Pathogenesis of Respiratory Viral and Fungal Coinfections
Fabián Salazar1, Elaine Bignell1, Gordon D Brown1
1Medical Research Council Centre for Medical Mycology, University of Exeter, Exeter, United Kingdom.
Abstract:
Individuals suffering from severe viral respiratory tract infections have recently emerged as "at risk" groups for developing invasive fungal infections. Influenza virus is one of the most common causes of acute lower respiratory tract infections worldwide. Fungal infections complicating influenza pneumonia are associated with increased disease severity and mortality, with invasive pulmonary aspergillosis being the most common manifestation. Strikingly, similar observations have been made during the current coronavirus disease 2019 (COVID-19) pandemic. The copathogenesis of respiratory viral and fungal coinfections is complex and involves a dynamic interplay between the host immune defenses and the virulence of the microbes involved that often results in failure to return to homeostasis. In this review, we discuss the main mechanisms underlying susceptibility to invasive fungal disease following respiratory viral infections. A comprehensive understanding of these interactions will aid the development of therapeutic modalities against newly identified targets to prevent and treat these emerging coinfections.
Insights
Severe viral respiratory infections, like influenza and COVID-19, increase the risk of invasive fungal infections. Understanding these complex coinfections is crucial for developing new treatments.
Area of Science:
- Medical Microbiology
- Infectious Diseases
- Immunology
Background:
- Severe viral respiratory infections, including influenza and COVID-19, place individuals at high risk for secondary invasive fungal infections.
- Fungal coinfections, particularly invasive pulmonary aspergillosis, significantly increase disease severity and mortality in patients with viral pneumonia.
Purpose of the Study:
- To review the mechanisms underlying increased susceptibility to invasive fungal disease after respiratory viral infections.
- To explore the complex copathogenesis of viral and fungal coinfections.
Main Methods:
- Literature review focusing on mechanisms of fungal susceptibility post-viral infection.
- Analysis of host-pathogen interactions in viral-fungal coinfections.
Main Results:
- Viral infections disrupt host immune defenses, creating opportunities for fungal pathogens.
- The interplay between host immunity and microbial virulence contributes to poor outcomes and failure to achieve homeostasis.
Conclusions:
- A deeper understanding of the mechanisms driving these coinfections is essential.
- Identifying novel therapeutic targets is critical for preventing and treating emerging viral-fungal coinfections.
More Related Videos
09:02Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
09:01An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Related Concept Videos
Pneumonia II: Pathophysiology
COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
Pneumonia I: Introduction
Risk Factors
Various factors influence the likelihood of developing pneumonia. Age plays a crucial role, with infants, children under two, and individuals over 65 at increased risk due to their...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
Common Respiratory Disorders
Upper respiratory disorders impact the airways above the vocal cords, encompassing areas like the nose, sinuses, and throat. Various conditions fall under this category, including the common cold and allergic rhinitis. These disorders can stem from several causes,...
Cystic Fibrosis: Pathogenesis
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,...
