Abstract

Simple SummaryThis review is focused on enlisting viral proteins from different host sources, irrespective of their origin, that may act as future cancer curatives. Unlike the viral proteins that are responsible for tumor progression, these newly emerged viral proteins function as tumor suppressors. Their ability to regulate various cell signaling mechanisms specifically in cancer cells makes them interesting candidates to explore their use in cancer therapy. The discussion about such viral components may provide new insights into cancer treatment in the absence of any adverse effects to normal cells. The study also highlights avian viral proteins as a substitute to human oncolytic viruses for their ability to evade pre-existing immunity.Viruses are obligatory intracellular parasites that originated millions of years ago. Viral elements cover almost half of the human genome sequence and have evolved as genetic blueprints in humans. They have existed as endosymbionts as they are largely dependent on host cell metabolism. Viral proteins are known to regulate different mechanisms in the host cells by hijacking cellular metabolism to benefit viral replication. Amicable viral proteins, on the other hand, from several viruses can participate in mediating growth retardation of cancer cells based on genetic abnormalities while sparing normal cells. These proteins exert discreet yet converging pathways to regulate events like cell cycle and apoptosis in human cancer cells. This property of viral proteins could be harnessed for their use in cancer therapy. In this review, we discuss viral proteins from different sources as potential anticancer therapeutics.

Highlights

  • Viruses have proven to be drivers of evolution since more than 500 million years ago

  • We recently showed that p17 is able to inhibit motility, migration, and angiogenesis in human macrovascular (HUVEC) and microvascular endothelial cells (EC) (HMVEC)

  • It was earlier shown that alphaviral structural proteins contribute to cell death by apoptosis as virus replicon particles (VRP) lacking E1 and E2, showed a delay in caspase activation thereby concluding that structural proteins contribute to apoptotic activity in cancer cells [109]

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Summary

Introduction

Viruses have proven to be drivers of evolution since more than 500 million years ago. Rep has been observed to exert antiproliferative effects by blocking cell cycle in all of the phases and by inducing apoptosis independently of p53 via the caspase-3 dependent pathway [24]. In light of these findings, exploring the role of Rep in other cancer types and replicating the same in vivo may mark another milestone in virus-based anticancer therapy. The HHV-6/U94 gene, known as Rep, is highly conserved in both HHV-6A and B It is a single-stranded DNA binding, exonuclease, helicase-ATPase protein which might be involved in DNA replication. Since U94 mRNA was detected in the peripheral blood mononuclear cells (PBMC) from latently infected healthy individuals, U94 was considered as a molecular marker of viral latency [28]

Mechanism of Action
Role of U94 in Blocking Angiogenesis
Role in Cell Cycle
Role in Angiogenesis
SINV E1 and E2
Administration Tools
Conclusions and Future Directions
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