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Wang2019 - A mathematical model of oncolytic virotherapy with time delay

ABSTRACT: A mathematical model describing oncolytic virotherapy with incorporation the viral lytic cycle and the virus-specific CTL response. The thresholds for viral treatment and virus-specific CTl response are also obtained.

SUBMITTER: Johannes Meyer

PROVIDER: BIOMD0000000902 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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Publications

A mathematical model of oncolytic virotherapy with time delay.

Wang Zi Zi ZZ Guo Zhi Ming ZM Smith Hal H

Mathematical biosciences and engineering : MBE 20190301 4

Oncolytic virotherapy is an emerging treatment modality which uses replication-competent viruses to destroy cancers without causing harm to normal tissues. By the development of molecular biotechnology, many effective viruses are adapted or engineered to make them cancer-specific, such as measles, adenovirus, herpes simplex virus and M1 virus. A successful design of virus needs a full understanding about how viral and host parameters influence the tumor load. In this paper, we propose a mathemat ...[more]

PMID: 31137188

Publication: 1/2

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Wang2019 - A mathematical model of oncolytic virotherapy with time delay

Project description:A mathematical model describing oncolytic virotherapy with incorporation the viral lytic cycle and the virus-specific CTL response. The thresholds for viral treatment and virus-specific CTl response are also obtained.

2024-09-02 | BIOMD0000000772 | BioModels

Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

Project description:To investigate the ability for pevonedistat to sensitize renal 786-0 carcinoma cells to VSVd51 oncolyic virotherapy, we treated cells with monotherapies or combination and sequencinced the transcriptome for antiviral interferon impact

2023-09-28 | GSE206428 | GEO

Subclone of resistant CT26 murine tumor shows high sensitivity to VA7 virotherapy: A novel system to study innate immunity and antigen dominance in oncolytic immuno-virotherapy

Project description:Recently, attenuated Semliki Forest virus vector VA7 completely eliminated type I interferon (IFN) unresponsive human U87 glioma xenografts while IFN responsive mouse GL261 and CT-2A gliomas proved refractory to the oncolytic virotherapy. Here we describe in two clones of a well established Balb/c mouse tumor cell line, CT26 murine colon carcinoma, diametrically opposed IFN responsiveness and sensitivity to oncolytic virus. Both CT26WT and CT26LacZ clones secreted biologically active type I IFN in vitro upon infection but virus replication was self-limiting only in CT26WT cells. Total transcriptome sequencing (RNA-Seq) and western blotting experiments revealed that in sharp contrast to CT26LacZ cells, CT26WT cells had strong constitutive expression of 56 different genes associated with pattern recognition and type I interferon signaling pathways, spanning two reported anti-RNA virus gene signatures and22 genes that have been reported to have direct anti-Alphaviral activity. Correspondingly, only CT26LacZ tumors were infectable in vivo, resulting in rapid central necrosis of the tumors by 96 hours post infection and complete tumor eradication both in immunocompetent and in SCID mice. CT26LacZ tumor eradication by oncolysis induced 100% protective immunity against homologous CT26LacZ challenge but only 50% protection against heterologous CT26WT challenge, indicating LacZ immune dominance over shared antigens. We believe the two clone CT26 system described herein constitutes a challenging yet realistic model for clonally and immunologically heterogeneous cancer where a strong therapy efficacy bias toward sensitive tumor subpopulations might falsely predict therapeutic success on a broad patient scale highlighting the necessity of successful pre-screening for responsive tumors. RNA-Seq in CT26 tumor cell line

2014-09-05 | E-GEOD-53001 | biostudies-arrayexpress

Single-cell RNA sequencing reveals a strong connection between Gadd45g upregulation and oncolytic HSV infection in tumor tissue

Project description:The oncolytic effect of virotherapy derives from the intrinsic capability of the applied virus in selectively infecting and killing tumor cells. Although oncolytic viruses of various constructions have been shown to efficiently infect and kill tumor cells in vitro, the efficiency of these viruses to exert the same effect on tumor cells within tumor tissues in vivo has not been extensively investigated. Here we report our studies using single-cell RNA sequencing to comprehensively analyze the gene expression profile of tumor tissues following herpes simplex virus 2-based oncolytic virotherapy. Our data revealed the extent and cell types within the tumor microenvironment that could be infected by the virus. Moreover, we observed changes in the expression of cellular genes, including antiviral genes, in response to viral infection. One notable gene found to be upregulated significantly in oncolytic virus-infected tumor cells was Gadd45g, which is desirable for optimal virus replication. These results not only help reveal the precise infection status of the oncolytic virus in vivo, but also provide insight that may lead to the development of new strategies to further enhance the therapeutic efficacy of oncolytic virotherapy.

2021-10-31 | GSE186753 | GEO

Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

Project description:Pevonedistat sensitizes cancer cells to oncolytic VSVd51 virotherapy

| PRJNA850784 | ENA

Subclone of resistant CT26 murine tumor shows high sensitivity to VA7 virotherapy: A novel system to study innate immunity and antigen dominance in oncolytic immuno-virotherapy

2014-09-05 | GSE53001 | GEO

Phan2017 - innate immune in oncolytic virotherapy

Project description:The paper describes a model on the key components for tumor–immune dynamics in multiple myeloma. Created by COPASI 4.25 (Build 207) This model is described in the article: The Role of the Innate Immune System in Oncolytic Virotherapy Tuan Anh Phan and Jianjun Paul Tian Computational and Mathematical Methods in Medicine (2017) 6587258 Abstract: The complexity of the immune responses is a major challenge in current virotherapy. This study incorporates the innate immune response into our basic model for virotherapy and investigates how the innate immunity affects the outcome of virotherapy. The viral therapeutic dynamics is largely determined by the viral burst size, relative innate immune killing rate, and relative innate immunity decay rate. The innate immunity may complicate virotherapy in the way of creating more equilibria when the viral burst size is not too big, while the dynamics is similar to the system without innate immunity when the viral burst size is big. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2024-09-02 | BIOMD0000000748 | BioModels

Wodarz2001 - Viruses as antitumor weapons

Project description:This mathematical model of the dynamics between tumor, virus and virus-specific CTL populations is described by the publication: Wodarz D. "Viruses as antitumor weapons: defining conditions for tumor remission". Cancer Res. 2001 Apr 15;61(8):3501-7. PMID: 11309314 Comment: Reproduction of Fig. 3A was achieved by using the initial conditions infected_tumor_cells = 0.01, uninfected_tumor_cells = 0.0001, virus-specific_CTLs = 0, and with modified parameter sets. For Fig. 3A non-cytotoxic virus, k = 17 and beta= 0.5. For Fig. 3A cytotoxic virus, beta = 0.5. These simulation conditions yield plots similar to Fig. 3A in the manuscript. Abstract: Recent research has indicated that viruses specifically infecting tumor cells could be used as an alternative therapeutic approach in cancer patients. A particular example is the adenovirus ONYX-015, which has entered clinical trials in the context of head and neck cancer. Successful therapy crucially requires an understanding about how viral and host parameters influence tumor load. The interactions between the growing tumor, the replicating virus, and possible immune responses are multifactorial and nonlinear. Hence, a complete understanding of how virus and host characteristics influence the outcome of therapy requires mathematical models. In this study, such mathematical models are presented and analyzed. The study investigates three possible scenarios that could be relevant for therapy: (a) viral cytotoxicity alone kills tumor cells; (b) a virus-specific lytic CTL response contributes to killing of infected tumor cells; (c) the virus elicits immunostimulatory signals within the tumor that promote the development of tumor-specific CTL. The models precisely define conditions required for successful therapy. They identify the parameters that need to be measured and modulated to evaluate and refine the existing therapy regimes.

2024-09-02 | BIOMD0000001043 | BioModels

Changes in cellular transcriptome in response to inhibitors of Epstein-Barr virus

Project description:Burkitt lymphoma cells can be latently infected with Epstein-Barr virus (EBV). The virus may be activated into its lytic cycle by small molecules, such as sodium butyrate. Other molecules, such as valproate and valpromide, block viral lytic reactivation. These pharmacological agents alter the cellular physiology that controls viral lytic gene expression. Changes in the cellular transcription were measured in response to one activator and two inhibitors of the Epstein-Barr virus lytic cycle in order to identify cellular genes that are potential regulators of the viral life cycle.

2024-03-13 | GSE135794 | GEO

Murine cytotoxic CD4 T cells

Project description:Cytotoxic CD4 T lymphocytes (CD4-CTL) are important in anti-viral immunity.  For example, we have previously shown that in mice, CD4-CTL are important to control ectromelia virus (ECTV) infection.  How viral infections induce CD4-CTL responses remains incompletely understood. Here we demonstrate that not only ECTV but also vaccinia virus and Lymphocytic Choriomeningitis virus induce CD4-CTL, but that the response to ECTV is stronger.  Using ECTV, we also demonstrate that in contrast to CD8-CTL, CD4-CTL differentiation requires constant virus replication and ceases once the virus is controlled.  We also show that Major Histocompatibility Complex Class II molecules on CD11c+ cells are required for CD4-CTL differentiation and for mousepox resistance.  Transcriptional analysis indicated that anti-viral CD4-CTL and non-cytolytic T Helper 1 (Th1) CD4 T cells have similar transcriptional profiles, suggesting that CD4-CTL are terminally differentiated classical Th1 cells.  Interestingly, CD4-CTL and classical Th1 cells expressed similar mRNA levels of the transcription factors ThPOK and GATA-3, necessary for CD4 T cell linage commitment; and Runx3, required for CD8 T cell development and effector function.  However, at the protein level, CD4-CTL had higher levels of the three transcription factors suggesting that further post-transcriptional regulation is required for CD4-CTL differentiation.  Finally, using CRISPR-Cas9 deletion of Runx3 in CD4 T cells, we demonstrate that the development of CD4-CTL but not of classical Th1 CD4 T cells requires Runx3 following ECTV infection.  These results further our understanding of the mechanisms of CD4-CTL differentiation during viral infection and the role of post-transcriptionally regulated Runx3 in this process.

2021-07-06 | GSE179289 | GEO

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