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A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation

A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation

Published on: April 2, 2012

Viral entry shapes HCMV latency establishment.

Yaarit Kitsberg¹, Aharon Nachshon¹, Tamar Arazi¹

¹Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

Nature Communications

|December 28, 2025

Summary

This summary is machine-generated.

Human cytomegalovirus (HCMV) infection latency in monocytes is linked to inefficient viral entry. Enhancing entry allows productive infection, revealing entry as a key factor in HCMV latency.

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Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds

Published on: October 29, 2015

Area of Science:

Virology
Immunology
Cell Biology

Background:

Human cytomegalovirus (HCMV) establishes lifelong persistence through latent infection.
Monocytes support latent HCMV, while macrophages support productive infection, largely attributed to chromatin regulation.
Differences in viral transcription between monocytes and macrophages are observed early in infection.

Purpose of the Study:

To investigate the factors contributing to differential HCMV infection outcomes in monocytes versus macrophages.
To explore the role of viral entry efficiency in HCMV latency and productive infection.
To identify specific cellular factors influencing HCMV entry during monocyte differentiation.

Main Methods:

Metabolic labeling of newly synthesized RNA to assess viral transcription.
Comparative analysis of viral entry and nuclear genome delivery in monocytes and macrophages.
Ectopic expression of HCMV entry receptors in monocytes.
Identification of cell surface proteins involved in HCMV entry using integrin β3 as a marker.

Main Results:

Monocytes exhibit significantly lower viral transcription and inefficient viral entry compared to macrophages.
Ectopic expression of HCMV entry receptors in monocytes rescues viral entry and enables productive infection.
Integrin β3 is identified as a differentiation-induced protein crucial for efficient HCMV entry into macrophages.
Cells with reduced viral genome entry are more prone to establishing latent infection and reactivation.

Conclusions:

Viral entry efficiency is a critical, previously unrecognized factor in establishing HCMV latency in monocytes.
Monocyte differentiation into macrophages enhances HCMV entry, partly via integrin β3 upregulation.
Understanding entry mechanisms provides new insights into HCMV persistence and reactivation dynamics.