scholarly journals Significance of Epigenetics in Sars-CoV-2 Infection and Proposed Epi-Drugs for Covid-19

Author(s):  
Pragya Chaturvedi ◽  
Sudhanshu Singh

We frequently come in contact with animal viruses through the food which we eat, the pets which we have, and our connections with nature. The enormous majority of viruses which enter our bodies pass inoffensively through our physiological systems or eradicate by our immune systems. However, on rare circumstances, a human-encounters by a virus which begins to replicate itself, accomplishing its entire lifecycle within human cells and intensifying themselves into a large number. Replication of an animal virus inside the human body is the key instant in the zoonotic process. SARS CoV-2 is one of these viruses which cause COVID-19 disease. To enter the target cell SARS-CoV-2 uses angiotensinconverting enzyme 2 (ACE2) and the cellular protease transmembrane protease serine 2 (TMPRSS2). Genome stability and maintenance of cellular equilibrium are the main parameters influenced by epigenetically regulated chromatin structure. Implication of regulation by epigenetic machinery has also been found in the physiopathology of the virus infection. By varying the function of gene locus. such regulation links genotype and phenotype without changing the original DNA sequences. However antiviral drugs have been used to treat various viral diseases since long, epi-drugs are now proposed to treat these diseases due to the epigenetic implications found in these infections. Epi-drugs are small agents that are able to reverse some epigenetic changes. This review is aimed to find implication of epigenetics in infection caused due SARS C0V-2 and if there is any epi-drugs approach possible to treat this infection.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yu-Ching Teng ◽  
Aishwarya Sundaresan ◽  
Ryan O’Hara ◽  
Vincent U. Gant ◽  
Minhua Li ◽  
...  

AbstractATRX is a tumor suppressor that has been associated with protection from DNA replication stress, purportedly through resolution of difficult-to-replicate G-quadruplex (G4) DNA structures. While several studies demonstrate that loss of ATRX sensitizes cells to chemical stabilizers of G4 structures, the molecular function of ATRX at G4 regions during replication remains unknown. Here, we demonstrate that ATRX associates with a number of the MCM replication complex subunits and that loss of ATRX leads to G4 structure accumulation at newly synthesized DNA. We show that both the helicase domain of ATRX and its H3.3 chaperone function are required to protect cells from G4-induced replicative stress. Furthermore, these activities are upstream of heterochromatin formation mediated by the histone methyltransferase, ESET, which is the critical molecular event that protects cells from G4-mediated stress. In support, tumors carrying mutations in either ATRX or ESET show increased mutation burden at G4-enriched DNA sequences. Overall, our study provides new insights into mechanisms by which ATRX promotes genome stability with important implications for understanding impacts of its loss on human disease.


EMBO Reports ◽  
2018 ◽  
Vol 20 (1) ◽  
Author(s):  
Thomas S Emden ◽  
Marta Forn ◽  
Ignasi Forné ◽  
Zsuzsa Sarkadi ◽  
Matías Capella ◽  
...  

1998 ◽  
Vol 10 (8) ◽  
pp. 671 ◽  
Author(s):  
Kurt A. Zuelke

The application of transgenic technologies in dairy cattle has been restricted largely to producing potential pharmaceutical or nutriceutical products in the mammary gland. Broader application of transgenesis in dairy cattle production will require identifying target traits that are both amenable to transgenic modification and economically important to the dairy industry. The casein proteins are the most valuable component of cows milk destined for value-added processing. The four bovine casein genes lie within a single, multi-gene locus of approximately 200 kb in length. The working hypothesis is that this multi-gene locus contains all of the DNA sequences required to regulate the coordinated expression of all four individual casein genes (i.e. a locus control region or LCR). The initial research aim is to clone the entire casein locus into a bacterial artificial chromosome (BAC) vector, thus preserving the extended 5′and 3′ regions that flank the locus, as well as maintaining the spatial integrity of the four individual casein genes that comprise the locus. The author's laboratory has prepared a bacterial artificial chromosome (BAC) library of genomic DNA from elite dairy cattle. Partial, non-elite BAC clones of the casein gene locus are being tested in transgenic mice to establish proof of concept. Advances in nuclear transfer of transfected somatic cells should improve the efficiency of producing transgenic calves that possess a BAC casein construct introduced into an elite genetic background.


2012 ◽  
Vol 109 (38) ◽  
pp. 15229-15234 ◽  
Author(s):  
Bethany A. Buck-Koehntop ◽  
Robyn L. Stanfield ◽  
Damian C. Ekiert ◽  
Maria A. Martinez-Yamout ◽  
H. Jane Dyson ◽  
...  

Methylation of CpG dinucleotides in DNA is a common epigenetic modification in eukaryotes that plays a central role in maintenance of genome stability, gene silencing, genomic imprinting, development, and disease. Kaiso, a bifunctional Cys2His2 zinc finger protein implicated in tumor-cell proliferation, binds to both methylated CpG (mCpG) sites and a specific nonmethylated DNA motif (TCCTGCNA) and represses transcription by recruiting chromatin remodeling corepression machinery to target genes. Here we report structures of the Kaiso zinc finger DNA-binding domain in complex with its nonmethylated, sequence-specific DNA target (KBS) and with a symmetrically methylated DNA sequence derived from the promoter region of E-cadherin. Recognition of specific bases in the major groove of the core KBS and mCpG sites is accomplished through both classical and methyl CH···O hydrogen-bonding interactions with residues in the first two zinc fingers, whereas residues in the C-terminal extension following the third zinc finger bind in the opposing minor groove and are required for high-affinity binding. The C-terminal region is disordered in the free protein and adopts an ordered structure upon binding to DNA. The structures of these Kaiso complexes provide insights into the mechanism by which a zinc finger protein can recognize mCpG sites as well as a specific, nonmethylated regulatory DNA sequence.


2017 ◽  
Vol 32 (3) ◽  
pp. 235-244 ◽  
Author(s):  
Dong-Ying Liu ◽  
Jing Liu ◽  
Bing-Yu Liu ◽  
Yuan-Yuan Liu ◽  
Hai-Rong Xiong ◽  
...  

1992 ◽  
Vol 5 (1) ◽  
pp. 49-73 ◽  
Author(s):  
E O Major ◽  
K Amemiya ◽  
C S Tornatore ◽  
S A Houff ◽  
J R Berger

Studies of the pathogenesis and molecular biology of JC virus infection over the last two decades have significantly changed our understanding of progressive multifocal leukoencephalopathy, which can be described as a subacute viral infection of neuroglial cells that probably follows reactivation of latent infection rather than being the consequence of prolonged JC virus replication in the brain. There is now sufficient evidence to suggest that JC virus latency occurs in kidney and B cells. However, JC virus isolates from brain or kidney differ in the regulatory regions of their viral genomes which are controlled by host cell factors for viral gene expression and replication. DNA sequences of noncoding regions of the viral genome display a certain heterogeneity among isolates from brain and kidney. These data suggest that an archetypal strain of JC virus exists whose sequence is altered during replication in different cell types. The JC virus regulatory region likely plays a significant role in establishing viral latency and must be acted upon for reactivation of the virus. A developing hypothesis is that reactivation takes place from latently infected B lymphocytes that are activated as a result of immune suppression. JC virus enters the brain in the activated B cell. Evidence for this mechanism is the detection of JC virus DNA in peripheral blood lymphocytes and infected B cells in the brains of patients with progressive multifocal leukoencephalopathy. Once virus enters the brain, astrocytes as well as oligodendrocytes support JC virus multiplication. Therefore, JC virus infection of neuroglial cells may impair other neuroglial functions besides the production and maintenance of myelin. Consequently our increased understanding of the pathogenesis of progressive multifocal leukoencephalopathy suggests new ways to intervene in JC virus infection with immunomodulation therapies. Perhaps along with trials of nucleoside analogs or interferon administration, this fatal disease, for which no consensus of antiviral therapy exists, may yield to innovative treatment protocols.


1983 ◽  
Vol 23 (1) ◽  
pp. 109-145 ◽  
Author(s):  
Luis Carrasco ◽  
Juan Carlos Lacal
Keyword(s):  

Author(s):  
A. Taqaddas

Viral infections have always been of major concern in communities, health care settings and medical fields including radiotherapy and Radiology. Recently corona virus infection has attained global attention in the wake of covid-19 outbreak and consequently highlighted importance of viral prevention, diagnostic and therapeutic strategies to control and treat viral disease. In view of the recent events, the author reviewed the current and past literature to discuss contagious versus infectious viral transmission, as well as simple and effective ways of preventing the spread of viral diseases in community and health care setting so that this information can be used for preventing viral transmission at all levels. The article is written for a wide variety of audiences i.e. scientific and medical communities policy makers and general public.


Viruses ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1377
Author(s):  
Yonggang Pei ◽  
Erle S. Robertson

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.


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