**2. Genome of the virus**

Japanese encephalitis virus belongs to the *Flaviviridae* family, it is an RNA virus measuring ~ 40-50 nm in diameter and structurally it is a spheroid having cubical symmetry. It is an en‐ 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 perinuclear location, and matures on intracellular membranes.

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‐

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

Japanese encephalitis virus belongs to the *Flaviviridae* family, it is an RNA virus measuring ~ 40-50 nm in diameter and structurally it is a spheroid having cubical symmetry. It is an en‐

man population.

162 Encephalitis

**2. Genome of the virus**

**Figure 2.** The genome of Japanese Encephalitis Virus, constituting the 3 Structural genes: C, prM, E and 7 Non-struc‐ tural genes: NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5.

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‐ mission (Mathur et al., 1982). Symptomatic infections are usually present in the form of nonspecific febrile illness, including diarrhoea and rigors followed by headache, vomiting and reduced levels of consciousness and aseptic meningitis or encephalitis. The incubation peri‐ od after JEV exposure varies from 6 to 16 days (Saxena et al., 2009). One in 200/800 infected people develop clinical signs like high fever and nausea. A quarter of patients with symp‐ toms die; a third of survivors suffer brain damage.

east Asia and northern Australasia (Cambodia, Indonesia, Laos, Malaysia, Papua New Guinea, Thailand, and the Torres Strait islands of northern Australia), and to southern Asia (Bangladesh, Bhutan, India, Myanmar, Nepal, and Sri Lanka) (Fig. 3). Evidences have also been seen for Pakistan. JE is largely a disease of rural areas, especially associat‐ ed with irrigated rice agriculture. During endemics, no seasonal pattern exists and spora‐ dic cases of encephalitis occur throughout the year, most often in infants and young children. There is a peak in vector density and virus activity during October-December in endemic zones. However, epidemic activity in temperate and subtropical areas occurs

Japanese Encephalitis Virus: The Complex Biology of an Emerging Pathogen

http://dx.doi.org/10.5772/54111

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**Figure 3.** Epidemiology of JE globally. The areas highlighted in black display the regions under the attack of JEV infec‐

From past 75 years the major focus of JE coverage was on China and Southeast Asia, but now it has extended its horizons to westward towards India and Pakistan, northern to eastern Russia, eastward towards Philippines and southward to Australia. Occurrence of JE is more closely related to temperature and humidity in the atmosphere (Misra and Kalita, 2010). JEV is also engulfing new geographical regions which are shown by JEV sequencing analysis and results exhibit that JEV is expanding alarmingly to the new re‐ gions of Papua New Guinea and Australia. GI strains are often isolated from Northern Thailand, Cambodia, Korea, China, Japan, Vietnam, Taiwan and Australia between 1967 and the present. GII are isolated from Southern Thailand, Malaysia, Indonesia, Papua

tions and are high infection prone areas.

most commonly in summer and early autumn (van den et al., 2009).
