**1. Introduction**

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Servis: (2008).

160 Encephalitis

Japanese encephalitis virus (JEV) is a flavivirus, which is an emerging threat globally, major‐ ly being southern and Southeast Asia and Australia. Even though most JEV infections are asymptomatic, it is estimated that only 0.3% leads to disease causing and results in over 35,000 cases including 10,000 deaths annually worldwide, and remaining cases which some‐ how escape death produce permanent sequelae, proving to be as a persistent threat (Singh et al., 2012). The human infections caused by encephalitic flaviviruses are more often asympto‐ matic or they cause mild febrile illness but sometimes this low percentage of mild infection turns into a dangerous and life-threatening encephalitis. The conditions which support viral survival are concerned to both viral and host factors that allow virus entry from the blood into the central nervous system (CNS). Host factors play important role in disease suscepti‐ bility. Japanese encephalitis, caused by JEV which belongs to arthropod-borne virus family and transmitted through *Culex* mosquito, is centrally a pediatric disease which causes acute infection and inflammation of the brain. Historically, in 1817 JE was first identified in Japan, but the causative agent (JEV) was later isolated from a fetal human case in 1934 (Erlanger *et al.,* 2009). First report of JE in India was in 1955, and since then this deadly virus has en‐ gulfed thousands of lives and has shaken several economies. The total numbers of cases re‐ ported annually are about 35,000-50,000 (Zheng *et al.,* 2012). Out of these reported cases ~30-50 % patients suffer from neurological sequelae and ~20-40 % cases turn to be fatal (Nett *et al*., 2009). The actual counts are still higher than reported due to lack of reach of technolo‐ gy and surveillance towards extreme rural areas, which contain more vulnerable and needy population. The natural cycle of JEV consists of pig-mosquito-pig or bird-mosquito-bird (van den Hurk *et al.,* 2009) circulation of virus. When an infected mosquito bites a healthy

© 2013 Saxena et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

individual, it may lead to febrile illness or a severe meningoencephalomyelities illness which is life taking. The incidence of the disease intensifies in rainy season as the environ‐ ment supports the viral growth because of temperature, moistness and dampness which are plus factors letting the virus to bloom and flourish (Saxena *et al*., 2008) (Fig.1). Today the need is to fight against this reemerging virus by the aid of high level of immunization and therapeutic and preventive measures to slow down the spread of the disease amongst hu‐ man population.

veloped virus having single stranded RNA as a genome which is infectious. The genome is of ~11kb with positive sense and a 5' cap but it lacks a 3' poly tail (Vashist et al., 2011). It contains nucleocapsid which is surrounded by a lipid envelope. The genomic RNA contains a single open reading frame (ORF) and codes for a polyprotein of ~3400 amino acids. This polyprotein is cleaved by viral and host proteases into 10 proteins. Structural genes are three in number and are involved in antigenicity since they are expressed on the virus coded by capsid protein and involved in capsid formation: core (C), pre membrane (prM) and enve‐ lope (E). Among all three the E gene is the most important and is the most studied one. There are seven non structural genes: NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5 (Fig.2) and these are involved in virus replication (Saxena et al., 2011). A novel mutation in domain II of the envelop gene of JEV circulating in North India has been reported (Pujhari et al., 2011). The high rate of mutation in JEV is due to RNA dependent RNA polymerase (RdRp) coded by NS5 (Neyts et al., 1999). JEV replicates exclusively in the cytoplasm of infected cells, in a

Japanese Encephalitis Virus: The Complex Biology of an Emerging Pathogen

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**Figure 2.** The genome of Japanese Encephalitis Virus, constituting the 3 Structural genes: C, prM, E and 7 Non-struc‐

Japanese encephalitis (JE), caused by Japanese encephalitis virus (JEV), is the most impor‐ tant form of viral encephalitis in Asia. The epidemiology of JE has changed in the past 50 years and the area affected by JEV has expanded to India, China, Southeast Asia and West‐ ern Pacific regions. About 50, 000 cases and 10 000 deaths are reported in JEV-endemic areas among a population of 3 billion people. However, the true number is unknown, because most areas where JEV occurs lack diagnostic facilities. Most JEV infections are subclinical. JEV is a member of the JEV serological complex, which causes significant morbidity and mortality. Pigs are the most important biological amplifiers and reservoirs. Generally direct person to person spread of JEV does not or rarely occurs until it is through intrauterine transmission (Guy et al., 2010). Blood and organ transplantation also serve as a mode of transmission. JEV infection transmits from mother to foetus through vertical mode of trans‐

perinuclear location, and matures on intracellular membranes.

tural genes: NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5.

**Figure 1.** Displaying the contributing factors, which are responsible for the emergence and reemergence of JEV.
