How to Conquer Tamiflu Influenza Virus

The virus, a parasite living beings, are also constantly by mutating in order to trick the host cell's defense system. This method allows the virus to enter the cell and makes the virus can escape from the attack of the host cell. The virus could then multiply within the host cells and can lead to death of the infected organism. Not only that, by mutating, the virus can become resistant to the drugs used to suppress human virus.

One of the viruses that are harmful to humans are influenza virus. In the last five years the world community shocked by the spread of one subtype of influenza A, which is called the H5N1 bird flu. The virus is reported to have killed 262 people worldwide. In Indonesia alone victims reached 115 people.

Unfinished face of H5N1, now the world community was shocked by the spread of infection and transmission of influenza A virus subtype H1N1. In a relatively short time, the virus has killed more than 400 people worldwide. The world was declared in a state of pandemic influenza.

On fears the pandemic, reported that it started there influenza virus, both H5N1 and H1N1, which is resistant to Tamiflu. In fact, the mainstay antiviral drug Tamiflu used to counteract the spread of H5N1 or H1N1.

Inhibition "neuraminidase"

Oseltamivir, influenza antiviral drug known as Tamiflu, works by inhibiting neuraminidase, which is a protein enzyme present on the surface of the virus. In inhibiting neuraminidase, oseltamivir attaches to the enzyme active site so that the neuraminidase enzyme becomes inactive. Neuraminidase instrumental in releasing the new virus is formed so that this new virus can spread and infect other cells.

Virus newly formed as a result of proliferation in cells initially still attached to the cell surface via sialic acid residues. To release the virus from the host cell membrane, neuraminidase cut the sialic acid residues. If the neuraminidase activity is inhibited by oseltamivir, the newly formed virus cannot escape to spread so that the proliferation of the virus can be stopped.

This condition will help the immune system to win the battle against the influenza virus was attacking so that an infected person can recover.

However, if oseltamivir fails to inhibit the activity of neuraminidase, the virus will continue to multiply and can spread from one cell to another cell, although patients given the drug Tamiflu. This situation is very dangerous and can threaten the lives of patients. For example, cases of patient deaths due to H5N1 resistant to Tamiflu, among others, have been reported in Vietnam and the consequences of Tamiflu-resistant H1N1 infection have been reported in the Netherlands.

Gene mutation "neuraminidase"

The influenza virus can become resistant to Tamiflu because of a mutation in the neuraminidase gene, the gene coding for the protein neuraminidase. Mutations are changes in the nucleotide bases in a DNA molecule or gene, for example, changes in the base cytosine (C) into the base thymine (T). These base changes lead to changes in the genetic code that could further alter the amino acid residues of the proteins encoded.

Neuraminidase genes measuring 1,362 base pairs and encodes a protein neuraminidase, which consists of 454 amino acid residues. C to T mutation at nucleotide bases 763 to change the amino acid residues at all 454 of the neuraminidase protein histidine to tyrosine.

These changes resulted in oseltamivir attachment points on neuraminidase protein changes so that oseltamivir can no longer be bound to the neuraminidase (see Figure). As a result, could not be inhibited neuraminidase activity and viral replication cannot be stopped by Tamiflu. Other mutations were also reported to cause resistance to Tamiflu is a mutation that changed amino acid residue 292 from arginine to lysine and transform into the residue to 294 from asparagine into serine.

To anticipate the emergence of a dangerous mutation in the influenza virus, sequences or the nucleotide sequences of DNA virus that is endemic need to be analyzed regularly. Neuraminidase gene changes need to be monitored to anticipate the outbreak of the virus resistant to Tamiflu. In addition, influenza antiviral drug alternatives should be developed. Treatment using several compounds with different ways of working should also be considered.















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