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Fig. 2.

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Fig. 2. Models of viral and host regulation related to chromatin conformation. (A) In herpesviruses, host architectural proteins (i.e., CTCF and cohesin) bind the viral episome and influence viral gene expression depending on the state of the virus (i.e., latent vs. lytic) via conformational changes to the episome. (B) Viral gene products can modulate host gene expression by targeting host enhancers or promoters (i.e., EBNAs and LANA). (C) The herpesvirus episome is associated with a repressed compartment in the host genome during latency. Upon reactivation, the interaction between the episome and euchromatin may increase. This viral-host chromosomal interplay could modulate both viral and host gene expression. (D) CTCF binding at the E2 promoter acts as a suppressor of viral oncogene E6/E7 by modulating HPV chromatin architecture. Disruption of CTCF binding causes transcriptional activation of E6/E7 in the HPV episome. (E) Viral integration into the host genome weakens looping between the E2 and E6/E7 loci, which also results in activation of the latter. The integrated viral sequence can hijack host enhancers for transcription of viral gene products or can act as an enhancer itself to stimulate neighboring cancer-associated genes. (F) Upon IAV infection, the viral protein NS1 inhibits the termination of transcription in a subset of highly transcribed genes. This inhibition leads to RNA Pol II-dependent dissociation of CTCF from its binding sites and disruption of chromatin loops (left). IAV protein NP competitively binds the host protein Suv4-20h2 to release Suv4-20h2- bound cohesin. Liberated cohesin is then recruited to the HoxC8-HoxC6 locus where it induces gene expression by forming an active chromatin loop (right).
J. Microbiol. Biotechnol. 2022;32:1515~1526
© J. Microbiol. Biotechnol.