymphoma cells enhances EBV lytic genes expression and replicationPMID 26335716Read ↗

Epstein-Barr Virus Blocks the Autophagic Flux and Appropriates the Autophagic Machinery To Enhance Viral ReplicationSemantic proximity Read ↗

EBV and KSHV Infection Dysregulates Autophagy to Optimize Viral Replication, Prevent Immune Recognition and Promote TumorigenesisSemantic proximity Read ↗

Advancing therapeutic strategies for Epstein-Barr virus-associated malignancies through lytic reactivationSemantic proximity Read ↗

Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survivalSemantic proximity Read ↗

Inhibition of the Epstein–Barr virus lytic cycle by Zta-targeted RNA interferenceSemantic proximity Read ↗

A switch from canonical to noncanonical autophagy shapes B cell responsesSemantic proximity Read ↗

Enhancement of Autophagy during Lytic Replication by the Kaposi's Sarcoma-Associated Herpesvirus Replication and Transcription ActivatorSemantic proximity Read ↗

Entry into the lytic cycle exposes EBV-infected cells to NK cell killing via upregulation of the MICB ligand for NKG2D and activation of the CD56bright and NKG2A+KIR+CD56dim subsetsSemantic proximity Read ↗

Therapies based on targeting Epstein‐Barr virus lytic replication for EBV ‐associated malignanciesSemantic proximity Read ↗

Cyclophilin A binds to AKT1 and facilitates the tumorigenicity of Epstein-Barr virus by mediating the activation of AKT/mTOR/NF-κB positive feedback loopSemantic proximity Read ↗

EBV lytic infection enhances transformation of B‐lymphocytes infected with EBV in the presence of T‐lymphocytesSemantic proximity Read ↗

EBV and Apoptosis: The Viral Master Regulator of Cell Fate?Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.