Editorial: Interaction between virus and host cell: how do viruses cause cellular dysregulation?
Résumé
Viruses are opportunistic pathogens that hijack host cell machinery including control of host cell cycle, apoptosis, immunity and essential cellular signalling cascades to be employed only for their own replication. Other viruses, namely oncogenic viruses, are controlling the cellular oncogenic pathways and dysregulating them leading directly or indirectly to the development of carcinoma or malignancy. For instance, hepatitis B virus (HBV, DNA virus), human papillomavirus (HPV, DNA virus), human herpesvirus-8 (HHV-8, DNA virus), and Merkel cell polyomavirus (MCPyV, DNA virus), Epstein-Barr Virus (EBV, DNA virus), hepatitis C virus (HCV, RNA virus) and human T-cell lymphotropic virus-1 (HTLV-1, RNA virus). The high prevalence and extended epidemiology of these oncogenic viral infections in developing countries including Sub-Saharan African countries [1] are alarming to consider early and affordable precancer molecular marker with high reliability and predictive value in these populations. For the early diagnosis of these viral infections and understanding the role of the cellular factors in establishing viral infections and their long-term consequences (e.g. carcinoma), the transcriptomic and proteomic studies of virus-infected cells and single-cell analysis could recently attract more attention. These studies can globally revolutionize the approach of translational research. Interestingly, the viral infection consequences may extend beyond virus clearance due to treatment with direct-acting antivirals [2]. To this point, Elbahrawy and his colleagues emphasized the importance to follow up the pretreatment and posttreatment predictors of hepatocellular carcinoma (HCC) and recommended the indication of HCC surveillance in recovered HCV patients with compensated advanced chronic liver disease [2]. The post-treatment complications in HCV patients might be caused by remaining HCV-induced epigenetic alterations, immune dysregulations, and hepatic parenchymal injuries, leading to de novo HCC occurrence [2].This Research Topic gathers also contributions that highlight the intracellular trafficking networks of human-cytomegalovirus (HCMV) and elucidated the strategies that the HCMV employs to hijack and dysregulate the intracellular trafficking networks to permit viral fitness and replication [3]. In addition, cell infection with viruses is always associated with the intracellular release of different types of RNAs including long non-coding RNA (IncRNA), MicroRNA (miRNA), protein coding mRNA and other RNAs. These RNA species play important roles in virus–host interactions, viral pathogenicity and regulating innate antiviral responses. In the minireview article by Nangare and his colleagues, the authors highlighted the importance of secreted miRNA species during Chikungunya viral infections and their possible role to develop candidate cellular miRNA-based therapies against Chikungunya viral infections [4]. This collection could spotlight the necessity to intensify research effort and funding to understand the cellular networks that are induced following viral infections and to define regulated and dysregulated cellular elements/pathways during viral infections. This could pave the way to apply these elements as markers of virus-induced complications such as malignancy or provide novel approaches as druggable targets.
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