Mammalian orthoreovirus type 3 Dearing (MRV-3 Dearing)

Mammalian orthoreovirus type 3 Dearing (MRV-3 Dearing) is a prototype strain of mammalian orthoreovirus, a non-enveloped, double-stranded RNA virus with a segmented genome that infects mammals, including humans[4][5]. The virus has a broad host range and is notable for its capacity to infect transformed or tumorigenic cells preferentially, leading to cell death—an effect exploited in oncolytic virus therapy for cancer[1][4]. MRV-3 Dearing attaches to host cells via the σ1 protein using the junctional adhesion molecule-A as its main receptor, and sialic acid as a co-receptor, particularly for type 3[4]. In humans, MRV-3 Dearing infection is usually asymptomatic, but serological evidence suggests widespread exposure. Its oncolytic mechanism relies on tumor cell abnormalities (e.g., Ras activation, p53 mutation), rendering malignant cells more susceptible to reovirus-induced apoptosis, while sparing most normal cells[1]. The viral genome consists of 10 dsRNA segments encoding structural and non-structural proteins needed for replication, packaging, cell entry, and modulation of host defenses[2][5]. MRV-3 Dearing is under investigation as a therapeutic agent (not a classical pharmacological "target" in the sense of a human receptor or enzyme), with relevance as a biomarker-driven therapy and unique safety/efficacy profile in cancer therapy[1][4][5].

Other names

Reovirus type 3 DearingReovirus 3-DearingMRV-3 DearingOrthoreovirus type 3 DearingMammalian reovirus 3 Dearing

For oncolytic therapy, exploits oncogene- and tumor suppressor-related vulnerabilities in transformed (cancer) cells to induce selective cell lysis and apoptosis; modulates host death receptors (TRAIL, TNFR, Fas), interferes with host antiviral responses (PKR inhibition via σ3 protein)[1][4][5].