Professor Nigel Dimmock and colleagues at the University of Warwick have developed a genetically altered version of the influenza virus, a so-called “protecting virus”, which slows down the infection by accelerating its own reproduction rate. Here’s how it works:
‘Protecting virus’ has a significant alteration to one of the virus’s genes. The genetic material of a flu virus consists of 8 individual segments of single stranded RNA. Professor Dimmock’s protecting influenza virus has a huge but specific deletion of around 80% of the RNA of one of these 8 strands.
This deletion makes the virus harmless and prevents it from reproducing by itself within a cell, so that it cannot spread like a normal influenza virus. However, if it is joined in the cell by another influenza virus, it retains its harmless nature but starts to reproduce – and at a much faster rate than the new influenza virus. This fast reproduction rate – spurred by the new flu infection – means that the new invading influenza is effectively crowded out by the ‘protecting virus’. This vastly slows the progress of the new infection, prevents flu symptoms, and gives the body time to develop an immune response to the harmful new invader. In effect the protecting virus converts the virulent virus into a harmless live vaccine.
Research indicates that the ‘protecting virus’ would have the same beneficial effect whatever strain of influenza is infecting you. This is because the coat of the virus is irrelevant to the protection process – the effect works on the virus genes inside the cell. It thus promises to be a highly effective tool when combating the spread of any new strain of virus, as well existing strains. One could give it as a preventive measure without the need to tailor it to a particular flu strain or mutation. This has obvious benefits when dealing with the sudden outbreak of a major epidemic, as one would not need to know the exact make up of the new strain before deploying the protecting virus making it much more useful than vaccines, which are effective only against particular existing strains of virus. In addition it protects instantly, whereas protection generated by conventional flu vaccination takes 2-3 weeks to become fully effective. Experiments so far show that a single dose of protecting virus can be given 6 weeks before an infection with flu virus and be effective. This could also have a substantial advantage over anti-viral drugs that only give less than 24-hour protection. Another advantage is that influenza virus does not appear to become resistant to ‘protecting virus’, although drug-resistance is a serious problem with many microbes.
‘Protecting virus’ also protects when given up to 24 hours after infection (and possibly longer) . It is thus able to counter an actual infection. It could therefore also be used as a treatment for family and other direct contacts of infected individuals.