Antibody response to common human viruses is shaped by genetic factors

Significant interindividual variation exists among “normal” human humoral immune responses to viral infection. However, although the genetic etiology of immunologic extremes such as primary immunodeficiency has been well characterized, little is known about the genetics of normal interindividual variation in immune response. The classical twin design, which compares the phenotypic similarity between monozygotic (MZ) twin pairs and dizygotic (DZ) twin pairs, can be used to estimate the proportion of interindividual variation due to genetic factors. For example, the classical twin design has been used to demonstrate that antibody response to vaccination against certain pathogens is likely to be influenced by genetic factors.1 The present study used twin and sibling data to estimate the genetic and environmental determinants of antibody titers to 6 common human viruses: EBV, Coxsackie B virus (CVB), parvovirus B-19 (PV-B19), herpes simplex virus 1 (HSV-1), human herpes virus 6 (HHV-6), and cytomegalovirus (CMV). Although these viruses usually cause relatively mild symptoms or are asymptomatic, many are also observationally associated with the development of more severe diseases, including autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, type 1 diabetes, and systemic lupus erythematosus.2