Research into the West Nile virus has hit a breakthrough, signalling the possibility that this serious infection could eventually be eradicated.
Li Ka Shing Institute of Virology's Faculty of Medicine & Dentistry researcher Tom Hobman has conducted research published in the journal PLoS One that discovered how the virus that causes the condition crosses the blood-brain barrier.
The mosquito-spread disease often results in flu-like symptoms, with many people who contract the ailment displaying no sickness at all.
However, seizures, paralysis and inflammation of the brain have been seen in a significant number of sufferers, with around ten per cent of these individuals dying.
Some people purchase expatriate health insurance to ensure they can be protected if they contract the condition, which was first identified in Uganda in 1937.
It is now found throughout the globe and has been seen in Africa, Asia, the Middle East, Oceania and North America.
Researchers discovered that the disease enters the central nervous system by breaking down two proteins – the junctional adhesion molecule (jam) and claudin – in the "tight junction", which is part of the blood-brain barrier.
Mr Hobman hypothesised that the virus can cause the pathways that regulate this junction to stop working properly, which causes jam and claudin to endure an accelerated breakdown.
"We've looked in at least three different cell types and we see the same thing happening," he remarked, explaining: "The virus replication is causing degradation of two very important molecules that form these intra-cellular barriers."
"Once we understand how West Nile virus affects the pathways that control the tight junctions of the blood-brain barrier, it may be possible to design drugs that prevent infection of the brain," the researcher added.
These international healthcare treatments could also help professionals to treat a number of other viruses that target the central nervous system, Mr Hobman asserted.
Previously, his laboratory published studies that showed the West Nile virus became 100 times less infectious when a specific cellular protein's expression was inhibited.