Abstract
Epigenetics is a versatile player in manipulating viral infection and a potential therapeutic target for the treatment of viral-induced diseases. Both epigenetics and metabolism are crucial in establishing a highly specific transcriptional network, which may promote or suppress virus infection. Human herpesvirus infection can induce a broad range of human malignancies and is largely dependent on the status of cellular epigenetics as well as its related metabolism. However, the crosstalk between epigenetics and metabolism during herpesvirus infection has not been fully explored. Here, we describe how epigenetic regulation of cellular metabolism affects herpesvirus infection and induces viral diseases. This further highlights the importance of epigenetics and metabolism during viral infection and provides novel insights into the development of targeted therapies.
Highlights
Human herpesvirus family is a group of important DNA viruses that are associated with a spectrum of human diseases [1]
The results demonstrated that human cytomegalovirus (HCMV) profoundly promoted fatty acid biosynthesis, while herpes simplex virus 1 (HSV-1) increased pyrimidine biosynthesis [33]
DNMT1 histone deacetylases, resulting in hypermethylation and suppression of through the JNK-AP-1 pathway and can recruit DNMT1 and histone deacetylases, resulting in Kaposi’s sarcoma-associated herpesvirus (KSHV) interacts and recruits DNMT3A to increase de novo promoter methylation of H-cadherin hypermethylation and suppression of E-cadherin [48]
Summary
Human herpesvirus family is a group of important DNA viruses that are associated with a spectrum of human diseases [1]. This family contains eight members that belong to three subgroups according to the cells they predominantly infect and the site of latency [1]. Epigenetics, a crucial factor that affects herpesvirus infection, is characterized by DNA methylation and histone modifications These epigenetic modifications control chromosome organization and transcriptional regulation and to a large extent determine success of infection [3]. Metabolic substrates or enzymes are key players in regulating cellular epigenetic levels via controlling DNA methylation and histone methylation or acetylation. Understanding the interactions of epigenetics and metabolism in herpesvirus infection could provide new insights for the development of novel therapeutic strategies against herpesvirus-associated diseases
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