Researchers have discovered how dengue and Japanese encephalitis (JE) viruses proliferate inside the host cells by activating a specific molecular pathway and blocking a host’s immune responses1.
They have shown that an inhibitor molecule can stop viral replication by disrupting the molecular pathway inside the host cells – a finding that could lead to potential therapies for dengue and JE.
It is known that viruses replicate by hijacking a host’s cellular machinery. But, the precise mechanism of such replication is not known.
Scientists from the Regional Centre for Biotechnology in Faridabad and the National Brain Research Centre in Manesar, shed light on how dengue and JE viruses rapidly propagate inside the host cells, in experiments with virus-infected cultured cells and virus-infected mice.
They have shown that dengue and JE viruses activate platelets, inducing these blood cells to release platelet factor 4 (PF4). This factor then inhibits the anti-viral activity of the host’s immune cells, such as monocytes. This, in turn, robs the immune cells of their ability to secrete specific immune proteins, including interferon, which is known to stop virus replication.
The team, led by Prasenjit Guchhait and Anirban Basu, found that PF4 acts by binding to a receptor, a cell-surface protein. The researchers claim that blocking this binding between PF4 and the receptor stopped the replication of dengue and JE viruses.
Since this mechanism may exist in other viruses, this finding may provide leads for developing therapies for various viral diseases, says Guchhait.
