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Related Concept Videos

Herpes01:28

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 Herpes01:23

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...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Cytomegalovirus Disease01:27

Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
Viral Replication: Lysogenic Cycle01:16

Viral Replication: Lysogenic Cycle

The lysogenic cycle is a crucial viral replication strategy that allows bacteriophages to persist within host cells without immediately destroying them. This process is primarily observed in temperate phages, such as bacteriophage lambda (λ), which infects Escherichia coli. The cycle allows the viral genome to persist across bacterial generations while keeping host cells viable.Integration of the Viral GenomeUpon infection, bacteriophage lambda attaches to the bacterial surface and injects its...

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Prefusion-specific glycoprotein B human antibodies protect against neonatal HSV-2 infection.

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Herpes simplex virus 1 ICP34.5 acts to maintain latency in human and mouse neurons.

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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

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

Published on: October 28, 2019

Xenophagy in herpes simplex virus replication and pathogenesis.

Diane E Alexander1, David A Leib

  • 1Department of Ophthalmology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

Autophagy
|November 15, 2007
PubMed
Summary

Herpes simplex virus type 1 (HSV-1) uses its ICP34.5 protein to block host autophagy, a defense mechanism. This protein antagonizes autophagy, promoting neurovirulence but not viral replication in cell cultures.

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

  • Cellular Biology
  • Virology
  • Immunology

Background:

  • Autophagy is a cellular process that acts as a host defense mechanism against intracellular pathogens, known as xenophagy.
  • Many pathogens have evolved strategies to evade or exploit xenophagy for their own benefit.
  • Herpes simplex virus type 1 (HSV-1) is known to counteract host autophagy.

Purpose of the Study:

  • To investigate the mechanism by which HSV-1's neurovirulence protein, ICP34.5, inhibits the host's autophagy pathway.
  • To understand the role of autophagy antagonism in the lifecycle and pathogenesis of HSV-1.

Main Methods:

  • Analysis of protein interactions between ICP34.5, protein phosphatase 1alpha, PKR, eIF2alpha, and Beclin 1.
  • Assessment of the impact of ICP34.5 on translational arrest and autophagosome formation.
  • Comparison of HSV-1 replication and neurovirulence in the presence and absence of autophagy antagonism.

Main Results:

  • ICP34.5 binds to protein phosphatase 1alpha, counteracting PKR-mediated phosphorylation of eIF2alpha, and also interacts with Beclin 1.
  • These interactions prevent translational arrest and inhibit autophagosome formation, thus down-regulating autophagy.
  • While autophagy antagonism by ICP34.5 promotes neurovirulence, it does not affect HSV-1 replication in permissive cell cultures.

Conclusions:

  • HSV-1's ICP34.5 protein effectively antagonizes the host autophagy pathway through specific protein interactions.
  • Autophagy antagonism is crucial for HSV-1 neurovirulence but dispensable for viral replication in cell culture.
  • Further research is needed to elucidate the precise mechanisms of ICP34.5-mediated autophagy inhibition and its broader role in HSV-1 pathogenesis.