Some features of rheumatic valvar disease resemble the histopathology of herpesvirus infection. While the prevalence of rheumatic fever (RF) has declined in developed countries, 15–20 million cases of RF occur each year in developing countries and RF remains the leading cause of acquired heart disease among children and young adults. A resurgence of RF has been observed in both Europe and the USA.¹ Chronic, acquired valvar disease is thought to be caused by RF, which parallels the incidence of throat infection with group A streptococci (GAS).² However, many patients with RF have no history of streptococcal pharyngitis, most throat infections with GAS do not result in RF, and RF does not follow repeated streptococcal infection at other sites such as skin. It is generally believed that RF results from an autoimmune response to streptococcal M proteins, cross-reactive with human tissue, but serum concentrations of creatine kinase or cardiac troponin type 1 (cTnI) do not increase during active rheumatic carditis indicating that anti-heart antibodies do not result in significant myocyte injury. Previous attempts to demonstrate streptococcal antigens in valvar tissue in rheumatic heart disease (RHD) were unsuccessful.

Acute pharyngitis is caused more often by viral infection than by streptococcal infection, with herpes simplex virus type 1 (HSV-1) being responsible for about 4% of all cases of sore throat. GAS, but …