La epidemia de gripe porcina y la gripe aviar/Swine flu outbreak and the Avian Flu

Un nuevo estudio de la Universidad de Maryland sugiere que el potencial del virus de la gripe avia para causar una pandemia es mayor de lo que se pensaba anteriormente. Los resultados ilustran también la forma más probable en la que se originó la actual gripe porcina.
Los virus de la gripe aviaria pueden infectar a humanos que entren en contacto con pájaros, pero estos virus no se transmiten fácilmente entre humanos. Sin embargo, una reciente investigación del Dr. Daniel Perez de la Universidad de Maryland, ha demostrado que después de recombinarse con virus de gripe humana, proceso que suele tener lugar en especies intermediarias como el cerdo, los virus de la gripe aviar precisan de relativamente pocas mutaciones para ser capaces de propagarse entre mamíferos mediante la respiración. Según Pérez "esto es similar al método por el cual es probable que se haya formado el actual virus de la gripe del cerdo".
En su estudio, Perez utilizó el virus de gripe aviar H9N2, uno de los que está en la lista de candidatos para causar una pandemia. Mediante técnicas de ingeniería genética inversa, Perez y su equipo crearon un virus híbrido humano-aviar. Este virus fue permitido mutar en hurones y al poco tiempo el virus fue capaz de transmitirse por vía respiratoria.
Al comparar las secuencias genéticas del virus híbrido original y del virus mutante, solo se encontraron 5 aminoácidos mutados: tres en la superficie y dos intenros. Dos de los superficiales son los responsables de la transmisión por vía respiratoria. Ya que se necesitan tan pocas mutaciones para hacer trnasmisible por esa vía al virus híbrido H9N2, los investigadores concluyeron que después de que se forme en la naturaleza un virus híbrido humano-aviar, el riesgo de que se produzca una pandemia humana está solo a unas pocas mutacioens más allá.

A new study by University of Maryland researchers suggests that the potential for an avian influenza virus to cause a human flu pandemic is greater than previously thought. Results also illustrate how the current swine flu outbreak likely came about.
Avian flu viruses can infect humans who have contact with birds, but these viruses tend not to transmit easily between humans. However, in research recently published by Dr. Daniel Perez from the University of Maryland showed that after reassortment with a human influenza virus, a process that usually takes place in intermediary species like pigs, an avian flu virus requires relatively few mutations to spread rapidly between mammals by respiratory droplets. "This is similar to the method by which the current swine influenza strain likely formed," said Perez.
In his study, Perez used the avian H9N2 influenza virus, one that is on the list of candidates for human pandemic potential. Using reverse genetics Perez and his team created a hybrid human-avian virus. This virus was infected to ferrets, and soon after the virus was able to transmit by respiratory droplets.
When the genetic sequences of the mutant virus and original hybrid virus were compared, the only differences were five amino acid mutations, three on the surface, and two internally. Two of the surface mutations were determined to be solely responsible for supporting respiratory droplet transmission. Because so few mutations were necessary to make the hybrid H9N2 transmissible this way, they concluded that after an animal-human hybrid influenza virus forms in nature, a human pandemic of this virus is potentially just a few mutations away.

Tomado de Science Daily

Resumen de la publicación/Abstract of the paper
Minimal molecular constraints for respiratory droplet transmission of an avian–human H9N2 influenza A virus.
Erin M. Sorrell, Hongquan Wan, Yonas Araya, Haichen Song and Daniel R. Perez
http://www.pnas.org/content/early/2009/04/17/0900877106
Abstract
Pandemic influenza requires interspecies transmission of an influenza virus with a novel hemagglutinin (HA) subtytpe that can adapt to its new host through either reassortment or point mutations and transmit by aerosolized respiratory droplets. Two previous pandemics of 1957 and 1968 resulted from the reassortment of low pathogenic avian viruses and human subtypes of that period; however, conditions leading to a pandemic virus are still poorly understood. Given the endemic situation of avian H9N2 influenza with human-like receptor specificity in Eurasia and its occasional transmission to humans and pigs, we wanted to determine whether an avian–human H9N2 reassortant could gain respiratory transmission in a mammalian animal model, the ferret. Here we show that following adaptation in the ferret, a reassortant virus carrying the surface proteins of an avian H9N2 in a human H3N2 backbone can transmit efficiently via respiratory droplets, creating a clinical infection similar to human influenza infections. Minimal changes at the protein level were found in this virus capable of respiratory droplet transmission. A reassortant virus expressing only the HA and neuraminidase (NA) of the ferret-adapted virus was able to account for the transmissibility, suggesting that currently circulating avian H9N2 viruses require little adaptation in mammals following acquisition of all human virus internal genes through reassortment. Hemagglutinin inhibition (HI) analysis showed changes in the antigenic profile of the virus, which carries profound implications for vaccine seed stock preparation against avian H9N2 influenza. This report illustrates that aerosolized respiratory transmission is not exclusive to current human H1, H2, and H3 influenza subtypes.