Editorial [Hot topic: Antiretroviral, Anti-Inflammatory and Dopaminergic Substances in the Treatment of HIV-Infection (Guest Editor: Gabriele Arendt)]

Welcome to the 2009 Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry (HOT TOPIC) Vol. 8, June 2009. The topic we have chosen for this volume is the treatment of HIV-infection, antiretroviral as well as anti-inflammatory and dopaminergic. We highlight the current therapeutic state-of-the-art as well as future therapeutic options. In particular, Arendt and Nolting analyse the current knowledge on the role of interferons, interleukins, tumor-necrosis factor- alpha, colony-stimulating factors, adhesion molecules and chemokines in neuropathogenesis of HIV-infection and the resulting options for therapeutic procedures. This is important, because it is well-known that antiretroviral therapy alone is not a causative treatment for HIV-related brain disease. Because HIV-patients live longer due to modern antiretroviral therapy, they are endangered of developing virus-related complications as central nervous system disease, so that there is urgent need for adjunctive therapies. Speth and colleagues describe resident immune effector mechanisms in the HIV-infected brain. They emphasize the significance of complement factors and microglia in neuropathogenesis of HIV-infection, especially the diverse antiviral mechanisms exerted by complement and microglia. The authors underline the exploitation of complement to improve cell infection as well as the function of microglia as a viral reservoir and producer of progenitor virus. They present complement and microglia as integral parts of the immune system with positive protective and detrimental abilities in virus infected brains. Eva Neuen-Jacob presents another pathogenetic trait of viral brain infection, i.e., glutamate-mediated neurodysfunction in human (HIV) and simian (SIV) immunodeficieny virus associated encephalitis. From a morphological point of view, she contributes to the glutamate hypothesis for the development of HIV-associated dementia and underlines that the impairment of glutamate clearing plays an important pathogenetic role. Furthermore, she highlights the significance of the N-methyl-Daspartate (NMDA)-receptor activation in the pathogenetic cascades of neurodegenerative disorders including HIV-associated dementia, which thus, is not only an inflammatory, but also a neurodegenerative disorder.