Polyoma Virus Receptor (PVR)

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γδ T cells play an important role in tumor resistance in a naturally occurring virus-induced tumor model. And reports about the interaction of polyomavirus and γδ T cells have intrigued researchers.

Introduction of Polyoma Virus Receptor

The entry of viruses into cells can occur via several different mechanisms, most of which require interaction with a specific cellular receptor. While this interaction is not sufficient to guarantee successful virus entry, it is a necessary step. The specificity of virus-host interactions, therefore, relies heavily on the specificity of the virus attachment protein cellular receptor interaction. Identification of cellular virus receptor moieties will be important for understanding the mechanisms of virus infection and tissue tropism and for the development of antiviral agents. Polyomavirus attaches to mouse kidney cells (MKC) via two physically and kinetically distinguishable binding mechanisms. Following attachment to the saturable, specific receptor, the virus is internalized, and infection ensues. Nonspecific binding results in virus internalization and eventual degradation in lysosomes. The receptor thus appears to play an important role in determining the course of polyomavirus infection which is to follow.

Schematic representation of the polyomaviruses genome organization. Fig.1 Schematic representation of the polyomaviruses genome organization. (Delbue, 2012)

Polyoma Virus and γδ T

Virus-induced tumors mostly develop in immune-compromised hosts, suggesting that the immune system protects against the induction and/or progression of these tumors. T cells expressing α and β TCR and recognizing viral peptide epitopes are thought to be important for this protection. However, other cell types of the immune system, including NK cells and γδ T cells, are also endowed with effector functions similar to those of αβ T cells, but their role in the control of virus-induced tumors is largely unexplored.

Previous research reported that γδ T and NK cells can prevent tumor formation in Polyoma virus-infected αβ T cell-deficient mice. Polyoma virus-induced tumor cell lines activate γδ T cells and NK cells in vitro and in vivo. Moreover, these tumor cell lines express Rae-1 ligands recognized by NKG2D, an activating receptor expressed on all NK cells and some γδ T cells, they are efficiently killed by NK cells in vitro and this killing is NKG2D-mediated. These data taken together show a major role for γδ T cells and NK cells in tumor resistance in a naturally occurring virus-induced tumor model, implicate NKG2D-NKG2D ligand interactions in these antitumor responses, and suggest that αβ T cells, γδ T cells, and NK cells may work together to prevent tumor formation during life-long virus persistence. Besides, DNAM-1 expressed on the Vγ9Vδ2 T cells recognizes its ligands nectin-2 and polyoma virus receptor (PVR) that are widely expressed in tumor cells, which helps Vγ9Vδ2 T cells target tumor cells. This suggests a possible interaction mechanism between γδ T and polyoma virus.

The tumor cell recognition of γδ T cells. Fig.2 The tumor cell recognition of γδ T cells. (Liu, 2020)

The recent identification of many components of the Polyomaviridae family that can infect humans represents a strong incentive for the scientific community to improve and increase the research on the oncogenic potentialities of these viruses. In particular, since the association between the viral aetiology of the tumors and the state of the host immune system is well established, it is urgent to focus future studies on the nature of the relationship between the host immune system and polyomaviruses infection.


  1. Delbue, S.; et al. Review on the relationship between human polyomaviruses-associated tumors and host immune system. Clin Dev Immunol. 2012, 2012: 542092.
  2. Liu, Y.; Zhang, C. The role of human γδ t cells in anti-tumor immunity and their potential for cancer immunotherapy. Cells. 2020, 9(5).
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