Investigadores descubren cómo la influenza daña el tejido pulmonar

Una proteína del virus de la influenza que lo ayuda a multiplicarse también daña las células epiteliales pulmonares causando acumulación de fluidos en los pulmones de acuerdo con una nueva investigación de la Universidad de Alabama en Birmingham (UAB) y el Instituto de Investigación del Sur. Publicado online en la revista de la Federación de Sociedades Americanas para la Biología Experimental, los investigadores señalan que estos hallazgos brindan mejor comprensión sobre como la influenza ataca los pulmones a la vez que brinda objetivos para nuevos tratamientos.
En casos severos de influenza, el líquido se acumula en los pulmones haciendo difícil la respiración evitando que el oxígeno llegue al torrente sanguíneo. Los investigadores reportan que la M2, una proteína del virus de la influenza, daña una proteína responsable de la eliminación de fluidos de los pulmones al incrementar la cantidad de oxidantes o radicales libres dentro de las células. Los oxidantes son necesarios para la función adecuada de las células pero pueden tornarse tóxicos si no son controlados
“Bajo condiciones normales, los oxidantes juegan un papel muy importante ya que destruyen patógenos dentro de las células. Pero nuestros hallazgos sugieren que disminuyendo el número de oxidantes o evitando su incremento, se podría evita el daño causado a los pulmones por la proteína M2, dijo Sadis Matalon, Ph.D., vicepresidente de investigación y profesor de anestesiología en la UAB y principal investigador del estudio”.

http://www.eurekalert.org/pub_releases/2009-07/uoaa-urs071709.php

The researchers say the recent outbreak of H1N1 influenza and the rapid spread of this strain across the world highlight both the need to better understand how the virus damages the lungs and the urgency to find new treatments. Influenza is a contagious disease leading to about 36,000 human deaths and 200,000 hospitalizations every year in the United States alone.
Matalon, along with co-investigators Ahmed Lazrak, Ph.D., and Karen E. Iles, Ph.D., from the Department of Anesthesiology at UAB, and James W. Noah, Ph.D., and Diana L. Noah, Ph.D., of Southern Research, injected frog eggs with M2 protein and the lung protein involved with fluid removal. Using molecular biology techniques, they removed part of the flu protein until they could isolate the segment responsible for the lung injury.
“We found that when the flu protein was shortened in length, it did not damage the lung protein responsible for removing fluid from the lungs,” said Diana Noah. “This is important information as it will enable us to design drugs that will hopefully prevent this M2 flu protein from functioning properly, making it possible for those infected with the flu to recover faster.”
Another set of experiments involved injecting intact flu proteins and their target lung proteins into frog eggs along with agents that remove oxidants. The findings of the study show that following this procedure the lung proteins were no longer damaged by the flu viruses.
The team then repeated the experiments in cells from human lungs and found the same results. “We were able to understand the basic mechanisms by which the flu damages key components of the lungs in a simple system, such as the frog eggs, and then confirm these findings in human lung cells,” said Matalon.
The researchers are hesitant to say that these results indicate a simple antioxidant, such as vitamin C, can prevent or minimize flu. “The issue is too complex and we simply can’t answer that yet,” said James Noah. “Vaccination is our leading defense against flu and we have anti-viral drugs that are effective in some cases, but flu viruses show a remarkable ability to mutate, rendering vaccines and drugs less effective. Having a new target for potential interventions opens up an entirely new approach to combating influenza.”