Immunological response to COVID-19 and its role as a predisposing factor in invasive aspergillosis

Document Type : Reviews

Authors

1 Invasive Fungi Research Center, Communicable Diseases Research Institute, Mazandaran University of Medical Sciences, Sari, Iran

2 Department of Medical Parasitology and Mycology, School of Medicine, Babol University of Medical Sciences, Babol, Iran

3 Department of Medical Mycology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran

4 Institute of Hygiene and Medical Microbiology, Medical University of Innsbruck, Innsbruck, Austria

5 Division of Infectious Diseases and Global Health, University of California San Diego, La Jolla, California

10.18502/cmm.6.4.5442

Abstract

The world is involved with a pandemic coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2. The clinical manifestations of reported COVID-19-associated pulmonary impairments range from asymptomatic infections to a pneumonia-induced acute respiratory distress syndrome that requires mechanical ventilation. Fungal superinfections complicating the clinical course remain underexplored. Angiotensin-converting enzyme 2, the receptor for COVID-19 that is mainly expressed in airway epithelia and lung parenchyma, is considered an important regulator of innate immunity. With regard to the viral-cell interaction, imbalanced immune regulation between protective and altered responses caused by the exacerbation of inflammatory responses should be considered a major contributor to secondary pulmonary aspergillosis. In addition, the complex inherited factors, age-related changes, and lifestyle may also affect immune responses. The complication and persistence of invasive aspergillosis have been well described in patients with severe influenza or COVID-19. However, there is a scarcity of information about the immunological mechanisms predisposing patients with COVID-19 to fungal co-infections. Therefore, this study was conducted to investigate the aforementioned domain.
 

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