The comparative ease of identifying compounds that safely cured bacterial infections was more difficult to duplicate in treatments of fungal and viral infections. Antibiotic research led to great strides in the knowledge of biochemistry, establishing large differences between the cellular and molecular physiology of the bacterial cell and that of the mammalian cell. This explained the observation that many compounds that are toxic to bacteria are non-toxic to human cells. In contrast, the basic biochemistries of the fungal cell and the mammalian cell are much more similar. Most antifungal drugs have targeted steps in the synthesis of the fungal cell membrane (e.g., imidazole, triazole, and allylamine antifungals) or target components of the formed cell wall (e.g., polyene antifungals). However, toxicity is not fully avoided in the case of polyene antifungals since they can target human membrane cholesterol, mistaking it for fungal ergosterol.
 

This restricts the development and use of therapeutic compounds that attack a fungal cell, while not harming mammalian cells. Similar problems exist in antibiotic treatments of viral diseases. Human viral metabolic biochemistry is very closely similar to human biochemistry, and the possible targets of antiviral compounds are restricted to very few components unique to a mammalian virus.

For related articles, see fungicide, antifungal drug, and antiviral drug