British Prime Minister Boris Johnson recently announced the establishment of an antiviral working group to “strengthen” the development of new antiviral drugs. At the Downing Street press conference, Johnson said: “Most scientific opinions in the UK still firmly believe that another wave of COVID-19 will occur at some stage this year.” The Prime Minister hopes to develop antiviral drugs before the fall to help quell the third wave. epidemic.
Anti-inflammatory drugs such as dexamethasone and tocilizumab can reduce the risk of death in patients with new coronary disease, but these drugs are only used for patients who are hospitalized due to severe illness. Johnson wanted a pill-like medicine that could be taken at home to prevent people from ending their lives while wearing ventilators in the hospital.
It usually takes years to develop and approve new antiviral drugs because the discovery process is extremely difficult. This process involves identifying compounds that target viruses and then testing them for effectiveness and safety. For this reason, scientists are also considering reusing existing drugs that have been approved to treat other viruses or diseases. Broad-spectrum antibiotics can be used to treat many bacterial infections, but the difference is that drugs that are effective against one virus are rarely effective against other viruses. For example, Remdesivir, which was originally developed to treat hepatitis C, was once recommended for the treatment of the new coronavirus, but clinical trials have shown that it has limited effect on this coronavirus. There are few effective broad-spectrum antiviral drugs because viruses are much more diverse than bacteria, including the way they store genetic information (some in the form of DNA, some in the form of RNA). Unlike bacteria, the virus itself has fewer protein building blocks that can be targeted by drugs.
For a drug to work, it must achieve its goal. This is especially difficult for viruses because they replicate in human cells by hijacking our cellular machinery. The drug needs to enter these infected cells and act on the processes necessary for the normal function of the body. Unsurprisingly, this usually leads to collateral damage to human cells, namely side effects. For viruses outside the cell, preventing them from gaining a foothold before replication is possible, but it is also very difficult. Because the outer shell of the virus is very strong, it can resist the negative impact of the environment on its host. Only when the virus reaches the target, its outer shell will decompose or eject substances containing its genetic information. This process may be a weakness in the life cycle of the virus, but the conditions for controlled release are very specific. Although drugs targeting the virus shell sound attractive, some drugs may be toxic to humans.
Despite these difficulties, drugs to treat viruses such as influenza and HIV have been developed. Some of these drugs target the process of virus replication and virus shell assembly and have also identified promising coronavirus drug targets. But it takes a long time to develop new drugs, and the virus mutates quickly. Therefore, even if a drug is developed, the evolving virus may quickly become resistant to it.
Another problem in the fight against viruses is that some viruses such as HIV, papillomavirus, and herpes virus may enter sleep mode. In this state, the infected cells will not produce any new viruses. The genetic information of the virus is the only virus information present in the cell. Drugs that interfere with virus replication or the outer shell have no activity, so the virus survives.
When the sleeping virus becomes active again, the symptoms are likely to reappear, and additional medications are needed at this time. This increases the chance of drug resistance because the virus takes longer to mutate after being induced by the drug. Although we are only just beginning to understand the life cycle of coronaviruses, there are signs that they can last longer, especially in patients with weakened immunity, leading to another problem of the production of more drug-resistant virus strains. Research to understand how the coronavirus works have made progress in a short period of time, but there are still many problems to be solved in the development of antiviral drugs. It is expected that later this year, the virus infection may make a comeback, so the work of the anti-virus task force will be cut.
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