Why are there so many germicides but so few anti-virus?

At the end of World War II, mass production of a newly discovered antibiotic, penicillin, saved many wounded wounded victims.

Since then, penicillin and many other antibiotics have successfully treated numerous infections.

But antibiotics do not fight viruses, only antiviral drugs do this. Since the outbreak of the covid-19 epidemic, researchers and pharmaceutical companies have been working day and night trying to find an antiviral drug to treat the disease.

So why are there so few antiviral drugs? The general answer is still biological, namely that the virus uses our own cells to multiply and grow . So it's very difficult to kill the virus without killing our cells.

Take advantage of the differences between humans and germs

Differences between bacterial and human cells are key to the effectiveness of antibiotics.

Picture 1 of Why are there so many germicides but so few anti-virus?
Remdesivir is an antiviral drug that researchers are trying to treat covid-19, but so far, the results are mixed, unclear.

Germs are independent life forms, they can live without invading a part of the host body. They are similar to our cells, but also have many other characteristics with us.

For example, penicillin works because it interferes with the formation of the cell wall of bacteria. The cell walls are made by a polymer called peptidoglycan . Human cells have no walls or any peptidoglycans. So antibiotics that prevent peptidoglycan-producing bacteria can neutralize germs without harming the user, or can be interpreted as selective toxic antibiotics.

Viruses use our own cells to duplicate

Unlike germs, viruses cannot replicate outside a host cell. Scientists are still debating whether or not they are truly living things.

To clone, the virus enters a host cell and hijacks the cell. Once inside the cell, some viruses are dormant, others replicate slowly and exit the cell over a long process, others replicate with too many cells. The host cell is broken and dead. Newly formed virus particles disperse and infect new host cells.

An antiviral treatment that interferes with the virus' 'life' cycle can be successful. The problem is that if this treatment targets the replication process, but the process is also important for the host cell, then this approach will be toxic not only to the virus but also to the host cells. It is easy to kill the virus, but keeping the host cell alive is difficult.

Successful antiviral drugs are drugs that disrupt the processes or structure of the virus itself, thereby preventing the virus from replicating and minimizing damage to the patient. The more the virus is dependent on the host, the fewer targets the antiviral drug is targeting, making it harder to kill the virus. The difficulty is that most viruses have very few unique differences that the drug can target.

Another problem is that viruses vary a lot, not like germs. All germs have their own double strand DNA genome and clone independently by growing and then splitting into two, similar to a human cell. As for the viruses, the difference is huge and varied. Some viruses have a DNA genome, but some have an RNA genome, some with a single strand gene, others with a double strand. This makes it practically impossible to create a broad-spectrum antiviral drug to kill many viruses.

Stories of 'fighting' success with viruses

Despite many difficulties, there are many differences between humans and viruses, and taking advantage of these differences has brought some success. An example is the case of influenza A virus, a type of influenza virus. Influenza A tricked human cells into invading. Once inside the cell, the virus needs to ' take off the clothes' , that is, remove its shell to release its RNA into the cell.

There is a viral protein called matrix-2 protein , which is key for the process of breaking down the envelope of the virus, facilitating the release of RNA from the virus particle. Once the viral RNA is released into the host cell, that RNA is transported to the nucleus to begin the viral replication process.

But if a drug blocks or blocks the matrix-2 protein, the viral RNA cannot escape from the virus particle into the cell nucleus, so it cannot replicate. Therefore, the infection process is interrupted. Amantadine and rimantadine are successful antiretroviral drugs at an early age when targeting the matrix-2 protein.

New drugs that have been successful in treating patients with influenza A or B infection are zanamivir (brand name Relenza) and oseltamivir (nickname Tamiflu). These two drugs work by neutralizing the viral main enzyme, preventing the virus from releasing itself in cells, slowing the spread from one cell to another inside the host, and minimizing damage. harm caused by virus infection to patients.

We need to find out what is the difference of the new corona virus

Picture 2 of Why are there so many germicides but so few anti-virus?
Tamiflu is a successful antiviral drug that slows the spread of influenza in humans. So far, we have not had any effective antiviral drug for Covid-19.

Getting a vaccine for Covid-19 is difficult. Therefore, testing antiviral drugs to find a type that can effectively treat the disease is still an important goal.

Much of this will depend on understanding the complexity of this virus and how it interacts with human cells. If researchers can identify the unique characteristics of this virus in the way it survives and replicate, then its weaknesses can be used to create an effective treatment.