In our most recent work we compared the frequency of HHV-6A and/or HHV-6B infections in children with febrile seizures (including FSE) and a control group of febrile children without seizures to see if there was a link between HHV-6A/B infection and febrile seizures.
Children infected by Human Herpesvirus 6B with febrile seizures are more likely to develop febrile status epilepticus: A case-control study in a referral hospital in Zambia
Background: Human herpesvirus 6B (HHV-6B) is the causative agent of Roseola infantum, and has also been suggested to play a role in the pathogenesis of febrile seizures in young children, a percentage of whom go on to develop febrile status epilepticus (FSE), but the existing data is conflicting and inconclusive. HHV-6A is a distinct species, rarely detected in most parts of the world, but prior studies suggest a higher prevalence in febrile African children. We describe a case-control study comparing the frequency of HHV-6A and/or HHV-6B infections in children with febrile seizures (including FSE) and a control group of febrile children without seizures.
Methods: We recruited children aged 6 to 60 months admitted with a febrile illness with (cases) or without (controls) seizures presenting within 48 hours of commencement of fever. Three milliliters of whole blood was centrifuged and plasma stored at -80°C for pooled screening for HHV-6B and HHV-6A by Taqman real-time polymerase chain reaction.
Results: 102 cases and 95 controls were recruited. The prevalence of HHV-6B DNA detection did not differ significantly between cases (5.8% (6/102)) and controls (10.5% (10/95)) but HHV-6B infection was associated with FSE (OR, 15; 95% CI, [1.99-120]; P= 0.009). HHV-6A was not detected.
Conclusion: Prevalence of HHV-6B was similar among cases and controls. Within the FS group, HHV-6B infection was associated with FSE, suggesting HHV-6B infections could play a role in the pathogenesis of FSE.
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ViralZone – excellent entry ports into the magical world of viruses from ExPASy and the Swiss Institute of Bioinformatics (SIB)
There are nine herpesvirus species for which humans are the natural reservoir. They cause a diverse set of diseases affecting a broad range of tissues and organ systems. Primary infection results in life-long latent infection with periodic reactivations which are more common for some species than others. Disease presentation often differs between primary infection and reactivation, or re-infection with different strains.
Herpesviruses are well established as causal pathogens in many well characterised diseases which result from direct pathology of the virus in a specific tissue or organ, but they are also associated with several neurological conditions and malignancies, where the exact causal mechanisms are less clear.
There is a long and expanding list of conditions in which herpesviruses may play a causal role, and one of the greatest challenges to the herpesvirus researcher or practitioner, is to differentiate active infections causing pathology which might respond to treatment, from sub-clinical infections.