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Updated: May 4, 2026
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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
Published on: September 14, 2010
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Kv1.3-induced hyperpolarization is required for efficient Kaposi's sarcoma-associated herpesvirus lytic replication.
Holli Carden1, Katherine L Harper1, Timothy J Mottram1
1School of Molecular and Cellular Biology and Astbury Centre for Structural Molecular Biology, University of Leeds, LS2 9JT Leeds, UK.
Science Signaling
|July 16, 2024
Summary
Voltage-gated potassium channel Kv1.3 in B cells promotes Kaposi's sarcoma-associated herpesvirus (KSHV) replication. Blocking Kv1.3 inhibits KSHV lytic replication and infectious virion production, identifying it as a therapeutic target.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Kaposi's sarcoma-associated herpesvirus (KSHV) causes Kaposi's sarcoma.
- KSHV establishes latent infections in B cells, with reactivation leading to lytic replication and virion production.
Purpose of the Study:
- To investigate the role of voltage-gated potassium channel Kv1.3 in KSHV lytic replication.
- To identify Kv1.3 as a potential therapeutic target for KSHV infection.
Main Methods:
- Pharmacological and genetic silencing of Kv1.3 in B cells.
- Assessing KSHV replication and infectious virion production.
- Measuring intracellular calcium (Ca2+) levels and protein localization.
Main Results:
- Kv1.3 channel activity enhanced KSHV lytic replication.
- KSHV RTA protein increased Kv1.3 abundance and activity, leading to B cell membrane hyperpolarization.
- Enhanced Kv1.3 activity promoted Ca2+ influx, nuclear localization of KSHV RTA and NFAT, and increased NFAT1 target gene expression.
- Kv1.3 blockers or silencing inhibited KSHV replication and virion production.
Conclusions:
- Kv1.3 is a critical host factor for KSHV lytic replication.
- Kv1.3 represents a druggable target for inhibiting KSHV replication and potentially treating KSHV-associated diseases.
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