The swine-origin influenza a (HINI) virus that is responsible for the current pandemic clearly has the ability to leap from one human to another. The chain of transmission, aided by global air travel, has taken the virus from Mexico among humans in late march to countries around the globe.
Yet scientists who have been studying the virus say that changes is its genetic makeup could make it even more efficient at spreading and infecting people. Viruses are mostly genetic material packaged in protective coating and have no way of reproducing by themselves. So they are obligate parasites that must enter and take over a living cell, using the latter to make copies of themselves. Flu viruses use a protein on their outer surface known as hemagglutinin (HA) to gain entry into cells. Infection begins with the viral HA latching onto a receptor molecule on a cell’s surface.
Receptor molecule:
The receptor molecule has sialic acid linked to a sugar. Human-adapted flu viruses attach themselves to receptors with an ‘alpha-2-6’linkage between sialic acid and the sugar. bird flu viruses, on the one hand, bind to receptors with an ‘alpha-2-3’linkage.the alpha-2-6 receptors are found on cell along the human upper airway, such as the nose and throat.
Flu viruses that colonise these cells are then able to spread through tiny droplets that spray out when an infected person sneezes orcoughs.such iruses get transmitted much more easily and rapidly among humans. The HA of the amino acids necessary for”high affinity binding” to the alpha-2-6 receptor, according to research by ram sasisekharan and his colleagues at the Massachusetts institute of technology(MIT)that was published in nature biotechnology last month Dr.sasisekharan is Edward hoop taplin professor and director of the Harvard-MIT division of health sciences and technology.
Even so, the binding affinity of the swine-origin virus to the alpha-2-6 receptor was less than that of the 1918 HINI virus that caused the worst flu pandemic of the 20th century, says a study from the MIT group and a team of scientists from the U.S.centers for disease control and prevention (CDC) that was published recently online by science.
The efficiency with which flu viruses are able to spread through droplets is also affected by their ‘polymerase basic protein 2’ (PB2).”A single amino acid substitution from glutamic acid to lysine at amino acid position 627 supports efficient influenza virus replication at the lower temperature (33 degree C) found in the mammalian airway and contributes to efficient transmission in mammals,“ the MIT and CDC scientists pointed out in their science paper.
Glutamic acid
But in contrast to the seasonal strains of HINI that in fect humans, the swine-origin HINI virus has glutamic acid at that position in its PB2, which too affects the efficiency of the latter’s droplet transmission. given the propensity for the flu virus to develop mutations in its genome as well as for it to swap gene segments with other flu viruses(a process known as reassortment),it is possible that the swine origin virus could become even more adept at human-to-human transmission.
“Based on this study, we anticipate that mutations in the (receptor-binding site0of HA combined with mutation/reassortment of PB2 would increase the transmission efficiency of the 2009 HINI (swine-origin virus),” observed Dr.Sasisekharan in an email to this correspondent. “We need to pay careful attention to the evolution of this virus,” he said in a press release issued by MIT.
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