Secondary fungal infections in severe acute viral diseases: clinical features and underlying immune mechanisms

TL;DR

This paper explores how severe viral diseases can lead to secondary fungal infections by weakening the immune system.

Contribution

The paper introduces a new framework called 'virus-driven immune reprogramming' to explain susceptibility to fungal infections after viral illness.

Findings

Viral infections disrupt immune barriers and impair the Th17-IL-17 antifungal axis.

Platelet immune function is attenuated during viral infections, increasing fungal susceptibility.

Unique pathogen interactions create a host environment favorable to fungal invasion.

Abstract

Secondary fungal infections are increasingly recognized as critical factors in the prognosis of severe acute viral infections, including influenza, SARS-CoV-2, Severe Fever with Thrombocytopenia Syndrome virus, and Dengue. This review outlines the clinical features of fungal complications, proposing a “virus-driven immune reprogramming” framework. It highlights how viral infections disrupt immune barriers, impair the Th17-IL-17 antifungal axis, attenuate platelet immune function, and involve unique pathogen interactions, creating a host immune microenvironment that is more susceptible to fungal invasion. Understanding these immune-injury mechanisms underscores the clinical importance of earlier surveillance of secondary fungal disease and informs the development of mechanism-guided therapeutic approaches to improve patient outcomes.

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