Genetic defects in fungal recognition and susceptibility to invasive pulmonary aspergillosis

Medical Mycology
Cristina Cunha, Agostinho Carvalho

Abstract

The interindividual variability in the onset and clinical course of invasive pulmonary aspergillosis (IPA) raises fundamental questions about its actual pathogenesis. Clinical and epidemiological studies have reported only a few examples of monogenic defects, however an expanding number of common polymorphisms associated with IPA has been identified. Understanding how genetic variation regulates the immune response to Aspergillus provides critical insights into the human immunobiology of IPA by pinpointing directly relevant immune molecules and interacting pathways. Most of the genetic defects reported to increase susceptibility to infection were described or suggested to impair fungal recognition by the innate immune system. In this review, we discuss the contribution of host genetic variation in pattern recognition receptors to the development of IPA. An improved understanding of the molecular and cellular processes that regulate human susceptibility to IPA is ultimately expected to pave the way toward personalized medical interventions based on host-directed risk stratification and individualized immunotherapy.

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Citations

Jan 30, 2020·FEBS Letters·Raffaella ParenteAntonio Inforzato
Jun 12, 2020·Current Fungal Infection Reports·Michail S Lionakis
Aug 30, 2020·Infectious Diseases and Therapy·Tananun TanpaibulePorpon Rotjanapan

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Aspergillosis is the name given to a wide variety of diseases caused by infection by fungi of the genus Aspergillus. Aspergillosis occurs in chronic or acute forms which are clinically very distinct. Most cases of acute aspergillosis occur in patients with severely compromised immune systems. Chronic colonization or infection can cause complications in people with underlying respiratory illnesses. Discover the latest research on aspergillosis here.

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