Target type: biologicalprocess
Any process in which a host organism modulates the frequency, rate or extent of viral transcription. [GOC:jl]
Viruses rely on host cellular machinery to replicate, and this includes transcription. Host cells possess a complex regulatory network that can modulate viral transcription in various ways. This modulation can either enhance or suppress viral gene expression, ultimately influencing the course of infection. Here's a detailed breakdown of how hosts can influence viral transcription:
* **Transcription Factors (TFs):** Host TFs can bind to specific DNA sequences within viral promoters, either activating or repressing transcription. Some TFs are constitutively expressed and may have general effects on transcription, while others are induced or repressed in response to viral infection. This induction or repression can be part of the innate immune response.
* **Chromatin Remodeling:** The structure of chromatin, the complex of DNA and proteins that forms chromosomes, influences accessibility of viral DNA to transcription machinery. Host factors can alter chromatin structure by modifying histones (proteins associated with DNA) via acetylation, methylation, or phosphorylation. These modifications can either promote or hinder transcription.
* **RNA Polymerase II (RNAP II):** This enzyme is crucial for transcribing DNA into RNA, including viral genes. Host cells can regulate RNAP II activity and its association with viral promoters, thereby influencing transcription rates.
* **Viral RNA Splicing:** Some viruses utilize host splicing machinery to process their pre-mRNAs into mature mRNAs. Host factors can influence the efficiency and specificity of splicing, ultimately determining which viral proteins are produced.
* **MicroRNAs (miRNAs):** These small RNA molecules play a significant role in post-transcriptional gene regulation. Host miRNAs can target viral transcripts, either degrading them or inhibiting their translation.
* **Interferon (IFN) Response:** IFN is a key component of the innate immune response. Upon viral infection, cells produce IFN, which triggers a cascade of events leading to the production of antiviral proteins that can directly inhibit viral transcription or indirectly suppress it by inducing the expression of antiviral genes.
* **Cellular Stress Responses:** Viral infection can induce cellular stress, which can activate various stress response pathways. These pathways often involve modulation of transcription factors and other cellular processes that influence viral gene expression.
The modulation of viral transcription by the host is a complex and dynamic process that involves multiple levels of regulation. Understanding these mechanisms is crucial for developing antiviral therapies that target the host-virus interaction. '
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Protein | Definition | Taxonomy |
---|---|---|
26S proteasome regulatory subunit 6A | A 26S proteasome regulatory subunit 6A that is encoded in the genome of human. [PRO:DNx] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
bortezomib | amino acid amide; L-phenylalanine derivative; pyrazines | antineoplastic agent; antiprotozoal drug; protease inhibitor; proteasome inhibitor | |
carfilzomib | epoxide; morpholines; tetrapeptide | antineoplastic agent; proteasome inhibitor | |
belactosin a | belactosin A: isolated from Streptomyces; structure in first source |