The reason why there are few effective broad-spectrum antivirals is that viruses are much more diverse than bacteria, including how they store their genetic information (some in DNA and some in DNA form). RNA). Unlike bacteria, viruses have less of their own protein building blocks that can be targeted with drugs.
For a drug to work, it must achieve its purpose. This is especially difficult with viruses because they replicate inside human cells by hijacking our cellular machinery. The drug must get inside these infected cells and act on processes that are essential for the normal functioning of the human body. Unsurprisingly, this often results in collateral damage to human cells, which is experienced as side effects.
Targeting viruses outside cells – to prevent them from gaining a foothold before they can replicate – is possible, but is also difficult due to the nature of the virus shell. The shell is extraordinarily robust, resistant to the negative effects of the environment on its host’s path. It is only when the virus reaches its target that its shell breaks down or ejects its contents, which contain its genetic information.
This process can be a weak point in the virus’s life cycle, but the conditions that control release are very specific. Although drugs targeting the virus shell appear attractive, some can still be toxic to humans.
Despite these difficulties, drugs that treat viruses such as influenza and HIV have been developed. Some of these drugs target viral replication and viral shell assembly processes. Promising drug targets for coronaviruses have also been identified. But the development of new drugs takes a long time, and viruses mutate quickly. So even when a drug is developed, the ever-evolving virus could soon develop resistance to it.