Innate Immunity in Infection Management

**3**

**Chapter 1**

**Abstract**

Pathogenesis and Host Immune

Response during Japanese

*and Shailendra K. Saxena*

Macrophages, Dendritic cells

**1. Introduction**

Encephalitis Virus Infection

*Swatantra Kumar, Rajni Nyodu, Vimal K. Maurya* 

Japanese Encephalitis Virus (JEV) is a mosquito borne flavivirus infection. Transmission of JEV starts with the infected mosquito bite where human dermis layer act as the primary site of infection. Once JEV makes its entry into blood, it infects monocytes wherein the viral replication peaks up without any cell death and results in production of TNF-α. One of the most characteristics pathogenesis of JEV is the breaching of blood brain barrier (BBB). JEV propagation occurs in neurons that results in neuronal cell death as well as dissemination of virus into astrocytes and microglia leading to overexpression of proinflammatory cytokines. JEV infection results in host cells mediated secretion of various types of cytokines including type-1 IFN along with TNF-α and IFN-γ. Molecule like nitrous oxide (NO) exhibits antiviral activities against JEV infection and helps in inhibiting the viral replication by blocking protein synthesis and viral RNA and also in virus infected cells clearance. In addition, the antibody can also acts an opsonizing agent in order to facilitate the phagocytosis of viral particles, which is mediated by Fc or C3 receptor. This chapter focuses on the crucial mechanism of JEV induced pathogenesis including neuropathogenesis viral clearance mechanisms and immune escape strategies.

**Keywords:** Japanese encephalitis virus, Neuropathogenesis, Dendritic cells,

Japanese Encephalitis Virus (JEV) infection is a mosquito-borne zoonotic infection in human which is the most common cause of viral encephalitis in Southeast Asia [1]. The first case of JEV was reported in Japan in the year of 1871. The virus was first isolated in the year 1935 from human brain, which was a fatal case. JEV is responsible for causing a high morbidity and high mortality specifically in the pediatrics age group [2]. Transmission cycle of JEV includes pigs which act as the reservoir/amplifying-host, water bird as carriers and mosquitoes as vector and humans are considered as the dead-end host. JEV is transmitted into human via infected Culex mosquitoes bite and thereby infected individuals develop viremia [3]. Transmission cycle starts mostly post-monsoon where the chance of mosquito breeding increases in paddy fields. JEV is single stranded positive- sense envelope RNA virus and is a member of family *Flaviviridae*. The genome of JEV encodes a

#### **Chapter 1**
