Related Experiment Video

Updated: Sep 20, 2025

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
09:01

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection

Published on: December 10, 2013

8.0K

The Impact of EPAC2-Associated Junction Plakoglobin on Respiratory Syncytial Virus Infection

Chaitra A Takle1, Eun-Jin Choi1, Eun Seok Choi1

  • 1Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.

Viruses
|May 28, 2025
PubMed

Insights

New research reveals junction plakoglobin (JUP) interacts with EPAC2, a key regulator in respiratory syncytial virus (RSV) infection. JUP is essential for viral replication and immune response, suggesting a new therapeutic target for RSV.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Respiratory syncytial virus (RSV) causes severe respiratory infections, particularly in vulnerable populations.
  • Current therapies for RSV are limited, highlighting the need for novel treatment strategies.
  • Exchange proteins directly activated by cAMP (EPAC) are implicated in viral pathogenesis, with EPAC isoform 2 (EPAC2) previously identified as crucial for RSV replication and immunity.

Purpose of the Study:

  • To elucidate the molecular mechanisms of EPAC2 in RSV infection.
  • To identify EPAC2-interacting proteins involved in RSV pathogenesis.
  • To investigate the role of junction plakoglobin (JUP) in RSV replication and host response.

Main Methods:

  • Proteomics and immunoprecipitation to identify EPAC2-interacting proteins.
  • Comparative analysis of RSV replication in JUP-deficient and control cells.
  • Assessment of viral budding, gene transcription, and cellular immune response.

Main Results:

  • Junction plakoglobin (JUP) was identified as an EPAC2-interacting protein, with enhanced interaction during RSV infection.
  • Downregulation of JUP significantly reduced infectious RSV particle production.
  • JUP deficiency impaired viral budding and gene transcription, and compromised cellular immune response to RSV.

Conclusions:

  • EPAC2 and JUP cooperatively regulate RSV replication and dissemination.
  • JUP plays a critical role in supporting viral propagation and modulating the host immune system during RSV infection.
  • Targeting the EPAC2-JUP interaction may offer a novel therapeutic approach for managing RSV infections.

Keywords:
EPAC2JUPRSVviral gene transcription and viral genome replication

More Related Videos

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses11:48

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses

Published on: April 4, 2019

16.2K
Generation and Assembly of Virus-Specific Nucleocapsids of the Respiratory Syncytial Virus09:08

Generation and Assembly of Virus-Specific Nucleocapsids of the Respiratory Syncytial Virus

Published on: July 27, 2021

3.9K

Related Concept Videos

Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:
622
Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
370
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
3.1K
Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
388
Acute Respiratory Failure-V01:29

Acute Respiratory Failure-V

The treatment for acute respiratory failure varies based on factors like the underlying cause, overall health, and severity. A collaborative healthcare team is essential for early detection, often through arterial blood gas analysis. Identifying the cause is the primary goal, with treatment strategies adjusted for ventilation/perfusion (V/Q) mismatch, shunting, or diffusion impairment.
Ensure that patients are monitored continuously for their response to therapy, including changes in...
216
Acute Respiratory Failure-I01:21

Acute Respiratory Failure-I

Acute respiratory failure is a condition characterized by the inability of the lungs to perform their primary function: gas exchange. This failure leads to insufficient oxygen levels (hypoxemia) in the blood, elevated carbon dioxide levels (hypercapnia), or both, causing critical impairment in organ function.
Definition: It is defined by specific criteria based on blood gas measurements. Hypoxemia happens when the partial pressure of oxygen (PaO2) falls below 60 mmHg. At the same time,...
350