Cold sores are caused by a strain of the herpes simplex virus – herpes simplex virus type 1 (HSV-1). Between 80 and 90 per cent of people are infected with the virus, but only about a quarter of them get frequent cold sores. Scientists analyzed thousands of genes to identify which ones expressed the proteins needed by the body’s immune system to prevent the virus from becoming active and – as a result – cold sores from developing. They then looked at blood samples from people with cold sores and found that one of the genes previously identified – IL28b – was mutated.This genetic mutation means that the body is not able to mount an adequate immune response to the virus, which results in cold sores.
The gene identified is also linked to treatment responses for hepatitis C patients. If this gene is mutated, patients are less likely to respond as well to treatment. The link is further evidence that a single genetic mutation can be linked to different viruses. The study, published in the journal Plos Pathogens, was funded by the Medical Research Council, the Biotechnology and Biological Sciences Research Council, the Wellcome Trust and the European Union.
Professor Juergen Haas, of the University of Edinburgh’s Division of Pathway Medicine, said: “Most people carry the cold sore strain of the herpes simplex virus, but until now we never knew why only some of them develop cold sores.
“Knowing that susceptibility to the virus involved relates to people’s genes reinforces the need to research, not only the evolution of viruses themselves, but also the susceptibility of hosts to infection.”
Source: Samantha J. Griffiths, Manfred Koegl, Chris Boutell, Helen L. Zenner, Colin M. Crump, Francesca Pica, Orland Gonzalez, Caroline C. Friedel, Gerald Barry, Kim Martin, Marie H. Craigon, Rui Chen, Lakshmi N. Kaza, Even Fossum, John K. Fazakerley, Stacey Efstathiou, Antonio Volpi, Ralf Zimmer, Peter Ghazal, Jürgen Haas. A Systematic Analysis of Host Factors Reveals a Med23-Interferon-λ Regulatory Axis against Herpes Simplex Virus Type 1 Replication. PLoS Pathogens, 2013; 9 (8): e1003514 DOI:10.1371/journal.ppat.1003514