Aspergillus
species contain pathogenic and opportunistic fungal pathogens which have the potential
to cause mycosis (invasive aspergillosis) in humans. The existing antifungal drugs have
limitation largely due to the development of drug-resistant isolates. To gain insight
into the mechanism of action and antifungal drug resistance in
Aspergillus
species including biofilm formation, we have reviewed protein
data of
Aspergillus
species during interaction with
antifungals drugs (polynes, azoles and echinocandin) and phytochemicals (artemisinin,
coumarin and quercetin). Our analyses provided a list of
Aspergillus
proteins (72 proteins) that were abundant during interaction
with different antifungal agents. On the other hand, there are 26 proteins, expression
level of which is affected by more than two antifungal agents, suggesting the more
general response to the stress induced by the antifungal agents. Our analysis showed
enzymes from cell wall remodelling, oxidative stress response and energy metabolism are
the responsible factors for providing resistance against antifungal drugs in
Aspergillus
species and could be explored further in clinical
isolates. Also, these findings have clinical importance since the effect of drug
targeting different proteins can be potentiated by combination therapy. We have also
discussed the opportunities ahead to study the functional role of proteins from
environmental and clinical isolates of
Aspergillus
during
its interaction with the antifungal drugs.
Abbreviations
IPA: invasive pulmonary aspergillosis; IA: invasive aspergillosis; AmB: Amphotericin B;
CAS: Caspofungin; VRC: Voriconazole; ITC: Itraconazole; POS: Posaconazole; ART:
Artemisinin; QRT: Quercetin; CMR: Coumarin; MIC: minimal inhibitory concentration