See my coat of many, many colours
But we could do better. Vaccines work by training your body
to recognise the coat that surrounds the flu virus. The big problem is that flu
mutates, changing its coat, hiding from our immune system. The gene machinery
encoded by the influenza virus is inefficient (leaky). Imagine using a
photocopier to make repeat copies of the same document each time using the copy
as the template for the next round; over time the quality of the copies
declines. DNA is copied in the same way with faults in the copies leading to
errors in genes (mutations), most of which are harmless, some harmful and some
beneficial – this is the driving engine of evolution. Eukaryotic cells (us)
have proofreading in the gene copying machinery, if a faulty copy is made it is
deleted, viruses do not have this, so the chance of a faulty copy increases.
This means that viruses can mutate/ change quickly leading to the emergence of
new viruses with new coats each year necessitating new vaccines.
Killer cells
A goal of influenza research is to develop vaccines that
cover a wider spectrum of viruses – the universal flu vaccine. But to achieve
this goal, we need to understand more about the way in which the body fights
off flu infection. This is what we set out to do in our recently published
paper: “DNA
Vaccines Encoding Antigen Targeted to MHC Class II Induce Influenza-Specific
CD8+ T Cell Responses, Enabling Faster Resolution of Influenza Disease”. Using
unique vaccines from our Norwegian collaborators, Vaccibody, we dissected one
aspect of the immune response called the CD8 T cell. These cells are able to
sense when other cells have viruses in them and then kill the infected cells. The
vaccines are designed to target different types of cells and can be used to
alter the flavour of the immune response. Using a CD8 T cells specific
Vaccibody, we showed was that vaccines that evoke a T cell response led to a
faster resolution of disease – infected animals got better, quicker. This is
important because the influenza virus may be less good at escaping CD8 T cells
than other parts of the immune response. Based on these studies, we believe
that the next generation of influenza vaccines need to increase the CD8 T cell
response. This idea is supported by research performed during the influenza
pandemic in 2009: patients who had a functional CD8 response were much less
likely to get sick after infection. The more we understand about the immune
response, the better vaccines get and the less people will get sick from infections.
