Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma, primary effusion lymphoma and multicentric Castleman's disease. Since the discovery of KSHV 20 years ago, there is still no standard treatment and the management of virus-associated malignancies remains toxic and incompletely efficacious. As the majority of tumor cells are latently infected with KSHV, currently marketed antivirals that target the virus lytic cycle have shown inconsistent results in clinic. Nevertheless, lytic replication plays a major role in disease progression and virus dissemination. Case reports and retrospective studies have pointed out the benefit of antiviral therapy in the treatment and prevention of KSHV-associated diseases. As a consequence, potent and selective antivirals are needed. This review focuses on the anti-KSHV activity, mode of action and current status of antiviral drugs targeting KSHV lytic cycle. Among these drugs, different subclasses of viral DNA polymerase inhibitors and compounds that do not target the viral DNA polymerase are being discussed. We also cover molecules that target cellular kinases, as well as the potential of new drug targets and animal models for antiviral testing.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246246PMC
http://dx.doi.org/10.3390/v6114731DOI Listing

Publication Analysis

Top Keywords

lytic replication
8
lytic cycle
8
viral dna
8
dna polymerase
8
kshv
5
kshv targeted
4
targeted therapy
4
therapy update
4
update inhibitors
4
inhibitors viral
4

Similar Publications

Bacteria are constantly threatened by their viral predators (phages), which has resulted in the development of defense systems for bacterial survival. One family of defense systems found widely across bacteria are OLD (for overcoming lysogeny defect) family nucleases. Despite recent discoveries regarding Class 2 and 4 OLD family nucleases and how phages overcome them, Class 1 OLD family nucleases warrant further study as there has only been one anti-phage Class 1 OLD family nuclease described to date.

View Article and Find Full Text PDF

KSHV hijacks the antiviral kinase IKKε to initiate lytic replication.

PLoS Pathog

January 2025

Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

IKKε is a traditional antiviral kinase known for positively regulating the production of type I interferon (IFN) and the expression of IFN-stimulated genes (ISGs) during various virus infections. However, through an inhibitor screen targeting cellular kinases, we found that IKKε plays a crucial role in the lytic replication of Kaposi's sarcoma-associated herpesvirus (KSHV). Mechanistically, during KSHV lytic replication, IKKε undergoes significant SUMOylation at both Lys321 and Lys549 by the viral SUMO E3 ligase ORF45.

View Article and Find Full Text PDF

ZBP1-driven cell death in severe influenza.

Trends Microbiol

January 2025

Center for Immunology, Fox Chase Cancer Center, Philadelphia, PA, USA. Electronic address:

Influenza A virus (IAV) infections can cause life-threatening illness in humans. The severity of disease is directly linked to virus replication in the alveoli of the lower respiratory tract. In particular, the lytic death of infected alveolar epithelial cells (AECs) is a major driver of influenza severity.

View Article and Find Full Text PDF

Background: Viruses that infect prokaryotes (phages) constitute the most abundant group of biological agents, playing pivotal roles in microbial systems. They are known to impact microbial community dynamics, microbial ecology, and evolution. Efforts to document the diversity, host range, infection dynamics, and effects of bacteriophage infection on host cell metabolism are extremely underexplored.

View Article and Find Full Text PDF

Modulation of Cell Cycle Kinases by Kaposi's Sarcoma-Associated Herpesvirus.

J Med Virol

January 2025

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

The cell cycle is governed by kinase activity that coordinates progression through a series of regulatory checkpoints, preventing the division of damaged cells. The Kaposi's sarcoma-associated herpesvirus (KSHV) encodes multiple genes that modulate or co-opt the activity of these kinases, shaping the cellular environment to promote viral persistence. By advancing the cell cycle, KSHV facilitates latent replication and subsequent transmission of viral genomes to daughter cells, while also contributing to the establishment of multiple cancer types.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!