To be kidnapped Dewi Sinta, Marica Mahapatih bersiluman a golden deer, while King Ravana turned into an old priest. The effort they do to trick and deceive the system guarding against Dewi Sinta. Ravana finally managed to steal Dewi Sinta. Similarly, the story is told in the Ramayana.
Viruses, which are parasites of living beings, are also constantly "bersiluman" by mutating in order to trick the host cell's defense system. This method allows the virus to enter cells and makes the virus can escape from the attack host cells. The virus can then multiply inside host cells and can result in death for the infected organism. Not only that, with the mutated, the virus can also become resistant to the drugs used by humans to suppress the virus.
One of the viruses that are harmful to humans are influenza viruses. In the last five years the world community shocked by the spread of one subtype of influenza A, which is called H5N1 bird flu. The virus is reported to have killed 262 people worldwide. In Indonesia alone the victims reached 115 people.
Unfinished face of H5N1, now the world community was surprised 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 a pandemic, it was reported that from there the influenza virus, both H5N1 and H1N1, which is resistant to Tamiflu. In fact, the mainstay of antiviral drug Tamiflu be used to counteract the spread of H5N1 or H1N1.
Inhibition "neuraminidase"
Oseltamivir, influenza antiviral drug known as Tamiflu, works by inhibiting neuraminidase, an enzyme which is a protein that resides on the surface of the virus. In inhibiting neuraminidase, oseltamivir is attached to the side so that the active enzyme neuraminidase enzyme becomes inactive. Neuraminidase plays a role in releasing newly formed virus so that this new virus can spread and infect other cells.
The new viruses formed as a result of proliferation in the cell initially remains attached to the cell surface through sialat acid residues. To remove the virus from host cell membranes, neuraminidase sialat acid residues are cut. If the activity of neuraminidase is inhibited by oseltamivir, the newly formed viruses can not escape to spread that virus proliferation can be stopped.
This condition will help the body's defense system to win the battle against the influenza virus that was attacking so that infected people can recover.
However, if oseltamivir failed 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 extremely dangerous and can threaten the lives of sufferers. For example, patient deaths due to H5N1 resistant to Tamiflu, among others, have been reported in Vietnam and as a result of Tamiflu-resistant H1N1 infection have been reported in the Netherlands.
Gene mutation "neuraminidase"
Influenza virus could become resistant to Tamiflu because of a mutation in the neuraminidase gene, the gene coding for the neuraminidase protein. Mutations are changes in nucleotide bases in the DNA molecule or gene, for example, changes in base cytosine (C) to thymine base (T). These base changes may result in changes in the genetic code that could further alter the amino acid residues of the encoded protein.
Neuraminidase gene size 1362 base pairs and encodes a protein neuraminidase, which consists of 454 amino acid residues. C to T mutation at nucleotide bases that alter the amino acid residues 763 to 454 of the neuraminidase protein of the histidine to tyrosine.
This change resulted in the attachment of the protein neuraminidase oseltamivir changed so that oseltamivir can no longer be bound to the neuraminidase (see Figure). As a result, could not be inhibited neuraminidase activity and virus replication can not be halted by Tamiflu. Other mutations are also reported to cause resistance to Tamiflu is a mutation that changed amino acid residue 292 from arginine to a lysine residue and a change to-294 from asparagine to serine.
To anticipate the emergence of a dangerous mutation in the influenza virus, or a sequence of nucleotide base sequences of DNA virus that is infectious to be analyzed routinely. Changes in the neuraminidase gene needs to be monitored in order 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.
Viruses, which are parasites of living beings, are also constantly "bersiluman" by mutating in order to trick the host cell's defense system. This method allows the virus to enter cells and makes the virus can escape from the attack host cells. The virus can then multiply inside host cells and can result in death for the infected organism. Not only that, with the mutated, the virus can also become resistant to the drugs used by humans to suppress the virus.
One of the viruses that are harmful to humans are influenza viruses. In the last five years the world community shocked by the spread of one subtype of influenza A, which is called H5N1 bird flu. The virus is reported to have killed 262 people worldwide. In Indonesia alone the victims reached 115 people.
Unfinished face of H5N1, now the world community was surprised 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 a pandemic, it was reported that from there the influenza virus, both H5N1 and H1N1, which is resistant to Tamiflu. In fact, the mainstay of antiviral drug Tamiflu be used to counteract the spread of H5N1 or H1N1.
Inhibition "neuraminidase"
Oseltamivir, influenza antiviral drug known as Tamiflu, works by inhibiting neuraminidase, an enzyme which is a protein that resides on the surface of the virus. In inhibiting neuraminidase, oseltamivir is attached to the side so that the active enzyme neuraminidase enzyme becomes inactive. Neuraminidase plays a role in releasing newly formed virus so that this new virus can spread and infect other cells.
The new viruses formed as a result of proliferation in the cell initially remains attached to the cell surface through sialat acid residues. To remove the virus from host cell membranes, neuraminidase sialat acid residues are cut. If the activity of neuraminidase is inhibited by oseltamivir, the newly formed viruses can not escape to spread that virus proliferation can be stopped.
This condition will help the body's defense system to win the battle against the influenza virus that was attacking so that infected people can recover.
However, if oseltamivir failed 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 extremely dangerous and can threaten the lives of sufferers. For example, patient deaths due to H5N1 resistant to Tamiflu, among others, have been reported in Vietnam and as a result of Tamiflu-resistant H1N1 infection have been reported in the Netherlands.
Gene mutation "neuraminidase"
Influenza virus could become resistant to Tamiflu because of a mutation in the neuraminidase gene, the gene coding for the neuraminidase protein. Mutations are changes in nucleotide bases in the DNA molecule or gene, for example, changes in base cytosine (C) to thymine base (T). These base changes may result in changes in the genetic code that could further alter the amino acid residues of the encoded protein.
Neuraminidase gene size 1362 base pairs and encodes a protein neuraminidase, which consists of 454 amino acid residues. C to T mutation at nucleotide bases that alter the amino acid residues 763 to 454 of the neuraminidase protein of the histidine to tyrosine.
This change resulted in the attachment of the protein neuraminidase oseltamivir changed so that oseltamivir can no longer be bound to the neuraminidase (see Figure). As a result, could not be inhibited neuraminidase activity and virus replication can not be halted by Tamiflu. Other mutations are also reported to cause resistance to Tamiflu is a mutation that changed amino acid residue 292 from arginine to a lysine residue and a change to-294 from asparagine to serine.
To anticipate the emergence of a dangerous mutation in the influenza virus, or a sequence of nucleotide base sequences of DNA virus that is infectious to be analyzed routinely. Changes in the neuraminidase gene needs to be monitored in order 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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