Related Experiment Videos
A study of childhood febrile convulsions with particular reference to HHV-6 infection: pathogenic considerations
M F Bertolani1, M Portolani, F Marotti
1Gynecological, Obstetrical and Pediatric Sciences Department, University of Modena, Italy.
Insights
Human herpesvirus 6 (HHV-6) is a key cause of febrile convulsions (FC) in infants. This study highlights the significant role of HHV-6 infection and family history in infant FC development.
Area of Science:
- Pediatrics
- Virology
- Immunology
Background:
- Febrile convulsions (FC) are common in infants, often linked to viral infections.
- Human herpesvirus 6 (HHV-6) is implicated as a significant pathogen in FC.
- Understanding the viral etiology and host factors is crucial for managing FC.
Purpose of the Study:
- To investigate the association between viral infections, particularly HHV-6, and first-time simple FC in infants.
- To compare the virological and immunological profiles of infants with FC versus those with febrile illness without FC.
- To explore the potential role of cytokines and family history in FC development.
Main Methods:
- A case-control study comparing 65 infants with a first episode of simple FC (G1) to 24 infants with febrile syndrome but no FC (G2).
- Virological analysis including PCR for HHV-6, adenoviruses, SRV, HSV-1, CMV, and HHV-7.
- Immunological assessment including IgM, IgA, and cytokine levels (IL-1β, TNF-β, GM-CSF).
Main Results:
- HHV-6 was detected in 23/65 (35.4%) of G1 and 12/24 (50%) of G2 infants.
- Adenoviruses were found in 9/65 (13.8%) of G1 infants but none in G2.
- Infants in G1 were more likely to have a family history of FC and elevated granulocytes, with lower IgM and alpha 2-globulin levels.
- Among HHV-6 infected infants, those with FC had a higher likelihood of family history and IgM, but lower IgA.
- Two-year follow-up revealed a second FC episode in 9/57 (15.8%) of G1 infants, with HHV-6 identified in 3 cases, 2 due to reactivation.
Conclusions:
- HHV-6 plays a significant role in the pathogenesis of FC in infants.
- Family history and patient immunity appear to influence FC susceptibility, as evidenced by altered IgM levels.
- The reactivation of HHV-6 is a potential factor in recurrent FC, warranting further investigation.
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 alpha 2-globulin were less probable. Some cytokines (IL 1 beta, TNF beta 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.