JEV Pathogenesis
A myriad of factors govern the severity of JEV pathogenesis. The failure of the host to produce antibodies against the virus is associated with an increased likelihood of the disease to turn lethal (Ghosh D, 2009). An important factor in the increase of pathogenesis is crossing the blood –brain barrier and this result in neurotropic viral infection. After entering the body through a mosquito bite, the virus reaches the central nervous system (CNS) via leukocytes where JEV virions bind to the endothelial surface of CNS and are internalised by endocytosis. But still it’s not clear that macrophages and B lymphocytes can also harbour JEV. In other infections flavivirus like West Nile virus (WNV), macrophages could serve as a reservoir, spreading
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It is possible that during this time, the virus resides and multiplies within host leukocytes, which act as carriers to the CNS. Tlymphocytes and IgM play a major role in the recovery and clearance of the virus after infection. A plausible therapy of clearing the virus load while in its incubation period in peripheral lymphatic tissues and spleen may actually prevent JEV pathogenesis. Besides neuronal cells, researchers have shown that astrocytes are also infected by JEV. Astrocytes are the component of the blood brain barrier, may hep in the transmission of JEV from peripheral tissues to the cerebrospinal fluid. The molecular pathogenesis of JEV infection is still unclear. It is known that JEV causes neuronal cell death in two …show more content…
NO profoundly inhibits viral RNA synthesis, viral protein accumulation and virus release from infected cells. So, NO plays a crucial role in innate immunity of the host and its ability to restrict the initial stages of JEV infection in the CNS. In contrast dysregulation of NO secretion may inflict a similar but toxic effect on uninfected host cells, which actually contributes to the pathogenesis of encephalitis. Neuronal death by secreted TNF is mediated by the TNF receptor–associated death domain protein (TRADD), which thereupon regulates a downstream apoptotic cascade in neurons. However, neuronal death also activates microglia and astrocytes and thus the inflammatory cycle goes on. (Ghosh et
It is possible that during this time, the virus resides and multiplies within host leukocytes, which act as carriers to the CNS. Tlymphocytes and IgM play a major role in the recovery and clearance of the virus after infection. A plausible therapy of clearing the virus load while in its incubation period in peripheral lymphatic tissues and spleen may actually prevent JEV pathogenesis. Besides neuronal cells, researchers have shown that astrocytes are also infected by JEV. Astrocytes are the component of the blood brain barrier, may hep in the transmission of JEV from peripheral tissues to the cerebrospinal fluid. The molecular pathogenesis of JEV infection is still unclear. It is known that JEV causes neuronal cell death in two …show more content…
NO profoundly inhibits viral RNA synthesis, viral protein accumulation and virus release from infected cells. So, NO plays a crucial role in innate immunity of the host and its ability to restrict the initial stages of JEV infection in the CNS. In contrast dysregulation of NO secretion may inflict a similar but toxic effect on uninfected host cells, which actually contributes to the pathogenesis of encephalitis. Neuronal death by secreted TNF is mediated by the TNF receptor–associated death domain protein (TRADD), which thereupon regulates a downstream apoptotic cascade in neurons. However, neuronal death also activates microglia and astrocytes and thus the inflammatory cycle goes on. (Ghosh et