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Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates

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Published on: July 6, 2013

Wnt modulating agents inhibit human cytomegalovirus replication.

Arun Kapoor¹, Ran He, Rajkumar Venkatadri

¹Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Antimicrobial Agents and Chemotherapy

|April 11, 2013

Summary

Compounds targeting the Wnt pathway, like nigericin, inhibit human cytomegalovirus (HCMV) replication by disrupting viral protein expression and Wnt signaling. This reveals a complex interplay between HCMV and Wnt, crucial for understanding viral control.

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Ex Vivo Infection of Human Lymphoid Tissue and Female Genital Mucosa with Human Immunodeficiency Virus 1 and Histoculture

Ex Vivo Infection of Human Lymphoid Tissue and Female Genital Mucosa with Human Immunodeficiency Virus 1 and Histoculture

Published on: October 12, 2018

Area of Science:

Virology
Molecular Biology
Cell Signaling

Background:

Human cytomegalovirus (HCMV) poses a significant threat to pregnant women and immunocompromised individuals.
Existing anti-HCMV therapies are limited, necessitating the development of novel therapeutic agents.
The Wnt signaling pathway is vital for embryonic and cancer stem cell development and is manipulated by other herpesviruses.

Purpose of the Study:

To investigate the role of the Wnt signaling pathway in human cytomegalovirus (HCMV) replication in vitro.
To evaluate the efficacy of Wnt pathway modulators (monensin, nigericin, salinomycin) in inhibiting HCMV replication.

Main Methods:

Treatment of HCMV-infected cells (Towne strain and clinical isolate) with monensin, nigericin, and salinomycin.
Assessment of viral replication, viral protein expression (IE2, UL44, pp65), and Wnt pathway components (LRP6, Wnt 5a/b, β-catenin, Dvl2/3, axin 1).
Correlation analysis between Wnt pathway modulation and HCMV inhibition.

Main Results:

Monensin, nigericin, and salinomycin significantly inhibited HCMV replication, affecting the entire replication cycle.
Viral protein expression (IE2, UL44, pp65) was significantly decreased.
HCMV infection led to decreased expression of key Wnt pathway components (LRP6, Wnt 5a/b, β-catenin) and increased axin 1; nigericin modulated these in both infected and non-infected cells.

Conclusions:

Modulation of the Wnt signaling pathway effectively inhibits HCMV replication.
HCMV infection alters Wnt pathway components, suggesting a complex interplay that can be targeted for antiviral therapy.
Further research is needed to fully elucidate how HCMV exploits the Wnt pathway for its replication.