Tetrameric glycoprotein complex gH/gL/gQ1/gQ2 is a promising vaccine candidate for human herpesvirus 6B.

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.

Inhibitory effect of the tea polyphenol, (-)-epigallocatechin gallate, on growth of cervical adenocarcinoma cell lines.

To investigate the effect of (-)-epigallocatechin gallate (EGCG) on cervical adenocarcinoma, we performed a cell proliferation assay. TRAP assay is used for telomerase activity, flow cytometry analysis and pKi-67 immunofluoroscein staining in cervical adenocarcinoma cell lines (OMC-4, TMCC-1). Our results showed that EGCG inhibited the proliferation assay, TRAP assay for telomerase activity of both cell lines. Although cell apoptosis was induced, we observed that the expression of pKi-67 was suppressed. Our data suggest that EGCG may be effective for the treatment of cervical adenocarcinoma. The mechanisms of the anti-tumor effects were revealed to be the inhibition of telomerase activity, the induction of apoptosis and cell cycle dysregulation.