Cold sores are fluid-filled blisters caused mainly by the highly contagious herpes simplex virus type 1 (HSV-1), which is passed on by close skin contact with someone with a cold sore. Most children come into contact with the virus by the age of five but many show no symptoms until puberty. HSV-1 is not cleared from the body by the immune system and, following initial infection of cells of the epidermis, the virus travels to the nerve root ganglia where it becomes dormant and causes no symptoms. As a result of the primary infection, the body produces antibodies against the virus – the majority of adults have antibodies against HSV-1 and 20 per cent of these individuals will have recurrent attacks of cold sores throughout their lives. The causes of reactivation are uncertain but are thought to include physical or psychological stress as well as changes to immune function.
Writing in the journal Nature Immunology, scientists from Canada and the US have now described a novel cellular process that helps the body to fight HSV-1 infection. In mouse cells infected with HSV-1, the researchers discovered a previously unknown type of autophagosome originating from the nuclear membrane. When conditions of low-grade fever were replicated by hyperthermia, or the cells were exposed to the pyrogenic cytokine, interleukin 1β, autophagy and vacuolar processing of viral peptides was observed. Viral peptides in autophagosomes were further processed by the proteasome, suggesting a complex interaction between the vacuolar and previously described MHC class I presentation pathways.
The research team hope that their discovery might eventually lead to novel therapies for HSV-1 infections, as well as for infections caused by other pathogens that are able to evade the immune system.