Abstract
Primary infection of human herpesvirus 6B (HHV-6B) occurs in infants after the decline of maternal immunity and causes exanthema subitum accompanied by a high fever, and it occasionally develops into encephalitis resulting in neurological sequelae. There is no effective prophylaxis for HHV-6B, and its development is urgently needed. The glycoprotein complex gH/gL/gQ1/gQ2 (called 'tetramer of HHV-6B') on the virion surface is a viral ligand for its cellular receptor human CD134, and their interaction is thus essential for virus entry into the cells. Herein we examined the potency of the tetramer as a vaccine candidate against HHV-6B. We designed a soluble form of the tetramer by replacing the transmembrane domain of gH with a cleavable tag, and the tetramer was expressed by a mammalian cell expression system. The expressed recombinant tetramer is capable of binding to hCD134. The tetramer was purified to homogeneity and then administered to mice with aluminum hydrogel adjuvant and/or CpG oligodeoxynucleotide adjuvant. After several immunizations, humoral and cellular immunity for HHV-6B was induced in the mice. These results suggest that the tetramer together with an adjuvant could be a promising candidate HHV-6B vaccine.
Highlights
Human herpesvirus 6B (HHV-6B) infects infants during the window of susceptibility after a decline of maternal immunity, usually at the ages 6–18 months
Human herpesvirus 6B (HHV-6B) is known as the cause of the common childhood febrile illness exanthem subitum in its primary infection, and it develops into a lifelong latent
This primary infection causes exanthema subitum with a symptom of fever followed by skin rash, and in the worst cases, it develops into encephalitis leaving neurological sequelae[1,2,3,4]
Summary
Human herpesvirus 6B (HHV-6B) infects infants during the window of susceptibility after a decline of maternal immunity, usually at the ages 6–18 months. This primary infection causes exanthema subitum with a symptom of fever followed by skin rash (roseola), and in the worst cases, it develops into encephalitis leaving neurological sequelae[1,2,3,4]. HHV-6B establishes life-long latency after the primary infection, as do other members of the human herpesvirus family. HHV-6B reactivation occurs after transplantation, and it leads to viremia and life-threating encephalitis at a significantly high rate, 10%–20% [5]. There is no effective prophylaxis for HHV-6B, and the establishment and maintenance of immunity against HHV-6B is necessary for human health
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