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Neonicotinoid insecticides are systemic pesticides authorised in Europe since 1991. From their introduction on the market, they have received significant attention from the scientific community, particularly regarding the assessment of lethal and sublethal effects on bees. The availability of scientific evidence alongside some concerns raised on the bee health led to the development of more articulate risk assessment methodologies for pesticides. To support the European Commission in its decision-making process, since 2012 EFSA has been requested to evaluate the risk to bees posed by the exposure to neonicotinoids. The outcome of the EFSA evaluations has been used by risk managers to revise the approval conditions of the substances clothianidin, imidacloprid and thiamethoxam and to impose severe restrictions on their use. Meanwhile, a number of new studies have been carried out. EFSA is evaluating these data in order to further support the decision-making process with updated scientific assessments., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Human herpesvirus 6 (HHV-6) is a potentially immunosuppressive agent that has been suggested to act as a cofactor in the progression of HIV disease. Exposure of human macrophages to HHV-6A or HHV-6B profoundly impaired their ability to produce interleukin 12 (IL-12) upon stimulation with interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS). By contrast, the production of tumor necrosis factor-alpha (TNF-alpha); regulated on activation, normal T-cell expressed and secreted (RANTES); and macrophage inflammatory protein 1 beta (MIP-1 beta) was not negatively affected. To exclude the involvement of IL-12-suppressive cytokines, such as IL-10 and TNF-alpha, the viral stocks were fractionated by ultra-centrifugation. The bulk of the suppressive activity was recovered within the virion-rich pelleted fraction that was virtually devoid of such cytokines. IL-12 suppression was independent of viral replication, and the effect was not abrogated upon ultraviolet-light inactivation of the viral inoculum. The mechanism of HHV-6-mediated IL-12 suppression was investigated by RNase protection assays, which demonstrated unaltered levels of IL-12 p35 mRNA and only a modest reduction in p40 mRNA, which was insufficient to account for the near-complete loss of both extracellular and intracellular IL-12 protein. Moreover, both the IFN-gamma and the LPS signaling pathways were intact in HHV-6-treated cells. These data suggest that HHV-6 can dramatically affect the generation of effective cellular immune responses, providing a novel potential mechanism of HHV-6-mediated immunosuppression.