Naturally oncolytic viruses.

Curr Opin Mol Ther

Wellstat Biologics Corp, 930 Clopper Road, Gaithersburg, MD 20878, USA.

Published: August 2006

Naturally oncolytic viruses are replication-competent viruses that have an innate ability to selectively infect and kill tumor cells. Despite being used in the original attempts to treat cancer with live viruses five decades ago, interest in naturally oncolytic viruses has lagged behind the support for engineered adenoviruses and herpesviruses as cancer therapeutics. Recently, however, there has been renewed interest in the high potency and selectivity of these naturally occurring agents. In this review, the mechanism of selectivity as well as the preclinical and clinical activity of naturally oncolytic viruses will be discussed.

Download full-text PDF

Source

Publication Analysis

Top Keywords

naturally oncolytic
16
oncolytic viruses
16
viruses
6
naturally
5
viruses naturally
4
viruses replication-competent
4
replication-competent viruses
4
viruses innate
4
innate ability
4
ability selectively
4

Similar Publications

Adaptive Immunity Determines the Cancer Treatment Outcome of Oncolytic Virus and Anti-PD-1.

Bull Math Biol

January 2025

Department of Mathematics, University of Manitoba, 340 UMSU University Centre, Winnipeg, MB, R3T 2N2, Canada.

The immune checkpoint inhibitor, anti-programmed death protein-1 (anti-PD-1), enhances adaptive immunity to kill tumor cells, and the oncolytic virus (OV) triggers innate immunity to clear the infected tumor cells. We create a mathematical model to investigate how the interaction between adaptive and innate immunities under OV and anti-PD-1 affects tumor reduction. For different immunity strength, we create the corresponding virtual baseline patients and cohort patients to decipher the major factors determining the treatment outcome.

View Article and Find Full Text PDF

Combined delivery of IL12 and an IL18 mutant without IL18BP-binding activity by an adenoviral vector enhances tumor specific immunity.

Sci Rep

January 2025

State Key Laboratory of Pharmaceutical Biotechnology, Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.

Cytokines play pivotal roles in anticancer immune response. We previously reported that adenovirus armed with an IL18 variant (DR18) that overcomes IL18BP neutralizing effect displayed powerful therapeutic effects in local and distant tumors when delivered intratumorally. Here, we tested a combined delivery of IL12 and DR18 in tumor models since IL12 and IL18 are known to act synergistically in potentiating IFNγ production and antitumor immunity.

View Article and Find Full Text PDF

Epigenetic modulation by oncolytic viruses: Implications for cancer therapeutic efficacy.

Biochim Biophys Acta Rev Cancer

January 2025

Xinyuan Institute of Medicine and Biotechnology, College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou, China. Electronic address:

Among various therapeutic agents, Oncolytic Viruses (OVs) are the most promising anticancer therapeutics because of their tumor-specific targeting and capability to mediate an antitumor immune response. In this review, we will discuss how epigenetic reprogramming of both the host and tumor can facilitate increased sensitivity of tumors to OV therapy. OVs infect tumor cells and modulate epigenetic landscapes, including DNA methylation, histone modifications, and chromatin remodeling, as well as non-coding RNA expression that consequently induces immune responses.

View Article and Find Full Text PDF

Background: Reovirus (RV) is an oncolytic virus with natural tropism for cancer cells. We previously showed that RV administration in multiple myeloma (MM) patients was safe, but disease control associated with viral replication in the cancer cells was not observed. The combination with proteasome inhibitors (PIs) has shown to enhance RV therapeutic activity, but the mechanisms of action have not been fully elucidated.

View Article and Find Full Text PDF

Tertiary lymphoid structures (TLSs) are de novo ectopic lymphoid aggregates that regulate immunity in chronically inflamed tissues, including tumours. Although TLSs form due to inflammation-triggered activation of the lymphotoxin (LT)-LTβ receptor (LTβR) pathway, the inflammatory signals and cells that induce TLSs remain incompletely identified. Here we show that interleukin-33 (IL-33), the alarmin released by inflamed tissues, induces TLSs.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!