Molecular insights into the pathogenesis and infection of Aspergillus fumigatus

Molecular insights into the pathogenesis and infection of Aspergillus fumigatus

The virulence of fungi is dependent on multiple factors, including the immune status of the patient and biological features of the fungi. In particular, the virulence of Aspergillus fumigatus is due to the complex interaction between various molecules involved in thermotolerance (such as ribosomal biogenesis proteins, α-mannosyltransferase and heat shock proteins), pigment production (DHN-melanin), immune evasion (such as melanin and hydrophobin) and nutrient uptake (such as siderophores and zinc transporters). Other molecules also play important roles in the virulence of A. fumigatus, including cell wall components and those that maintain its integrity (such as β-1-3 glucan, α- 1-3 glucan, chitin, galactomannan and mannoproteins) and adhesion (such as hydrophobins) and various hydrolytic enzymes (such as serine and aspartic protease, phospholipases, metalloproteinase and dipeptidyl peptidases). Signalling molecules (such as G-Protein, cAMP, Ras protein and calcineurin) also lead to increased virulence by altering the metabolic response to stress condition and toxins (such as gliotoxin, fumitremorgins, fumagatin and helvolic acid)