Expansion
Antifungals target ergosterol or the cell wall; antivirals target viral enzymes
Expansion
Antifungals
- Azoles (fluconazole, itraconazole, voriconazole): inhibit 14-alpha demethylase, blocking ergosterol synthesis. Potent CYP inhibitors, hence many interactions
- Polyenes (amphotericin, nystatin): bind ergosterol directly, forming pores. Amphotericin is nephrotoxic with hypokalaemia and hypomagnesaemia
- Echinocandins (caspofungin): inhibit beta-glucan cell wall synthesis; well tolerated
- Terbinafine: squalene epoxidase; used for dermatophytes
- Flucytosine: pyrimidine analogue
Antivirals
- Aciclovir: a guanosine analogue activated by viral thymidine kinase, which gives its selectivity for herpes simplex and varicella zoster
- Ganciclovir: for cytomegalovirus; marrow suppressive
- Oseltamivir: neuraminidase inhibitor for influenza
- Antiretrovirals: nucleoside and non-nucleoside reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, entry inhibitors
- Direct acting antivirals for hepatitis C: NS5A and NS5B inhibitors, now curative
The recurring theme is selective toxicity: fungi have ergosterol where humans have cholesterol, and viral enzymes have no human counterpart, which is why aciclovir is so remarkably safe.