Not the vaccine but the replication inhibitor against H1N1
Virurses are not living creatures, they do not breath, their heart do not beat. Their only aim is to replicate within the cell. To do that, viruses use the machinery of the host cell. Upon infection by the virus your cells do nothing but mass-replicating the virus. Eventually, your cells rapture and die, releasing the newly produced virus for further infections.
Recently, scientists in a collaborative study from Howard Hughes Medical Institute, Harvard Medical School, Massachusetts General Hospital, Yale Medical School, and the Wellcome Trust Sanger Institute in Cambridge, UK have identified 120 proteins that are affecting viral replication. By knocking out cellular genes one by one via small interfering RNA (siRNA) technology the group identified 120 proteins that are affecting the ability of the virus to replicate. Among those, the IFITM3 protein is of particular interest. When knocked down, IFITM3 results in a burst in viral reproduction. Over expression on the other hand results in a dramatic reduction in the viral load. The most distinctive property of the first-line IFITM3 defense is its preventive action before the virus can fuse with the cell, said study co-author and virologist Michael Farzan.
This group of proteins, particularly IFITM3 is of tremendous therapeutic importance. So far IFITM3 was able to block the replication of H1N1 and every other tested strain of the "Influenza A" virus type.
Once the mechanism is further identified it could be possible to engineer proteins for prophylactic treatment against other viral types. This approach is not restricted to humans only, other species can also be prevented from being viral sinks.
More to come in this field once the sequence- function relationship of IFITM3 is identified.
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