We faced several difficult logistic issues including prolonged and cumbersome travel between our center and the village. We were unable to carry out tests for viral RNA detection and viral load. However, the relevance of the study was increased by the fact that a well defined rural population was meticulously screened during the epidemic as per a strict protocol. A large number of clinical cases were evaluated by a an investigation team that has been engaged in epidemiological studies in the region since 1996. We have followed our survey cases for periods ranging from 12– 24 months and repeatedly collected blood samples for cytokines assay and other relevant autoantibodies in a prospective study. Our principal focus was on persistent chronic arthritis and a separate report will describe the results. Meanwhile, we have published two studies to demonstrate persistence of IL-6 upto 18 months of follow-up of cases with chronic musculoskeletal symptoms and minimal or nil effect of chloroquin on selected Th1 and Th 2 cytokines in a 24 week randomized blind control drug trial study. This is the first comprehensive clinical report on the pathophysiology of acute CHIKV based on Th1 and Th2 cytokines and anti CHIKV antibodies based on a rural population survey during the 2006 Indian epidemic. An early and intense up regulation of number of pro-inflammatory and anti inflammatory cytokines was demonstrated during the early period in subjects with a typical self limiting illness. However, this phenomenon, albeit a lesser intensity, was also evident in cases with extended symptoms and in asymptomatic individuals. An early specific IgM and IgG antibody response to CHIKV was also seen in a significant number of cases. Early persistent IgM and lower IgG to anti CHKV and intense Th2 cytokine phenotype seem to be associated with delay in resolution and prolonged MSK symptoms. Interestingly, maximum assay of TNF-a, IL-6 and IL-13 with low anti CHIKV IgM response were found in subjects recovered from CHIKV within one month of illness onset. with the clinical phenotype and specific anti CHIKV antibody response, a more comprehensive work-up of virus markers, cytokines and immune responses would be required to establish concrete causal and contributory relationships. The association of cognitive BAY-60-7550 impairment and a higher incidence of dementia in patients with chronic kidney disease has been increasingly acknowledged over the last few years and represents an important issue in an already vulnerable population. The prevalence of cognitive impairment in chronic hemodialysis patients has been estimated at 30–80%. In addition to being associated with cerebrovascular disease and potentially other types of brain injury, cognitive impairment may jeopardize treatment adherence by affecting the efficiency of every-day tasks, including correct medication and dietary rules.