Chikungunya: an emerging and spreading arthropod-borne viral disease.

The infection caused by the virus Chikungunya is known since the last 50 years, but since the disease was mainly diffuse in geographical areas located in developing countries, a few research work have been made available until the appearance of an important epidemiological outbreak in 2005 in the island of La Reunion, that is part of metropolitan France even if located in the Southern Eastern part of the Indian Ocean. In 2007, a smaller outbreak of Chikungunya developed in the Northern Eastern part of Italy, where the local transmission has been made possible by the enormous population of Aedes albopictus and the presence of a viremic patient coming from the Indian Ocean area. Nowadays, Chikungunya is spreading in Southeast Asia countries, including Indonesia, Malaysia, Thailand and Singapore. This paper reviews different aspects of the disease caused by Chikungunya virus, including: history, epidemiology, biological and pathogenetic aspects, clinical pictures, diagnosis and treatment.

Dual Mechanism of Impairment of Interleukin-7 (IL-7) Responses in Human Immunodeficiency Virus Infection: Decreased IL-7 Binding and Abnormal Activation of the JAK/STAT5 Pathway

ABSTRACT Interleukin-7 (IL-7) plays a central role in controlling the homeostasis of both naive and long-term-memory CD4+ T cells. To better understand how human immunodeficiency virus (HIV) perturbs CD4+ T-cell homeostasis, we performed a detailed analysis of IL-7R expression, IL-7 binding, and IL-7-dependent early and late signaling events in CD4+ T-cell subsets from viremic and efficiently treated patients. HIV infection differentially affected the expression of IL-7 receptor (IL-7R) chains, with decreases in IL-7Rα/CD127 expression in the memory subset and increases in γc/CD132 expression in all CD4+ T cells. This resulted in preserved IL-7 binding in the naive compartment and decreased IL-7 binding in the memory compartment of viremic patients. Accordingly, the percentages of cells signaling in response to IL-7, as measured by pSTAT5 induction, were decreased in memory subsets, including conventional CD4+ T cells and regulatory T cells. However, the levels of pSTAT5 induction per responding cell, as measured by pSTAT5 fluorescence intensity, were increased within all naive and memory CD4+ T-cell subsets of viremic patients. The basal level of pSTAT5 was also increased, indicating a constitutive activation of the JAK/STAT5 pathway. IL-7 functional responses, as measured by Bcl-2, CD25, and Foxp3 induction, were impaired in viremic patient CD4+ T cells, suggesting that chronic activation led to downstream defects in the STAT5 signaling pathway. Thus, HIV infection perturbs IL-7 responses at both receptor binding and signaling steps, which likely compromises the regenerative capacity of the CD4+ T-cell pool and may contribute to CD4+ T-cell depletion.