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Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
Published on: August 15, 2025
913
KSHV miRNAs decrease expression of lytic genes in latently infected PEL and endothelial cells by targeting host
Karlie Plaisance-Bonstaff1, Hong Seok Choi2, Tyler Beals3
1Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA. karliebonstaff@gmail.com.
Viruses
|October 25, 2014
Summary
Kaposi's sarcoma-associated herpesvirus (KSHV) microRNAs miR-K12-3 and miR-K12-11 help maintain viral latency. These KSHV microRNAs indirectly decrease viral replication by down-regulating key transcription factors.
Area of Science:
- Virology
- Molecular Biology
- Gene Regulation
Background:
- Kaposi's sarcoma-associated herpesvirus (KSHV) encodes microRNAs within its latency-associated region.
- These KSHV microRNAs play a role in regulating viral gene expression during latency.
Purpose of the Study:
- To investigate the function of KSHV-encoded microRNAs, specifically miR-K12-3 and miR-K12-11, in regulating viral latency and reactivation.
- To elucidate the molecular mechanisms by which these microRNAs control the expression of viral and cellular genes.
Main Methods:
- Utilizing cell culture models (BC-3, BCBL-1, iSLK cells) with KSHV infection.
- Employing knockdown techniques to reduce specific KSHV microRNA levels.
- Performing gene expression analysis and virus production assays.
- Using luciferase reporter assays to confirm microRNA target interactions.
Main Results:
- Knockdown of miR-K12-3 and miR-K12-11 increased the expression of KSHV lytic genes and virus production.
- Deletion mutants of miR-K12-3 and miR-K12-11 in KSHV led to increased spontaneous viral reactivation.
- miR-K12-3 and miR-K12-11 were predicted and confirmed to target cellular transcription factors MYB, Ets-1, and C/EBPα, which are involved in activating the KSHV replication and transcription activator (RTA).
- Knockdown of miR-K12-11 increased MYB transcript levels, while knockdown of miR-K12-3 increased C/EBPα and Ets-1 transcript levels.
Conclusions:
- KSHV microRNAs miR-K12-3 and miR-K12-11 are crucial for maintaining viral latency.
- These microRNAs contribute to latency by indirectly suppressing RTA expression through the down-regulation of MYB, Ets-1, and C/EBPα.
- These findings reveal a novel regulatory mechanism by which KSHV microRNAs control viral reactivation and persistence.
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