Human herpesvirus-6B (HHV-6B) is a T lymphotropic β-herpesvirus that is clearly distinct from human herpesvirus-6A (HHV-6A) according to molecular biological features. The International Committee on Taxonomy of Viruses recently classified HHV-6B as a separate species. The primary HHV-6B infection causes exanthem subitum and is sometimes associated with severe encephalopathy. More than 90% of the general population is infected with HHV-6B during childhood, and the virus remains throughout life as a latent infection. HHV-6B reactivation causes encephalitis in immunosuppressed patients. The cellular receptor for HHV-6A entry was identified as human CD46, but the receptor for HHV-6B has not been clear. Here we found that CD134, a member of the TNF receptor superfamily, functions as a specific entry receptor for HHV-6B. A T-cell line that is normally nonpermissive for HHV-6B infection became highly susceptible to infection when CD134 was overexpressed. CD134 was down-regulated in HHV-6B-infected T cells. Soluble CD134 interacted with the HHV-6B glycoprotein complex that serves as a viral ligand for cellular receptor, which inhibited HHV-6B but not HHV-6A infection in target cells. The identification of CD134 as an HHV-6B specific entry receptor provides important insight into understanding HHV-6B entry and its pathogenesis.H uman herpesvirus-6B (HHV-6B) is a T lymphotropic β-herpesvirus (1) and is clearly distinct from human herpesvirus-6A (HHV-6A) according to their genetic and antigenic differences and their cell tropism (2-5). Recently the International Committee on Taxonomy of Viruses classified HHV-6B as a separate species.The primary HHV-6B infection causes exanthem subitum (6) and is sometimes associated with severe encephalopathy, whereas the diseases caused by HHV-6A are still unknown. More than 90% of the general population is infected with HHV-6B during childhood, and the virus remains throughout life as a latent infection (7). HHV-6B reactivation causes encephalitis in immunosuppressed patients. HHV-6B reactivation is also associated with drug-induced hypersensitivity syndrome, and recent studies have suggested that it could be related to the severity of this disease (8, 9).HHV-6A can infect a broader variety of human cells than HHV-6B (10), although the homology between HHV-6A and -6B is almost 90% over their entire genome (11-13). Human CD46 has been shown to be a cellular receptor of , and its viral ligand is a glycoprotein (g) complex made up of viral glycoprotein H (gH)/glycoprotein L (gL)/glycoprotein Q1 (gQ1)/ glycoprotein Q2 (gQ2) (15). However, the HHV-6A gH/gL/gQ1/ gQ2 complex binds to its human cellular receptor, CD46, whereas the corresponding complex of HHV-6B does not bind to it (10, 15). Moreover, anti-CD46 antibody does not block HHV-6B infection into the cells, whereas it does HHV-6A infection, indicating that the cellular receptor exists specific for HHV-6B infection. Because HHV-6B remains as a lifelong latent infection in more than 90% of the population and causes severe disease, it is...

To investigate whether female fertility decreases with age due to poor oocyte quality, we examined the presence of DNA fragmentation in ovulated oocytes from young, mature and aged mice. Oocytes from three age groups of female mice (7-8, 20-24 and 40-48 weeks) were retrieved from the oviducts 15 h after human chorionic gonadotrophin (HCG) injection. Oocytes from each mouse were incubated in a CO2 incubator for 0-60 h in human tubal fluid (HTF). After incubation, each oocyte was stained with the terminal deoxynucleotidyl transferase-mediated dUDP nick-end labelling (TUNEL) method. The rate of DNA fragmentation (interpreted as apoptotic changes) was significantly higher for oocytes from aged mice, and the fertilization rate was significantly lower, compared with oocytes from young and mature mice. Our results suggest that DNA fragmentation of oocytes might be one of the reasons for poor oocyte quality and lower fertility in the aged group.

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While past work has examined password usage on a specific computer, web site, or organization, there is little work examining overall password usage in daily life. Through a diary study, we examine all usage of passwords, and offer some new findings based on quantitative analyses regarding how often people log in, where they log in, and how frequently people use foreign computers. Our analysis also confirms or updates existing statistics about password usage patterns. We also discuss some implications for design as well as security education.