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Epstein-Barr virus (EBV) is a persisting herpesvirus which is controlled by the adaptive immune response after primary infection and maintained in a latent state. However, reactivation or persistent replication is observed in situations where the immune response is compromised. Since intensive physical training has been reported to diminish immune function, increased EBV load may be a cause of reduced performance and decreased ability to sustain high training loads in competitive athletes. Samples drawn from 209 athletes during their regular follow-up appointments were tested. One hundred sixty-five individuals of similar age not active in competitive sports served as case-controls. EBV load was quantified in peripheral blood leucocytes (PBLs) by real-time PCR, and EBV antibodies were detected in plasma by ELISA and immunoblot analysis. EBV DNA was detectable in 25 of 209 athletes and in 26 of 165 controls. Of note, the EBV load per 10(5) PBLs was 6.44 +/- 1.75 in the case and 1.67 +/- 0.44 copies in the controls, yielding a high significant difference (P < 0.0001). However, EBV-specific IgG titers were significantly lower in athletes (150.4 +/- 10.73 U ml(-1) vs. 241.6 +/- 18.59 U ml(-1)). As monitored by immunoblotting, primary infections were detected with low prevalence, three in the case group and one in the control group. These findings demonstrate that EBV is present at higher levels in athletes, but the antibody response is lower in athletes than in the controls. J. Med. Virol. 82:446-451, 2010. (c) 2010 Wiley-Liss, Inc.

BackgroundThe fetal immune system is characterized by a Th2 bias but it is unclear how the Th2 predominance is established. Natural killer T (NKT) cells are a rare subset of T cells with immune regulatory functions and are already activated in utero. To test the hypothesis that NKT cells are part of the regulatory network that sets the fetal Th2 predominance, percentages of Vα24+Vβ11+ NKT cells expressing Th1/Th2-related chemokine receptors (CKR) were assessed in cord blood. Furthermore, IL-4 and IFN-γ secreting NKT cells were quantified within the single CKR+ subsets.ResultsCord blood NKT cells expressed the Th2-related CCR4 and CCR8 at significantly higher frequencies compared to peripheral blood NKT cells from adults, while CXCR3+ and CCR5+ cord blood NKT cells (Th1-related) were present at lower percentages. Within CD4negCD8neg (DN) NKT cells, the frequency of IL-4 producing NKT cells was significantly higher in cord blood, while frequencies of IFN-γ secreting DN NKT cells tended to be lower. A further subanalysis showed that the higher percentage of IL-4 secreting DN NKT cells was restricted to CCR3+, CCR4+, CCR5+, CCR6+, CCR7+, CCR8+ and CXCR4+ DN subsets in cord blood. This resulted in significantly decreased IFN-γ /IL-4 ratios of CCR3+, CCR6+ and CCR8+ cord blood DN NKT cells. Sequencing of VA24AJ18 T cell receptor (TCR) transcripts in sorted cord blood Vα24Vβ11 cells confirmed the invariant TCR alpha-chain ruling out the possibility that these cells represent an unusual subset of conventional T cells.ConclusionsDespite the heterogeneity of cord blood NKT cells, we observed a clear Th2-bias at the phenotypic and functional level which was mainly found in the DN subset. Therefore, we speculate that NKT cells are important for the initiation and control of the fetal Th2 environment which is needed to maintain tolerance towards self-antigens as well as non-inherited maternal antigens.

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Noroviruses are a major cause of viral gastroenteritis and have been detected with increasing prevalence in recent years. Currently, two main genogroups GI and GII with an increasing number of subtypes are differentiated. Because of a high genetic variability new variants emerge constantly allowing epidemiological tracing of viruses from year to year and location to location. A 282 bp sequence at the 5'end of the capsid gene was analyzed in isolates originating from the University hospital, Technische Universität München. Phylogenetic analysis was based on 20 GII positive samples from an outbreak in March/April 2006 and 8 samples from the following winter season 2006-2008. In the initial outbreak two distinct genotypes were identified. The GII.4 strain 2006a found in the majority of outbreaks in 2006 worldwide was isolated from all but two patients. These two individuals were infected with a GII.7 strain clustering mainly with isolates from Asia. Of note, they excreted noroviral RNA for 81 and 27 days, respectively. Longitudinal analysis of an extended 1381 bp sequence revealed positive selection in the P2 domain. The variant was very similar to GII.7 strains isolated in 1990 and 1994 suggesting slow evolution with evidence of recombination according to the SimPlot analysis. Strains found in the following years 2006-2008 clustered around the isolate GII.4 2006b, characterized in the spring of 2006 and reaching a high prevalence in 2006-2007. The results provide an insight into norovirus evolution at a University hospital over 3 years and describe intraindividual evolution within a patient infected chronically.