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Herpes

Herpes

Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1...

Genital Herpes

Genital Herpes

Genital herpes is a sexually transmitted infection primarily caused by herpes simplex virus type 2 (HSV-2), though herpes simplex virus type 1 (HSV-1) is increasingly implicated in genital infections, particularly among younger populations. Transmission occurs mainly through sexual contact, with asymptomatic viral shedding serving as a major route of spread. This characteristic makes HSV-2 difficult to control at a population level, as individuals may unknowingly transmit the virus even in the...

Inhibitors of Virion Maturation and Assembly

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...

Leaky Scanning

Leaky Scanning

During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA. Marilyn Kozak discovered that the sequence RCCAUGG (where R stands for...

Inhibitors of Viral Protein Synthesis

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

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Related Experiment Video

Updated: Jun 25, 2026

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

Published on: November 4, 2018

HSV-2 ICP34.5 protein modulates herpes simplex virus glycoprotein processing.

Somik Chatterjee¹, Jason W Wang, Mary J Cismowski

¹Integrative Medical Sciences, Northeastern Ohio Universities Colleges of Medicine and Pharmacy, Rootstown, 44272, USA.

Archives of Virology

|March 10, 2009

Summary

The herpes simplex virus type 2 (HSV-2) ICP34.5 gene improves viral glycoprotein processing. This contrasts with HSV-1, where ICP34.5 limits this process, suggesting HSV-2 ICP34.5 modulates glycoprotein processing.

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Last Updated: Jun 25, 2026

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

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Published on: October 28, 2019

Area of Science:

Virology
Molecular Biology
Genetics

Background:

Herpes simplex virus (HSV) infection involves complex viral protein processing.
The ICP34.5 gene plays a role in HSV pathogenesis and replication.
Differential functions of ICP34.5 between HSV-1 and HSV-2 are not fully understood.

Purpose of the Study:

To investigate the role of HSV-2 ICP34.5 in viral glycoprotein processing.
To compare the function of HSV-2 ICP34.5 with that of HSV-1 ICP34.5.

Main Methods:

Cloning of the ICP34.5 gene from HSV-2 strain 333.
Expression of HSV-2 ICP34.5 in Vero cells.
Analysis of glycoprotein C (gC1) processing during HSV-1 SP7 infection in the presence of HSV-2 ICP34.5.

Main Results:

Expression of HSV-2 ICP34.5 enhanced the efficiency and extent of glycoprotein C processing.
HSV-1 SP7 ICP34.5 was found to limit viral glycoprotein processing.
HSV-2 ICP34.5 demonstrated a distinct function compared to HSV-1 ICP34.5.

Conclusions:

The ICP34.5 gene from HSV-2 enhances viral glycoprotein processing, unlike its HSV-1 counterpart.
Modulation of viral glycoprotein processing is a function of the HSV-2 ICP34.5 protein.
These findings highlight functional differences in ICP34.5 between HSV-1 and HSV-2, impacting viral replication strategies.