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Dreadful Mutation in Avian Flu Sparks PANDEMIC Threat!

The H5N1 avian flu virus may have acquired a mutation capable of sharply boosting the likelihood of human-to-human transmission, says a new study. Leading scientists are calling for stakes up as this genetic alteration increases risk of another disastrous epidemic.

Dreadful Mutation in Avian Flu Sparks PANDEMIC Threat!
Dreadful Mutation in Avian Flu Sparks PANDEMIC Threat!


United States: Recent studies showed that a single shift in the protein on the exterior of the highly pathogenic avian influenza (HPAI) H5N1 virus, which is known to infect the current US dairy cows could increase the ability of the virus to spread from human to human.

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The findings highlight the necessity to always closely supervise HPAI H5N1 to track the genetic changes that may enhance its transmission in people.

Today, the avian (bird) H5N1 virus infects cows to humans, but human-to-human transmission is not possible.

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However, there has been a direct transmission from affected wild birds, poultry, and dairy cows, among others.

This is because, as a result of focusing efforts on global flu pandemics, H5N1 has been tested in work previous to this with regard to natural evolution, along with the corresponding changes in transmissibility probabilities.

Attack of Influenza virus

Influenza viruses attach to cells with a surface viral protein called hemagglutinin (HA).

Avian (bird) influenza viruses, including H5N1, have not normally infected people due to the lack of avian-type cell receptors in the human upper respiratory tract.

This is bothering people with ironic and distressing facts that a virus should be able to get hold of its human-type cell receptors on the upper respiratory tracts and hence be capable of infecting humans and passing through them.

Researchers employed the H5N1 strain derived from the first human infection came from the bovine strain to determine how variation in the HA gene sequence altered the interaction of that protein with avian or human-like cell receptors.

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The researchers used site-directed mutagenesis to engineer the HA protein with several naturally-seen mutations and discovered that one of them, Q226L, enhanced the binding affinity of the protein to receptors frequently expressed in human cells if another mutation was incorporated.

More importantly, the researchers established the genetic mutations solely into the HA surface protein and did not synthesize or perform the experiments using the full, pathogenic virus.

Furthermore, study findings revealed that the Q226L mutation alone does not signify that HPAI H5N1 is about to cause a widespread pandemic. Other forms of genetic mutations would be necessary for the virus to spread among people.

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