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OMICS ; 25(6): 358-371, 2021 06.
Article in English | MEDLINE | ID: covidwho-1243453


About a tenth of all cancers are caused by viruses or associated with viral infection. Recent global events including the coronavirus disease-2019 (COVID-19) pandemic means that human encounter with viruses is increased. Cancer development in individuals with viral infection can take many years after infection, demonstrating that the involvement of viruses in cancer development is a long and complex process. This complexity emanates from individual genetic heterogeneity and the many steps involved in cancer development owing to viruses. The process of tumorigenesis is driven by the complex interaction between several viral factors and host factors leading to the creation of a tumor microenvironment (TME) that is ideal and promotes tumor formation. Viruses associated with human cancers ensure their survival and proliferation through activation of several cellular processes including inflammation, migration, and invasion, resistance to apoptosis and growth suppressors. In addition, most human oncoviruses evade immune detection and can activate signaling cascades including the PI3K-Akt-mTOR, Notch and Wnt pathways associated with enhanced proliferation and angiogenesis. This expert review examines and synthesizes the multiple biological factors related to oncoviruses, and the signaling cascades activated by these viruses contributing to viral oncogenesis. In particular, I examine and review the Epstein-Barr virus, human papillomaviruses, and Kaposi's sarcoma herpes virus in a context of cancer pathogenesis. I conclude with a future outlook on therapeutic targeting of the viruses and their associated oncogenic pathways within the TME. These anticancer strategies can be in the form of, but not limited to, antibodies and inhibitors.

Epstein-Barr Virus Infections/virology , Neoplasms/virology , Papillomavirus Infections/virology , Retroviridae Infections/virology , Retroviridae/physiology , Sarcoma, Kaposi/virology , Tumor Virus Infections/virology , Alphapapillomavirus/physiology , Carcinogenesis , Cell Transformation, Viral , Epstein-Barr Virus Infections/pathology , Herpesvirus 4, Human/physiology , Herpesvirus 8, Human/physiology , Humans , Molecular Targeted Therapy , Neoplasms/pathology , Neoplasms/therapy , Papillomavirus Infections/pathology , Retroviridae Infections/pathology , Sarcoma, Kaposi/pathology , Signal Transduction , Tumor Microenvironment , Tumor Virus Infections/pathology
Int Immunopharmacol ; 91: 107331, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1065225


The present review provides an overview of recent advances regarding the function of Th17 cells and their produced cytokines in the progression of viral diseases. Viral infections alone do not lead to virus-induced malignancies, as both genetic and host safety factors are also involved in the occurrence of malignancies. Acquired immune responses, through the differentiation of Th17 cells, form the novel components of the Th17 cell pathway when reacting with viral infections all the way from the beginning to its final stages. As a result, instead of inducing the right immune responses, these events lead to the suppression of the immune system. In fact, the responses from Th17 cells during persistent viral infections causes chronic inflammation through the production of IL-17 and other cytokines which provide a favorable environment for tumor growth and its development. Additionally, during the past decade, these cells have been understood to be involved in tumor progression and metastasis. However, further research is required to understand Th17 cells' immune mechanisms in the vast variety of viral diseases. This review aims to determine the roles and effects of the immune system, especially Th17 cells, in the progression of viral diseases; which can be highly beneficial for the diagnosis and treatment of these infections.

Cell Transformation, Viral , Neoplasms/virology , Th17 Cells/virology , Tumor Virus Infections/virology , Viruses/pathogenicity , Animals , Host-Pathogen Interactions , Humans , Neoplasms/immunology , Neoplasms/metabolism , Th17 Cells/immunology , Th17 Cells/metabolism , Tumor Microenvironment , Tumor Virus Infections/immunology , Tumor Virus Infections/metabolism , Viruses/immunology
Transpl Infect Dis ; 23(1): e13465, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-772374


Kidney transplant recipients have been supposed vulnerable to severe Covid-19 infection, due to their comorbidities and immunosuppressive therapies. Mild-term complications of Covid-19 are currently unknown, especially in this population. Herein, we report two cases of BKV replication after non-severe SARS-CoV-2 infection. The first case was a 59-year-old man, transplanted 3 months ago, with recent history of slight BKV viremia (3.3 log10 DNA copies/ml). Despite strong reduction of maintenance immunosuppression (interruption of mycophenolic acid and important decrease of calcineurin inhibitors), BKV replication largely increased after Covid-19 and viremia persisted at 4.5 log copy/ml few months later. The second case was a 53-year-old woman, transplanted 15 years ago. She had a recent history of BKV cystitis, which resolved with a decrease of MPA dosage. Few weeks after SARS-CoV-2 infection, she presented recurrence of lower urinary tract symptoms. Our reports highlight that SARS-CoV-2 infection, even without severity, could disrupt immune system and particularly lymphocytes, thus leading to viral replication. Monitoring of viral replications after Covid-19 in kidney transplant recipients could permit to confirm these preliminary observations.

BK Virus , COVID-19 , Kidney Transplantation , Polyomavirus Infections/virology , SARS-CoV-2 , Tumor Virus Infections/virology , Female , Humans , Immunosuppressive Agents/administration & dosage , Male , Middle Aged , Transplant Recipients , Viremia