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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
Author(s) -
Tembo John,
Chandwe Kanta,
Kabwe Mwila,
Chilufya Moses,
Ciccone Ornella,
Mpabalwani Evans,
Ablashi Dharam,
Zumla Alimuddin,
Chen Tie,
Bates Matthew
Publication year - 2018
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.25269
Subject(s) - status epilepticus , human herpesvirus 6 , medicine , pathogenesis , febrile seizure , pediatrics , referral , immunology , case control study , epilepsy , herpesviridae , viral disease , virus , psychiatry , family medicine
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.