ArticleViruses2020
SV40 Polyomavirus Activates the Ras-MAPK Signaling Pathway for Vacuolization, Cell Death, and Virus Release.
Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 11 citations in OpenAlex.
- Minimal Genome, Maximal Effect: How Polyomavirus Genomes Are Capable of Complex Pathogenesis.Viruses · 2026Review
- Remodeling of the cellular membrane architecture in response to BK polyomavirus infection.Virology journal · 2026Review
- Updated practice for detection of viral infections in breeding macaques.Zoological research · 2025Review
- Review
- Intersection of inflammation and viral replication: the central role of MAPK signaling in viral respiratory infections.Frontiers in microbiology · 2025Review
- Nervous necrosis virus induced vacuolization is a Rab5- and actin-dependent process.Virulence · 2024Article
- Massive entry of BK Polyomavirus induces transient cytoplasmic vacuolization of human renal proximal tubule epithelial cells.PLoS pathogens · 2024Article
- Tubeimoside-2 Triggers Methuosis in Hepatocarcinoma Cells through the MKK4-p38α Axis.Pharmaceutics · 2023Article
- Revisiting Regulated Cell Death Responses in Viral Infections.International journal of molecular sciences · 2022Review
- Article
- Endoplasmic Reticulum Stress Mediates Renal Tubular Vacuolation in BK Polyomavirus-Associated Nephropathy.Frontiers in endocrinology · 2022Article
- Sending mixed signals: polyomavirus entry and trafficking.Current opinion in virology · 2021Review
- GRK2 mediates β-arrestin interactions with 5-HTJournal of virology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Polyomaviruses are a family of small, non-enveloped DNA viruses that can cause severe disease in immunosuppressed individuals. Studies with SV40, a well-studied model polyomavirus, have revealed the role of host proteins in polyomavirus entry and trafficking to the nucleus, in viral transcription and DNA replication, and in cell transformation. In contrast, little is known about host factors or cellular signaling pathways involved in the late steps of productive infection leading to release of progeny polyomaviruses. We previously showed that cytoplasmic vacuolization, a characteristic late cytopathic effect of SV40 infection, depends on the specific interaction between the major viral capsid protein VP1 and its cell surface ganglioside receptor GM1. Here, we show that, late during infection, SV40 activates a signaling cascade in permissive monkey CV-1 cells involving Ras, Rac1, MKK4, and JNK to stimulate SV40-specific cytoplasmic vacuolization and subsequent cell lysis and virus release. Inhibition of individual components of this signaling pathway inhibits vacuolization, lysis, and virus release, even though high-level intracellular virus replication occurs. Identification of this pathway for SV40-induced vacuolization and virus release provides new insights into the late steps of non-enveloped virus infection.
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Registered trials
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.