A PHP Error was encountered

Severity: Warning

Message: fopen(/var/lib/php/sessions/ci_session2837uhgib4lbu37kiad43qpcrrseg26h): Failed to open stream: No space left on device

Filename: drivers/Session_files_driver.php

Line Number: 177

Backtrace:

File: /var/www/html/index.php
Line: 316
Function: require_once

A PHP Error was encountered

Severity: Warning

Message: session_start(): Failed to read session data: user (path: /var/lib/php/sessions)

Filename: Session/Session.php

Line Number: 137

Backtrace:

File: /var/www/html/index.php
Line: 316
Function: require_once

Annexins in Influenza Virus Replication and Pathogenesis. | LitMetric

Annexins in Influenza Virus Replication and Pathogenesis.

Front Pharmacol

Department of Physiology, NUS Immunology Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

Published: November 2018

Influenza A viruses (IAVs) are important human respiratory pathogens which cause seasonal or periodic endemic infections. IAV can result in severe or fatal clinical complications including pneumonia and respiratory distress syndrome. Treatment of IAV infections is complicated because the virus can evade host immunity through antigenic drifts and antigenic shifts, to establish infections making new treatment options desirable. Annexins (ANXs) are a family of calcium and phospholipid binding proteins with immunomodulatory roles in viral infections, lung injury, and inflammation. A current understanding of the role of ANXs in modulating IAV infection and host responses will enable the future development of more effective antiviral therapies. This review presents a comprehensive understanding of the advances made in the field of ANXs, in particular, ANXA1 and IAV research and highlights the importance of ANXs as a suitable target for IAV therapy.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249340PMC
http://dx.doi.org/10.3389/fphar.2018.01282DOI Listing

Publication Analysis

Top Keywords

iav
5
annexins influenza
4
influenza virus
4
virus replication
4
replication pathogenesis
4
pathogenesis influenza
4
influenza viruses
4
viruses iavs
4
iavs human
4
human respiratory
4

Similar Publications

Wastewater monitoring has the potential to complement infectious disease surveillance systems. However, the absence of predefined viral signal thresholds in wastewater is often presented as a limiting factor in triggering public health action. To overcome this issue, the feasibility of defining alarm threshold for viral loads in wastewater samples was assessed by quantifying genome fragments of SARS-CoV-2, influenza A virus (IAV), respiratory syncytial virus (RSV), norovirus (NoV), and rotavirus (RoV) by RT-digital PCR (dPCR) in untreated wastewater samples from three treatment plants.

View Article and Find Full Text PDF

Exploring the Protective Role of Recombinant Type III Interferons in Respiratory Infections: Insights from an Mx1-Deficient Mouse Model.

Int J Antimicrob Agents

March 2025

Smorodintsev Research Institute of Influenza, Russian Ministry of Health, Prof. Popov St. 15/17, 197376 St. Petersburg, Russia; Institute of Biomedical Systems and Biotechnology, Peter the Great Saint-Petersburg Polytechnic University, Politekhnicheskaya 29, 194064 St. Petersburg, Russia.

Type III interferons (IFNs) are regarded as safe and effective preventive agents for viral infections of the respiratory tract. The antiviral effects of type I and III IFNs are mediated through the induction of interferon-stimulated genes (ISGs), the variability of which influences the course of the disease and an individual's susceptibility to viruses. The effectiveness of the preventive use of type III IFNs in patients with polymorphisms in critical antiviral ISGs is particularly relevant.

View Article and Find Full Text PDF

Background: Understanding virus-virus interactions is important for evaluating disease transmission and severity. Positive interactions suggest concurrent circulation, while negative interactions indicate reduced transmission of one virus when another is prevalent. This study examines interactions among seven respiratory viruses using a Bayesian approach that accounts for seasonality and long-term trends.

View Article and Find Full Text PDF

Nonstructural Protein 1 of Influenza A (NS1A) Demonstrates Strain-Specific dsRNA Binding Capabilities.

ACS Infect Dis

March 2025

Saint Joseph's University, Department of Chemistry & Biochemistry, University City Campus, 600 South 43rd Street, Philadelphia, Pennsylvania 19104, United States.

Nonstructural protein 1 of influenza A (NS1A) is a key virulence factor produced inside host cells infected with Influenza A Virus (IAV) and consists of an N-terminal dsRNA binding domain (RBD) and a C-terminal effector domain (ED), joined by a flexible linker. While NS1A is a highly promiscuous protein with a number of intracellular functions, its primary function is nonspecific dsRNA binding that enables influenza to evade our innate immune system. For this reason, NS1A has long been proposed as a potential drug target.

View Article and Find Full Text PDF

A novel method to assess antibody-dependent cell-mediated cytotoxicity against influenza A virus M2 in immunized murine models.

Biosaf Health

June 2024

Key Laboratory of Biosafety, National Health Commission of the People's Republic of China, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 102206, China.

The matrix protein 2 (M2) is a preferred target for developing a universal vaccine against the influenza A virus (IAV). This study aimed to develop a method for assessing antibody-dependent cell-mediated cytotoxicity (ADCC) associated with M2-based immunization in mice. We first established a stable cell line derived from mouse lymphoma cells (YAC-1) expressing M2 of H3N2.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!