Volume 5 Issue 6 Article 2



Arumugam Karthikeyan1, Subramaniyan Shanmuganathan2, Selvaraj Pavulraj3, Govinthasamy Prabakar4, Selvaraj Pavithra5, Kannan Porteen6, Govindaraj Elaiyaraja7, Yashpal Singh Malik8*


1Department of Veterinary Public Health and Epidemiology, Madras Veterinary College, Chennai 600007, Tamilnadu, India
2Division of Virology, Indian Veterinary Research Institute, Mukteswar, Uttarakhand-263138, India
3Institut fürVirologie, FreieUniversität Berlin, Berlin-14163, Germany
4Central Avian Research Institute, Izatnagar, Bareily-243122, India
5Department of Agronomy, Tamil Nadu Agricultural University, Coimbatore-641003, India
6Department of Veterinary Public Health and Epidemiology, Madras Veterinary College, Chennai-600007, India
7Department of Veterinary Microbiology, Madras Veterinary College, Chennai-600007, India
8Division of Biological standardization, Indian Veterinary Research Institute, Izatnagar-243122, India


Keywords: [ Japanese encephalitis virus, Virus genome, Transmission, Epidemiology, Diagnosis, Prevention]

Page No:730 – 748


Received – September 28, 2017; Revision – October 19, 2017; Accepted – December 08, 2017
Available Online – December 27, 2017




Japanese encephalitis (JE) is an emerging mosquito-borne zoonotic disease caused by Japanese encephalitis virus (JEV). Geographic and ecological factors such as global warming and climate change affect the demographic distribution of arthropod vectors and thereby favour the risk of JE epidemics across the world. It has become a devastating human disease that affects paediatric age group but people of all ages may get an infection. Furthermore, nearly 67,900 JEV incidences are occurring every year in 24 countries of South-East Asia and Western Pacific regions, wherein 10,426 cases were reported only in 2011. Although the mechanism for JEV pathogenesis is imprecise yet, significant scales of differences are professed in peripheral pathogenicity and neurovirulence between JEV strains. In addition to humans, a large number of vertebrate animal hosts viz. cattle, sheep, goat, dog, cat, and chicken get JEV infection. Of the note, birds and pigs serve as effective viraemic hosts and may help in dissemination of the disease in nature. Intervention strategies like vaccination as well as alteration inJournal of Experimental Biology and Agriculture Science http://www.jebas.org Japanese Encephalitis Recent Perspectives and future prospects 731 1 Introduction Japanese encephalitis (JE), an outrageous emerging mosquito-borne zoonotic disease, is caused by Japanese encephalitis virus (JEV) listed under Flaviviridae family (Saxena et al., 2013; Malhotra et al., 2015). A number of mosquito-borne viral diseases like Zika and Ebola have unrestrainedly spread in several parts of the world, even few claimed the status of ?International Emergency? due to the disease associated losses (Dhama et al., 2015; Singh et al., 2016; Singh et al., 2017; Munjal et al., 2017). In the recent years, Japanese encephalitis has become an overall human health hazard, especially in South-east Asia, Pacific regions (Western) and Australia. Though individuals of all the age groups are vulnerable to JEV infections, predominantly it affects children (less than 14 years of age) in endemic regions. Mainly, JEV infections remain asymptomatic in humans, but 1% of infections result in clinical disease with a fatality rate of 20-30%, further 30-50% of recovered individuals may undergo everlasting neuropsychiatric sequelae (Campbell et al., 2011; Sundari et al., 2016; Heffelfinger et al., 2017). JE is a notifiable disease as listed by World Organization for Animal Health (OIE) but its reporting is highly variable and incomplete due to lack of technology and observation in remote areas (Malhotra et al., 2015, More et al., 2017). Though actual incidence reports are still lacking, it was approximated that at present roughly 67,900 JEV incidences were occurring every year in 24 countries of South-East Asia and Western Pacific regions, wherein 10,426 cases reported in 2011 only (CDC, 2013). Recently, the global incidence of JE shows a progressive trend towards expansion along with geographical distribution. This review converses herein the virus genome, transmission, epidemiology, diagnosis and preventive measures to reduce the burden of JE amongst human and animal population. 2 Etiology JEV is listed under family Flaviviridae which shares similarities with other arthropod-borne flaviviruses namely, St. Louis encephalitis virus, Dengue virus, West Nile virus (WNV), Tick-Borne Encephalitis virus (TBEV) and Yellow fever virus (YFV)(Klema et al., 2015). Initially, JEV was categorized in group B of arbovirus under the family Togaviridae and afterward in the year 1985, listed in genus Flavivirus under the Flaviviridae family (Westaway et al., 1985). The genus Flavivirus comprises of more than 70 closely related enveloped small viruses with SS positive sense RNA genome (Liang et al., 2016). JEV is labile and susceptible to ultraviolet light, gamma radiation and common disinfectants like phenol, iodophors, ethanol (70 %), formaldehyde (3-8 %), iodine, glutaraldehyde (2%), bleach (1%), etc. In addition, JEV is inactive in acidic environmental conditions (pH between 1.0 and 3.0) but remain infectious in alkaline environments (pH between 7.0 and 9.0) (OIE, 2017). 3 Structure and Genome of the virus JEV is spherical in shape (40-50 nm in diameter), comprises of a lipid envelope decorated with glycoproteins containing an isometric nucleocapsid consists of single-stranded positive-sense RNA genome and core protein (Solomon et al., 2003). The genome contains single open reading frame (ORF) of about 11 kb size in which 5‘ end is capped and 3‘ end is not poly-adenylated with the potential to encode a large polyprotein of 3432 amino acids (Nain et al., 2017). This ORF carries genes for three structural proteins and seven non-structural proteins. The structural proteins are nucleocapsid or core protein (C), glycosylated envelope protein (E) and non-glycosylated membrane protein (M). Further, non-structural proteins are abbreviated as NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5 (Lindenbach et al., 2007; Saxena et al., 2011). The structural component of the nucleocapsid is formed by C protein (12-14 kDa) (Bharati & Vrati, 2006). The 8-9 kDa M protein serves as a transmission anchor which has hydrophobic domains (McAda et al., 1987). The M protein is initially synthesized as a precursor glycoprotein (prM) and cleaved to mature M protein by a furin-like cellular protease. It is worth to note here that incompletely cleaved prM act as an additional target on virions for neutralizing antibodies (Geiss et al., 2009). The envelope protein comprises of 3 domains (I, II and III) that helps in the penetration of the virion into host-cell, virulence, stimulation of neutralizing antibody and producing a protective immune response (Chambers et al., 1990). In addition, E protein acts as a major target for host antiviral immune response (Zhang et al., 2011). Non-structural proteins play a significant role in viral genome replication and expression. NS1 protein, a glycosylated protein found on the infected cell surface which may produce a deleterious response in the host if formed in huge amount agricultural practices, health education, integrated vector control programme, strengthening of diagnostic facilities together with active surveillance programs along with the =one health‘ approach might help to combat the emergence of this lethal pathogen and to safeguard human and animal health. This review abridges the updated information on virus genome, transmission, epidemiology, diagnosis and preventive measures to reduce the burden of JE amongst human and animal population.

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