Short Communication - Virology Research Journal (2023) Volume 7, Issue 2
The role of epigenetic modifications in viral gene expression regulation
Cortes Werghi*
Department of Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Iran
- Corresponding Author:
- Cortes Werghi
Department of Biochemistry
School of Medicine
Shiraz University of Medical Sciences, Iran
E-mail: cortes@sums.ac.ir
Received: 25-Feb-2023, Manuscript No. AAVRJ-23-90741; Editor assigned: 27-Feb-2023, PreQC No. AAVRJ-23-90741(PQ); Reviewed: 13-Mar-2023, QC No. AAVRJ-23-90741; Revised: 18-Mar-2023, Manuscript No. AAVRJ-23-90741(R); Published: 25-Mar-2023, DOI:10.35841/AAVRJ-7.2.139
Citation: Werghi C. The role of epigenetic modifications in viral gene expression regulation. Virol Res J. 2023;7(2):139
Introduction
Epigenetic modifications play a critical role in regulating gene expression, and recent research has highlighted their importance in viral gene expression as well [1]. In this article, we will discuss the role of epigenetic modifications in viral gene expression regulation.
Viral infections can have a significant impact on host gene expression, leading to changes in cellular processes and immune responses. The viral genome is often incorporated into the host genome, where it can be subject to epigenetic modifications that influence gene expression. Epigenetic modifications refer to changes in gene expression that are not caused by alterations in the DNA sequence but rather through modifications to DNA and its associated proteins. One of the most common epigenetic modifications is DNA methylation, which involves the addition of a methyl group to a cytosine nucleotide in DNA. DNA methylation typically leads to the silencing of gene expression by inhibiting transcription factors from binding to DNA, and thereby reducing gene expression. Viruses have evolved mechanisms to manipulate host DNA methylation to their advantage [2].
For example, human papillomavirus (HPV) has been shown to increase DNA methylation in the promoter regions of tumor suppressor genes, leading to their silencing and promoting viral persistence. This results in the development of HPV-associated cancers. Similarly, hepatitis B virus (HBV) and hepatitis C virus (HCV) have been shown to induce DNA methylation in host genes, leading to altered immune responses and promoting viral persistence. Histone modifications are another important epigenetic mechanism involved in regulating viral gene expression. Histones are proteins that package DNA into chromatin, and modifications to histones can influence the accessibility of DNA to transcription factors. Acetylation and deacetylation of histones are two common modifications that can alter gene expression [3]. Acetylation of histones typically leads to an increase in gene expression, whereas deacetylation leads to a decrease in gene expression. Viral proteins can interact with host proteins to manipulate histone modifications. For example, the human immunodeficiency virus (HIV) protein Tat interacts with the histone acetyltransferase p300, leading to increased acetylation of histones and activation of viral gene expression. Similarly, the Epstein-Barr virus (EBV) protein EBNA2 interacts with the histone acetyltransferase PCAF, leading to increased acetylation of histones and activation of viral gene expression [4,5].
In addition to DNA methylation and histone modifications, non-coding RNAs (ncRNAs) also play a role in regulating viral gene expression. ncRNAs are RNA molecules that do not code for proteins but instead regulate gene expression at the transcriptional and post-transcriptional levels. MicroRNAs (miRNAs) are a type of ncRNA that can bind to messenger RNA (mRNA) and inhibit its translation into protein. Several viruses, including herpes simplex virus (HSV) and human cytomegalovirus (HCMV), have been shown to manipulate host miRNAs to their advantage. For example, HCMV expresses a viral miRNA that targets a host mRNA involved in innate immune responses, leading to inhibition of the immune response and promoting viral persistence.
Epigenetic modifications can also influence the latency and reactivation of latent viruses. Latency is a state in which a virus remains dormant in the host cell without producing new viral particles. Reactivation occurs when the virus becomes active again and starts producing new viral particles. The transition between latency and reactivation is regulated by epigenetic modifications. For example, the herpes simplex virus type 1 (HSV-1) genome is subject to DNA methylation and histone modifications during latency. These modifications lead to the silencing of viral gene expression, allowing the virus to remain dormant. Reactivation of HSV-1 is associated with changes in epigenetic modifications, specifically the removal of repressive marks on histones and DNA demethylation, leading to the activation of viral gene expression and the production of new viral particles.
In summary, epigenetic modifications play a critical role in regulating viral gene expression. Viruses have evolved mechanisms to manipulate host epigenetic modifications to their advantage, leading to altered immune responses, viral persistence, and the development of viral-associated cancers. Epigenetic modifications can also influence the latency and reactivation of latent viruses, highlighting their importance in understanding the dynamics of viral infections. Understanding the role of epigenetic modifications in viral gene expression regulation has important implications for the development of antiviral therapies. Targeting host epigenetic modifications could potentially disrupt viral persistence and latency, leading to the clearance of the virus. For example, drugs that inhibit histone deacetylases (HDACs), which are involved in the removal of acetyl groups from histones, have been shown to reactivate latent viruses such as HIV and HSV-1, leading to the production of new viral particles and potential clearance of the virus.
In conclusion, epigenetic modifications are critical regulators of viral gene expression and play a key role in the pathogenesis of viral infections. Understanding the complex interplay between viruses and host epigenetic modifications will lead to the development of novel antiviral therapies and improve our understanding of the mechanisms underlying viral infections.
References
- Chen J. Activation of latent Kaposi's sarcoma-associated herpesvirus by demethylation of the promoter of the lytic transactivator. Proc Natl Acad Sci U S A. 2001;98(7):4119-24.
- Chang PC. Histone demethylase JMJD2A regulates Kaposi's sarcoma-associated herpesvirus replication and is targeted by a viral transcriptional factor. J Virol. 2011;85(7):3283-93.
- Toth Z, Brulois K, Jung JU. The chromatin landscape of Kaposi's sarcoma-associated herpesvirus. Viruses. 2013;5:1346–1373.
- Queen KJ Cve U, Scott RS. Epstein-Barr virus-induced epigenetic alterations following transient infection. Int J Cancer. 2013;132(9):2076-86.
- Caliskan M, Ober C. The effects of EBV transformation on gene expression levels and methylation profiles. Hum Mol Genet. 2011;20(8):1643-52.
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