Inactivated varicella vaccine given before hematopoietic-cell transplantation and during the first 90 days thereafter reduces the risk of zoster. The protection correlates with reconstitution of CD4 T-cell immunity against varicella-zoster virus.

PurposeTo determine the incidence of Herpes zoster in patients with one of 17 specific underlying diseases compared with that in patients with other underlying diseases.MethodsWe conducted a retrospective hospital-based cohort study using data from patients’ electronic medical records for the period 2001–2007 of the Kitano Hospital Research Database. These analyses included 55,492 patients with one of 17 underlying diseases, which were those reported as related to the contraction of Herpes zoster. Of these, 769 patients contracted Herpes zoster. The main outcome measure was the clinical diagnosis of Herpes zoster.ResultsThe adjusted hazard ratios (95% confidence interval) for Herpes zoster in patients with the 17 diseases were compared with other patients, with the following results: brain tumor [3.84 (2.51–5.88)], lung cancer [2.28 (1.61–3.22)], breast cancer [2.41 (1.52–3.82)], esophageal cancer [4.19 (2.16–8.11)], gastric cancer [1.95 (1.39–2.72)], colorectal cancer [1.85 (1.33–2.56)], gynecologic cancer [3.45 (2.08–5.70)], malignant lymphoma [8.23 (6.53–10.38)], systemic lupus erythematosus [3.90 (2.66–5.70)], rheumatoid arthritis [2.00 (1.60–2.50)], diabetes mellitus [2.44 (2.10–2.85)], hypertension [2.04 (1.75–2.38)], renal failure [2.14 (1.65–2.79)], and disk hernia [2.18 (1.52–3.13)].ConclusionsPatients with diabetes mellitus, renal failure, and malignancies have a 1.8–8.4-fold higher risk of a Herpes zoster event than patients with other diseases. Future studies should investigate alteration of the immune system in the underlying diseases and approaches for Herpes zoster prevention.

Human herpesvirus 6 (HHV-6), which belongs to the betaherpesvirus subfamily and infects mainly T cells in vitro, causes acute and latent infections. Two variants of HHV-6 have been distinguished on the basis of differences in several properties. We have determined the complete DNA sequence of HHV-6 variant B (HHV-6B) strain HST, the causative agent of exanthem subitum, and compared the sequence with that of variant A strain U1102. A total of 115 potential open reading frames (ORFs) were identified within the 161,573-bp contiguous sequence of the entire HHV-6 genome, including some genes with remarkable differences in amino acid identity. All genes with <70% identity between the two variants were found to contain deleted regions when ORFs that could not be expressed were excluded from the comparison. Except in the case of U47, these differences were found in immediate-early/regulatory genes, DR2, DR7, U86/90, U89/90, and U95, which may represent characteristic differences of variants A and B. Also, we have successfully typed 14 different strains belonging to variant A or B by PCR using variant-specific primers; the results suggest that the remarkable differences observed were conserved evolutionarily as variant-specific divergence.

To determine the relationship of human herpesvirus-6 (HHV-6) infection to febrile convulsions, cerebrospinal fluid (CSF) from patients with a history of febrile convulsion were tested by polymerase chain reaction (PCR) amplification for HHV-6 DNA. HHV-6 DNA was detected in 9 of 10 samples from patients with exanthem subitum who showed neurologic symptoms. Also, 8 of 10 CSF samples from 8 patients who had three or more febrile convulsions and 1 of 7 CSF samples from patients who had a single febrile convulsion contained HHV-6 DNA. These data suggest that HHV-6 may invade the brain during the acute phase of exanthem subitum and that recurrence of febrile convulsions may be associated with reactivation of HHV-6.