Viruses, cancer and non-self recognition

Abstract

Virus–host interactions form an essential part of every aspect of life, and this review is aimed at looking at the balance between the host and persistent viruses with a focus on the immune system. The virus–host interaction is like a cat-and-mouse game and viruses have developed ingenious mechanisms to manipulate cellular pathways, most notably the major histocompatibility (MHC) class I pathway, to reside within infected cell while evading detection and destruction by the immune system. However, some of the signals sensing and responding to viral infection are derived from viruses and the fact that certain viruses can prevent the infection of others, highlights a more complex coexistence between the host and the viral microbiota. Viral immune evasion strategies also illustrate that processes whereby cells detect and present non-self genetic material to the immune system are interlinked with other cellular pathways. Immune evasion is a target also for cancer cells and a more detailed look at the interfaces between viral factors and components of the MHC class I peptide-loading complex indicates that these interfaces are also targets for cancer mutations. In terms of the immune checkpoint, however, viral and cancer strategies appear different.

MYO1B as a prognostic biomarker and a therapeutic target in Arecoline‐associated oral carcinoma

“…As reported in the literature, viral infections may encode oncogenic viral proteins and cause disruption of gene expression, thus conveying cancer characteristics to the infected cells 47,48 . Similarly, viral infections have the capacity to affect our immune system and activate cellular pathways through immune evasion strategies, leading to cancer development 49 . Moreover, viral infections might cause a cellular stress response.…”

“…47,48 Similarly, viral infections have the capacity to affect our immune system and activate cellular pathways through immune evasion strategies, leading to cancer development. 49 Moreover, viral infections might cause a cellular stress response. Major oncogenic viruses in the body can be reactivated by glucocorticoids or catecholamines, and stress hormones stimulate oncogenic gene expression in human cells infected with oncogenic viruses.…”

Functional Interfaces, Biological Pathways, and Regulations of Interferon-Related DNA Damage Resistance Signature (IRDS) Genes

“…Evolution of the innate and adaptive immunity was shaped by species-specific viruses, and many elements of these networks are brought by viruses themselves [ 134 , 135 , 136 ]. The ability of retroviruses to integrate to the host DNA, expand and reintegrate allows for dispersing their sequences all over the genome.…”

Homology Modeling Epitopes of Kirsten Rat Sarcoma (KRAS) G12D, G12V and G12R as Pancreatic Ductal Adenocarcinoma Vaccine Candidates

“…The KRAS epitopes G12D, G12V and G12R were presented in major histocompatibility complexes (MHC) class I [22,24,25]. MHC I plays a very important key role in recognition of virus-infected and transformed cells [26,27]. HLA-A*11:01 is one of the MHC I molecules that can bind peptides with KRAS amino acid mutation at codon 12 [22,28,29].…”