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"Monster 14" is preparing to inhibit the virus
Each number associated with that "monster" is another step in the development of the project which, if successful, will become a medicine capable of inhibiting neuraminidase, a protein of the H1N1 virus used to spread the infection between cells
El Universal
Sunday November 29, 2009
In the laboratory of Dr. Enrique Pinera Rudin have made the discovery that has no name yet, so everybody in the place they call "monster version 14".
Each number associated with that "monster" is another step in the development of the project which, if successful, will become a medicine capable of inhibiting neuraminidase, a protein of the H1N1 virus used to spread the infection between cells .
In the market there are drugs that work on the same principle, but according to this researcher, "monster version 14" will be more effective because they act in areas not currently neuraminidase have been susceptible to attack by drugs such as Tamiflu or Relenza .
The difference between Tamiflu, Relenza and the "fourteenth monster" is that the latter is a larger molecule than the other drugs, allowing attacking several binding sites of the neuraminidase in infected cells.
The researcher is confident that within a year will have the first results. The pursuit and perfection of this molecule has four years and began when Henry Rudin was involved in the University of Oxford, England, in the design of inhibitors for other types of neuraminidase.
Today, a researcher at the Institute of Biotechnology, UNAM, Rudin Pi?era has resumed what he observed at the English laboratory.
During the interview, the doctor makes a basic understanding of concepts and then talk about his "monster version 14". "In the influenza virus envelope there are certain proteins to which they are known as spicules, because they resemble thorns. In these spicules are called H and N and the reason is that the one identified as H is known as hemagglutinin and N for a protein called neuraminidase "he explains. The HA has to do with the processes of anchoring the virus to a cell, where infection begins, and the neuraminidase has to do with the breakup of that cell to spread more viruses in the body.
The neuraminidase, he adds, has the ability to stick at two active sites of a cell via the sialic acid of the infected cell, but today Tamiflu and Relenza are only capable of attacking a neuraminidase active site and that has given more strength to the virus against both drugs.
The aim of the project being developed at the Institute of Biotechnology is to generate a molecule that prevents the virus produced in an infected cell and cut the sialic acid can go out to infect other cells. "For so strong that we use with Relenza or Tamiflu in large numbers have begun to detect certain strains of influenza viruses that are no longer susceptible to the molecule of these drugs," says the doctor.
- Do you become resistant?
- Exactly, and what we want to do is build this new molecule to no longer just attacking the zone of an active site. Thus we generate a larger molecule that can stick to two different places of neuraminidase, attacking the problem of influenza in two ways, trying to give us more time to the generation of resistant variants, and exploring an area that would be the second site union, which has not been forced to evolutionarily influenza viruses mutate and become resistant.
This molecule which its creator calls jocular manner "monster number 14" would lead to more drug-resistant mutation. The efforts are aimed at ensuring that bind to the neuraminidase. So far they have achieved a successful docking protein neuraminidase N2 and N6, which infect animals.
- How will be the pilot phase?
- We have neuraminidase types 1, 2, 4, 6 and 9 crystallized and what we will do is take it to obtain crystals. We do not work with live virus or anything. Once we have these compounds, crystals already formed, then placed in reactive and are spreading our molecule to see if they stick as we expect. If we block the activity of neuraminidase our compound works.
"Monster 14" is preparing to inhibit the virus
Each number associated with that "monster" is another step in the development of the project which, if successful, will become a medicine capable of inhibiting neuraminidase, a protein of the H1N1 virus used to spread the infection between cells
El Universal
Sunday November 29, 2009
In the laboratory of Dr. Enrique Pinera Rudin have made the discovery that has no name yet, so everybody in the place they call "monster version 14".
Each number associated with that "monster" is another step in the development of the project which, if successful, will become a medicine capable of inhibiting neuraminidase, a protein of the H1N1 virus used to spread the infection between cells .
In the market there are drugs that work on the same principle, but according to this researcher, "monster version 14" will be more effective because they act in areas not currently neuraminidase have been susceptible to attack by drugs such as Tamiflu or Relenza .
The difference between Tamiflu, Relenza and the "fourteenth monster" is that the latter is a larger molecule than the other drugs, allowing attacking several binding sites of the neuraminidase in infected cells.
The researcher is confident that within a year will have the first results. The pursuit and perfection of this molecule has four years and began when Henry Rudin was involved in the University of Oxford, England, in the design of inhibitors for other types of neuraminidase.
Today, a researcher at the Institute of Biotechnology, UNAM, Rudin Pi?era has resumed what he observed at the English laboratory.
During the interview, the doctor makes a basic understanding of concepts and then talk about his "monster version 14". "In the influenza virus envelope there are certain proteins to which they are known as spicules, because they resemble thorns. In these spicules are called H and N and the reason is that the one identified as H is known as hemagglutinin and N for a protein called neuraminidase "he explains. The HA has to do with the processes of anchoring the virus to a cell, where infection begins, and the neuraminidase has to do with the breakup of that cell to spread more viruses in the body.
The neuraminidase, he adds, has the ability to stick at two active sites of a cell via the sialic acid of the infected cell, but today Tamiflu and Relenza are only capable of attacking a neuraminidase active site and that has given more strength to the virus against both drugs.
The aim of the project being developed at the Institute of Biotechnology is to generate a molecule that prevents the virus produced in an infected cell and cut the sialic acid can go out to infect other cells. "For so strong that we use with Relenza or Tamiflu in large numbers have begun to detect certain strains of influenza viruses that are no longer susceptible to the molecule of these drugs," says the doctor.
- Do you become resistant?
- Exactly, and what we want to do is build this new molecule to no longer just attacking the zone of an active site. Thus we generate a larger molecule that can stick to two different places of neuraminidase, attacking the problem of influenza in two ways, trying to give us more time to the generation of resistant variants, and exploring an area that would be the second site union, which has not been forced to evolutionarily influenza viruses mutate and become resistant.
This molecule which its creator calls jocular manner "monster number 14" would lead to more drug-resistant mutation. The efforts are aimed at ensuring that bind to the neuraminidase. So far they have achieved a successful docking protein neuraminidase N2 and N6, which infect animals.
- How will be the pilot phase?
- We have neuraminidase types 1, 2, 4, 6 and 9 crystallized and what we will do is take it to obtain crystals. We do not work with live virus or anything. Once we have these compounds, crystals already formed, then placed in reactive and are spreading our molecule to see if they stick as we expect. If we block the activity of neuraminidase our compound works.