An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive Japanese encephalitis infection was also observed.Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage. In animals, key signs include infertility and abortion in pigs, neurological disease in horses, and systemic signs including fever, lethargy and anorexia. Cause
It is a disease caused by the mosquito-borne Japanese encephalitis virus (JEV). Virology
JEV is a virus from the family Flaviviridae, part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses, some which are particularly severe in horses, and four known to infect humans including West Nile virus. The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also.
It is stored in different depots to gynoid fat.Android fat cells are mostly visceral - they are large, deposited deep under the skin and are highly metabolically active. The hormones they secrete have direct access to the liver. The presence of fat in the trunk and upper body in males is facilitated by testosterone. Testosterone circulation causes fat cells to deposit around the abdominal and gluteofemoral region, whereas in women oestrogen circulation leads to fat deposits around areas such as thighs, breasts and buttocks. Therefore, measuring a persons oestrogen to testosterone ratio can reveal their predicted gynoid to android fat distribution. Android fat develops as a back-up source of energy when the male body is experiencing an imbalance, whereas gynoid fat develops after puberty, in order to better prepare the body for supporting a potential infant. 50% of the variance in abdominal fat mass observed in humans is due to genetic factors The cellular characteristics of adipose tissue in android and [gynoid] obese women are different. Android type have larger fat (hypertrophy) cells whereas gynoid type have increased number of fat cells (hyperplasia). This allows for hypertrophic obesity and hyperplastic obesity. Two different receptors, alpha and beta fat cell receptors, vary in their ability to facilitate or inhibit fat mobilization. Alpha-receptors are predominately in the lower body thus more abundant in gynoid patterns and Beta-receptors are predominantly in the upper body and so more abundant in android patterns.