ArticleCancer biology & therapy2019
Caprine herpesvirus 1 (CpHV-1) as a potential candidate for oncolytic virotherapy.
Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Caprine herpes virus-1 reduces cell viability and enhances chemosensitivity in breast cancer cells.Frontiers in oncology · 2025Article
- Antiviral Activity of Nitazoxanide and Miltefosine Against FeHV-1 In Vitro.Veterinary medicine international · 2024Article
- Transcriptomic insights into pseudorabies virus suppressed cell death pathways in neuroblastoma cells.Frontiers in microbiology · 2024Article
- Apoptosis is mediated by FeHV-1 through the intrinsic pathway and interacts with the autophagic process.Virology journal · 2023Article
- Modifications of the PI3K/Akt/mTOR axis during FeHV-1 infection in permissive cells.Frontiers in veterinary science · 2023Article
- Autophagy up-regulation upon FeHV-1 infection on permissive cells.Frontiers in veterinary science · 2023Article
- The MicroalgaMolecules (Basel, Switzerland) · 2022Article
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- Promising Activities of Marine Natural Products against Hematopoietic Malignancies.Biomedicines · 2021Review
- Potential ApproachesFrontiers in oncology · 2021Review
- Seneca Valley Virus 2C and 3CFrontiers in microbiology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caprine Herpesvirus type 1 (CpHV-1) is a species-specific herpes virus able to induce apoptosis in several biological systems. In the present study we aimed to investigate the ability of CpHV-1 to reduce cells viability, to replicate and to cause cell death also in human cancer cell lines. We tested the CpHV-1 effects on HEL-299, Vero, MDA-MB-468, HeLa, U2OS, PC3, A549 and K562 neoplastic cell lines and on MDBK cells. Firstly, we evaluated the effect of CpHV-1 infection on cell viability by MTT assay and our data showed that CpHV-1 can induce a marked cytopathic effect (CPE) in most of cell lines tested, except for HEL-299, Vero and K562 cells. The reduction of cell viability was associated with a significant increase of viral production. We next investigated if CpHV-1 was able to induce cell death and so through western blotting analysis we evaluated cleaved caspase 3, LC3II and p62 protein levels after infection. Caspase 3 activation was detected in MDBK cells and, even if at different times p.i., also in MDA-MB-468, U2OS, and PC3 cell lines, while LC3II increase and concomitant p62 protein reduction were observed only in U2OS, and A549 cells, no significant alteration of these proteins was observed in the other cell lines tested. Finally, to confirm virus ability to trigger apoptosis we performed an Annexin-V apoptosis test after 24 h p.i. Although we need to further explore mechanisms underlying CpHV-1 treatment, this study could serve as the basis for the development of new treatment options aiming to fight several cancer types.
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