scholarly journals DNA Geminivirus Infection Induces an Imprinted E3 Ligase Gene to Epigenetically Activate Viral Gene Transcription

2020 ◽  
Vol 32 (10) ◽  
pp. 3256-3272 ◽  
Author(s):  
Zhong-Qi Chen ◽  
Jian-Hua Zhao ◽  
Qian Chen ◽  
Zhong-Hui Zhang ◽  
Jie Li ◽  
...  
Keyword(s):  
Gene Transcription ◽  
E3 Ligase ◽  
Viral Gene ◽  
Viral Gene Transcription

scholarly journals Strategies to Inhibit Hepatitis B Virus at the Transcript Level

Viruses ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1327
Author(s):  
Bingqian Qu ◽  
Richard J. P. Brown
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Gene Transcription ◽  
Antigen Expression ◽  
Transcript Level ◽  
Viral Gene ◽  
Small Interfering Rnas ◽  
Viral Gene Transcription ◽  
Hbv Vaccination ◽  
B Virus

Approximately 240 million people are chronically infected with hepatitis B virus (HBV), despite four decades of effective HBV vaccination. During chronic infection, HBV forms two distinct templates responsible for viral transcription: (1) episomal covalently closed circular (ccc)DNA and (2) host genome-integrated viral templates. Multiple ubiquitous and liver-specific transcription factors are recruited onto these templates and modulate viral gene transcription. This review details the latest developments in antivirals that inhibit HBV gene transcription or destabilize viral transcripts. Notably, nuclear receptor agonists exhibit potent inhibition of viral gene transcription from cccDNA. Small molecule inhibitors repress HBV X protein-mediated transcription from cccDNA, while small interfering RNAs and single-stranded oligonucleotides result in transcript degradation from both cccDNA and integrated templates. These antivirals mediate their effects by reducing viral transcripts abundance, some leading to a loss of surface antigen expression, and they can potentially be added to the arsenal of drugs with demonstrable anti-HBV activity. Thus, these candidates deserve special attention for future repurposing or further development as anti-HBV therapeutics.

scholarly journals Swine Promyelocytic Leukemia Isoform II Inhibits Pseudorabies Virus Infection by Suppressing Viral Gene Transcription in Promyelocytic Leukemia Nuclear Bodies

2020 ◽  
Vol 94 (18) ◽  
Author(s):  
Cuilian Yu ◽  
Aotian Xu ◽  
Yue Lang ◽  
Chao Qin ◽  
Mengdong Wang ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Transcriptional Repression ◽  
Pseudorabies Virus ◽  
Promyelocytic Leukemia ◽  
Natural Host ◽  
Nuclear Bodies ◽  
Viral Gene ◽  
Viral Gene Transcription ◽  
C Terminus ◽  
Promyelocytic Leukemia Nuclear Bodies

ABSTRACT Promyelocytic leukemia nuclear bodies (PML-NBs) possess an important intrinsic antiviral activity against alphaherpesvirus infection. PML is the structural backbone of NBs, comprising different isoforms. However, the contribution of each isoform to alphaherpesvirus restriction is not well understood. Here, we report the role of PML-NBs and swine PML (sPML) isoforms in pseudorabies virus (PRV) infection in its natural host swine cells. We found that sPML-NBs exhibit an anti-PRV activity in the context of increasing the expression level of endogenous sPML. Of four sPML isoforms cloned and examined, only isoforms sPML-II and -IIa, not sPML-I and -IVa, expressed in a sPML knockout cells inhibit PRV infection. Both the unique 7b region of sPML-II and the sumoylation-dependent normal formation of PML-NBs are required. 7b possesses a transcriptional repression activity and suppresses viral gene transcription during PRV infection with the cysteine residues 589 and 599 being critically involved. We conclude that sPML-NBs inhibit PRV infection partly by repressing viral gene transcription through the 7b region of sPML-II. IMPORTANCE PML-NBs are nuclear sites that mediate the antiviral restriction of alphaherpesvirus gene expression and replication. However, the contribution of each PML isoform to this activity of PML-NBs is not well characterized. Using PRV and its natural host swine cells as a system, we have discovered that the unique C terminus of sPML isoform II is required for PML-NBs to inhibit PRV infection by directly engaging in repression of viral gene transcription. Our study not only confirms in swine cells that PML-NBs have an antiviral function but also presents a mechanism to suggest that PML-NBs inhibit viral infection in an isoform specific manner.

scholarly journals Evaluation of Cyprinid Herpesvirus 2 Latency and Reactivation in Carassius gibel

2020 ◽  
Vol 8 (3) ◽  
pp. 445
Author(s):  
Wenjun Chai ◽  
Lin Qi ◽  
Yujun Zhang ◽  
Mingming Hong ◽  
Ling Jin ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Genomic Dna ◽  
Primary Infection ◽  
Trichostatin A ◽  
Acute Infection ◽  
Culture Conditions ◽  
Gibel Carp ◽  
Viral Gene ◽  
Viral Gene Transcription

Cyprinid herpesvirus 2 (CyHV-2, species Cyprinid herpesvirus 2) causes severe mortality in ornamental goldfish, crucian carp (Carassius auratus), and gibel carp (Carassius gibelio). It has been shown that the genomic DNA of CyHV-2 could be detected in subclinical fish, which implied that CyHV-2 could establish persistent infection. In this study, the latency of CyHV-2 was investigated in the survival fish after primary infection. CyHV-2 genomic DNA was detected in multiple tissues of acute infection samples; however, detection of CyHV-2 DNA was significantly reduced in fish recovered from the primary infection on day 300 postinfection. No active viral gene transcription, such as DNA polymerase and ORF99, was detected in recovered fish. Following temperature stress, an increase of CyHV-2 DNA copy numbers and gene transcription were observed in tissues examined, which suggests that CyHV-2 was reactivated under stress. In addition, a cell line (GCBLat1) derived from the brain tissue from CyHV-2-exposed fish harbored CyHV-2 genome but did not produce infectious virions under normal culture conditions. However, CyHV-2 replication and viral gene transcription occurred when GCBLat1 cells were treated with trichostatin A (TSA) or phorbol 12-myristate 13-acetate (TPA). It suggests CyHV-2 can remain latent in vitro and can reactivate under stress condition.

scholarly journals BRD4 is associated with raccoon polyomavirus genome and mediates viral gene transcription and maintenance of a stem cell state in neuroglial tumour cells

2016 ◽  
Vol 97 (11) ◽  
pp. 2939-2948 ◽  
Author(s):  
Molly E. Church ◽  
Marko Estrada ◽  
Christian M. Leutenegger ◽  
Florante N. Dela Cruz ◽  
Patricia A. Pesavento ◽  
...  
Keyword(s):  
Stem Cell ◽  
Gene Transcription ◽  
Tumour Cells ◽  
Viral Gene ◽  
Viral Gene Transcription ◽  
Cell State ◽  
Stem Cell State

scholarly journals Alpha interferon suppresses hepatitis B virus enhancer activity and reduces viral gene transcription.

1990 ◽  
Vol 64 (4) ◽  
pp. 1821-1824 ◽  
Author(s):  
R Tur-Kaspa ◽  
L Teicher ◽  
O Laub ◽  
A Itin ◽  
D Dagan ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Gene Transcription ◽  
Alpha Interferon ◽  
Viral Gene ◽  
Enhancer Activity ◽  
Viral Gene Transcription ◽  
B Virus

scholarly journals Whitefly HES1 binds to the intergenic region of Tomato yellow leaf curl China virus and promotes viral gene transcription

Virology ◽  
2020 ◽  
Vol 542 ◽  
pp. 54-62 ◽  
Author(s):  
Yu-Meng Wang ◽  
Ya-Zhou He ◽  
Xin-Tong Ye ◽  
Wen-Ze He ◽  
Shu-Sheng Liu ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Intergenic Region ◽  
Tomato Yellow Leaf ◽  
Viral Gene ◽  
Yellow Leaf ◽  
Viral Gene Transcription ◽  
Leaf Curl

scholarly journals Glucocorticoids and chromosomal position modulate murine mammary tumor virus transcription by affecting efficiency of promoter utilization.

1983 ◽  
Vol 3 (4) ◽  
pp. 551-561 ◽  
Author(s):  
D S Ucker ◽  
G L Firestone ◽  
K R Yamamoto
Keyword(s):  
Gene Transcription ◽  
Mammary Tumor ◽  
Transcription Initiation ◽  
Viral Gene ◽  
Mammary Tumor Virus ◽  
Viral Gene Transcription ◽  
Murine Mammary Tumor Virus ◽  
Chromosomal Position ◽  
Murine Mammary Tumor ◽  
Tumor Virus

The rate of transcription of murine mammary tumor virus (MTV) sequences in MTV-infected rat hepatoma tissue culture cells is strongly affected by both glucocorticoid hormones and the chromosomal position of provirus integration. We have characterized MTV RNAs produced in J2.17 and M1.54, independent isolates containing, respectively, 1 and 10 proviruses integrated at distinct chromosomal loci. M1.54, but not J2.17, synthesized MTV RNA in the absence of glucocorticoids; the rate of hormone-stimulated viral gene transcription in M1.54 was 50- to 100-fold higher than in J2.17. In each case in which MTV genes were expressed (J2.17 induced, M1.54 basal and induced), the viral RNAs produced were indistinguishable. RNA blotting revealed accumulation of two transcripts, 7.8 and 3.8 kilobases; the latter was likely produced from the former by RNA splicing. Sites used for transcription initiation, polyadenylation, and splicing have been identified from the sizes of end-labeled hybridization probes protected from digestion with mung bean nuclease; the unique initiation and polyadenylation sites were both encoded within the MTV long-terminal-repeat sequence. The efficiencies of splicing and of utilization of the polyadenylation signal did not appear to vary as functions of chromosomal position or hormonal stimulation. Differences in rates of viral gene transcription were reflected in the differential accumulation of the 5'-terminal 136 nucleotides of MTV RNA. Thus, glucocorticoids and chromosomal position appeared to affect solely the efficiency of utilization of the MTV promoter, leaving unchanged the sites of initiation, splicing, and polyadenylation, as well as the efficiencies of the latter two processes.

Sign in / Sign up

Export Citation Format

Share Document