ArticleJournal of virology2000
Herpesvirus saimiri vFLIP provides an antiapoptotic function but is not essential for viral replication, transformation, or pathogenicity.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 52 citations in OpenAlex.
- c-FLIP as a master regulator of immune homeostasis and disease mechanisms.Cell death & disease · 2026Review
- Caspase cleavage of Kaposi sarcoma-associated herpesvirus proteins: a role for K5 in preventing caspase-mediated cell death during lytic replication.Journal of virology · 2025Article
- Emerging perspectives on RNA virus-mediated infections: from pathogenesis to therapeutic interventions.World journal of virology · 2023Review
- Self-Repairing Herpesvirus Saimiri Deletion Variants.Viruses · 2022Article
- Classical swine fever virus NJournal of virology · 2020Article
- Modulation of the extrinsic cell death signaling pathway by viral Flip induces acute-death mediated liver failure.Cell death & disease · 2019Article
- Identification of AIDS-Associated Kaposi Sarcoma: A Functional Genomics Approach.Frontiers in genetics · 2019Article
- The interplay of reovirus with autophagy.BioMed research international · 2014Review
- Evasion of adaptive and innate immune response mechanisms by γ-herpesviruses.Current opinion in virology · 2013Review
- The ephrin receptor tyrosine kinase A2 is a cellular receptor for Kaposi's sarcoma–associated herpesvirus.Nature medicine · 2012Article
- Viral FLICE inhibitory protein of rhesus monkey rhadinovirus inhibits apoptosis by enhancing autophagosome formation.PloS one · 2012Article
- Human herpesvirus 8 viral FLICE-inhibitory protein retards cell proliferation via downregulation of Id2 and Id3 expression.Molecular and cellular biochemistry · 2010Article
- Viruses associated with human cancer.Biochimica et biophysica acta · 2008Review
- Tyrosine phosphorylation of the Tio oncoprotein is essential for transformation of primary human T cells.Journal of virology · 2005Article
- Kaposi's sarcoma-associated herpesvirus encoded vFLIP induces cellular IL-6 expression: the role of the NF-kappaB and JNK/AP1 pathways.Oncogene · 2003Article
- The latency-associated nuclear antigen homolog of herpesvirus saimiri inhibits lytic virus replication.Journal of virology · 2003Article
- Kaposi's sarcoma-associated herpesvirus mitochondrial K7 protein targets a cellular calcium-modulating cyclophilin ligand to modulate intracellular calcium concentration and inhibit apoptosis.Journal of virology · 2002Article
- FLICE-inhibitory proteins: regulators of death receptor-mediated apoptosis.Molecular and cellular biology · 2001Review
- Herpesvirus saimiri.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Viruses and apoptosis.International journal of experimental pathology · 2001Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis of infected cells is an important host defense mechanism, and many viruses have exploited antiapoptotic proteins that interfere with crucial cellular pathways. Viral FLICE inhibitory proteins (vFLIPs) are encoded by rhadinoviruses like herpesvirus saimiri, the related Kaposi's sarcoma-associated herpesvirus-human herpesvirus 8 (KSHV/HHV8), and the poxvirus responsible for molluscum contagiosum. The vFLIPs can block the interaction of the death receptor-adapter complex with the cellular effector FLICE (caspase-8), and this prevents the initiation of the downstream caspase cascade. KSHV/HHV8 vFLIP overexpression can confer resistance to T-cell-mediated apoptosis and acts as a tumor progression factor in a murine B-cell lymphoma model. To analyze the function of herpesvirus vFLIPs in the genetic background of the virus and in a model for viral pathogenesis, we deleted the vFLIP gene (open reading frame 71) from the genome of herpesvirus saimiri strain C488. The viral deletion mutant was viable and replicated like the wild-type virus. An antiapoptotic effect could be attributed to the vFLIP gene, but we also show that the vFLIP gene of herpesvirus saimiri is dispensable for viral transformation of T cells in vitro and for pathogenicity in cottontop tamarins in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.