A study of childhood febrile convulsions with particular reference to HHV-6 infection: Pathogenic considerations

Abstract

Most febrile convulsions (FC) in infants occur during a viral infection, particularly in children of less than 3 years of age; human herpesvirus 6 (HHV-6) has an important pathogenic role. To evaluate the link between this and other viruses and FC, a group of 65 children (mean age 18.46 months, SD ± 9.19) with a first episode of simple FC (G1) was compared with 24 children (mean age 19.29 months, SD ± 13.17) with a febrile syndrome but without FC (G2). Virological study showed the following infections: HHV-6 in 23/65 of G1 and in 12/24 of G2, adenoviruses (ADV) in 9/65 of G1 and in 0/24 of G2, syncytial respiratory virus (SRV) in 3/28 of G1 and in 0/2 of G2, HSV-1 in 6/65 of G1 and in 1/24 of G2, cytomegalovirus (CMV) in 2/65 of G1 and in 0/24 of G2 and HHV-7 in 1/42 of G1 and in 1/13 of G2. Children in G1, statistically compared with G2, were significantly more likely to have a family history of FC and circulating granulocytes, while IgM and α2-globulin were less probable. Some cytokines (IL1β, TNFβ and GM-CSF) were found in 24 children in G1 and 12 in G2; no differences were found between the two groups. In the light of our data and of the recent literature, the possibility that the cytokines may act on the nervous system cannot be excluded. Among the HHV-6-infected children, those suffering from convulsions were statistically more likely to have a family history of FC and IgM, while IgA were less likely. In G1, 57 cases were followed up over 2 years: 9 of them had a second episode of FC. Virological diagnosis at the first episode of FC revealed HHV-6 infection in 3 cases, 2 of these being due to viral reactivation. We underline the important role of HHV-6 infection in FC and postulate a relationship between family history and the immunity of the patient; this is confirmed by the loss of statistical significance in the reduction of IgM in G1 compared with G2 with no family history of FC. The reactivation of FC by HHV-6 is a possibility to be borne in mind; an increased number of cases would be needed to confirm this hypothesis.