ArticlePloS one2016
Experimental Adaptation of Rotaviruses to Tumor Cell Lines.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Experimental adaptation of pigeon rotavirus A (pRVA) in human colorectal cancer cells reveals interferon-driven host responses and immune checkpoint modulation.New microbes and new infections · 2026Article
- Preclinical evaluation of oncolytic potential human rotavirus Wt 1-5 in gastric adenocarcinoma.PloS one · 2023Article
- Article
- Cell surface heat shock protein-mediated entry of tumor cell-adapted rotavirus into U-937 cells.Folia microbiologica · 2021Article
- Role of heat-shock proteins in infection of human adenocarcinoma cell line MCF-7 by tumor-adapted rotavirus isolates.Colombia medica (Cali, Colombia) · 2021Article
- Repurposing Infectious Diseases Vaccines Against Cancer.Frontiers in oncology · 2021Review
- Induction of Cell Death in the Human Acute Lymphoblastic Leukemia Cell Line Reh by Infection with Rotavirus Isolate Wt1-5.Biomedicines · 2020Article
- Assessing the oncolytic potential of rotavirus on mouse myeloma cell line Sp2/0-Ag14.Biomedica : revista del Instituto Nacional de Salud · 2020Article
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A number of viruses show a naturally extended tropism for tumor cells whereas other viruses have been genetically modified or adapted to infect tumor cells. Oncolytic viruses have become a promising tool for treating some cancers by inducing cell lysis or immune response to tumor cells. In the present work, rotavirus strains TRF-41 (G5) (porcine), RRV (G3) (simian), UK (G6-P5) (bovine), Ym (G11-P9) (porcine), ECwt (murine), Wa (G1-P8), Wi61 (G9) and M69 (G8) (human), and five wild-type human rotavirus isolates were passaged multiple times in different human tumor cell lines and then combined in five different ways before additional multiple passages in tumor cell lines. Cell death caused by the tumor cell-adapted isolates was characterized using Hoechst, propidium iodide, 7-AAD, Annexin V, TUNEL, and anti-poly-(ADP ribose) polymerase (PARP) and -phospho-histone H2A.X antibodies. Multiple passages of the combined rotaviruses in tumor cell lines led to a successful infection of these cells, suggesting a gain-of-function by the acquisition of greater infectious capacity as compared with that of the parental rotaviruses. The electropherotype profiles suggest that unique tumor cell-adapted isolates were derived from reassortment of parental rotaviruses. Infection produced by such rotavirus isolates induced chromatin modifications compatible with apoptotic cell death.
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