Japanese encephalitis

Last updated
Japanese encephalitis
Other namesJapanese B encephalitis
Japanese encephalitis distribution 2022.png
The geographic distribution of Japanese encephalitis (dark green)
Specialty Infectious disease
Symptoms Headache, fever, vomiting, confusion, seizures [1]
Usual onset5 to 15 days after infection [1]
Causes Japanese encephalitis virus (spread by mosquitoes)
Diagnostic method Blood or cerebrospinal fluid testing [2]
Prevention Japanese encephalitis vaccine, avoiding mosquito bites [2]
Treatment Supportive care [1]
Prognosis Permanent neurological problems occur in up to half of survivors [2]
Frequency68,000 [2]
Deaths17,000 [2]

Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV). [3] While most infections result in little or no symptoms, occasional inflammation of the brain occurs. [3] In these cases, symptoms may include headache, vomiting, fever, confusion and seizures. [1] This occurs about 5 to 15 days after infection. [1]

Contents

JEV is generally spread by mosquitoes, specifically those of the Culex type. [2] Pigs and wild birds serve as a reservoir for the virus. [2] The disease occurs mostly outside of cities. [2] Diagnosis is based on blood or cerebrospinal fluid testing. [2]

Prevention is generally achieved with the Japanese encephalitis vaccine, which is both safe and effective. [2] Other measures include avoiding mosquito bites. [2] Once infected, there is no specific treatment, with care being supportive. [1] This is generally carried out in a hospital. [1] Permanent problems occur in up to half of people who recover from JE. [2]

The disease primarily occurs in East and Southeast Asia as well as the Western Pacific. [2] About 3 billion people live in areas where the disease occurs. [2] About 68,000 symptomatic cases occur a year, with about 17,000 deaths. [2] Often, cases occur in outbreaks. [2] The disease was first described in Japan in 1871. [2] [4]

Signs and symptoms

The Japanese encephalitis virus (JEV) has an incubation period of 2 to 26 days. [5] The vast majority of infections are asymptomatic: only 1 in 250 infections develop into encephalitis. [6]

Severe rigors may mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38–41 °C (100.4–105.8 °F). The mortality rate of the disease is around 25% and is generally higher in children under five, the immuno-suppressed and the elderly. Transplacental spread has been noted. Neurological disorders develop in 40% of those who survive with lifelong neurological defects such as deafness, emotional lability and hemiparesis occurring in those who had central nervous system involvement. [7]

Japanese encephalitis virus enters the brain through two ways and leads to infection of neurons and encephalitis. Pathogens-08-00111-g003.png
Japanese encephalitis virus enters the brain through two ways and leads to infection of neurons and encephalitis.

Increased microglial activation following Japanese encephalitis infection has been found to influence the outcome of viral pathogenesis. Microglia are the resident immune cells of the central nervous system (CNS) and have a critical role in host defense against invading microorganisms. Activated microglia secrete cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α), which can cause toxic effects in the brain. Additionally, other soluble factors such as neurotoxins, excitatory neurotransmitters, prostaglandin, reactive oxygen, and nitrogen species are secreted by activated microglia. [8]

In a murine model of JE, it was found that in the hippocampus and the striatum, the number of activated microglia was more than anywhere else in the brain, closely followed by that in the thalamus. In the cortex, the number of activated microglia was significantly less when compared to other regions of the mouse brain. An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive Japanese encephalitis infection was also observed.Shukla M, Garg A, Dhole TN, Chaturvedi R (2023). "Exaggerated levels of some specific TLRs, cytokines and chemokines in Japanese encephalitis infected BV2 and neuro 2A cell lines associated with worst outcome". Virol. J. 20 (1): 16. doi: 10.1186/s12985-023-01966-8 . PMC   9881527 . PMID   36707891.

Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage. [9] In animals, key signs include infertility and abortion in pigs, neurological disease in horses, and systemic signs including fever, lethargy and anorexia. [10]

Cause

It is a disease caused by the mosquito-borne Japanese encephalitis virus (JEV). [11]

Virology

Japanese encephalitis virus
Ijms-20-04657-g002.webp
Flavivirus structure and genome
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Flasuviricetes
Order: Amarillovirales
Family: Flaviviridae
Genus: Flavivirus
Species:
Japanese encephalitis virus

JEV is a virus from the family Flaviviridae , part of the Japanese encephalitis serocomplex of nine genetically and antigenically related viruses, some of which are particularly severe in horses, and four of which, including West Nile virus, are known to infect humans. [12] The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase, and NS5 is the viral polymerase. It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER) [13] [14] and rapidly accumulates substantial amounts of viral proteins.

Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype V is the earliest recognized ancestral strain. [15] The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Complete genomes 372 strains of this virus have been sequenced as of 2024. [16]

Diagnosis

Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and/or cerebrospinal fluid, for example by IgM capture ELISA. [17]

JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed. [18] Confirmatory testing in the US is available only at the CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining. [10]

Prevention

Japanese encephalitis vaccine "ENCEVAC" in the Japanese language Japanese encephalitis vaccine "ENCEVAC"2016.jpg
Japanese encephalitis vaccine "ENCEVAC" in the Japanese language

Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IXIARO (IC51, also marketed in Australia, New Zealand as JESPECT and India as JEEV [19] ) and ChimeriVax-JE (marketed as IMOJEV). [20] All current vaccines are based on the genotype III virus.[ citation needed ]

A formalin-inactivated mouse-brain-derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program. [11]

The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. [21] However where the vaccine is not produced in mouse brains but in vitro using cell culture there are few adverse effects compared to placebo, the main side effects being headache and myalgia. [22]

The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. [23] [24] The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every 11 months for people who remain at risk. [25] Some data are available regarding the interchangeability of other JE vaccines and IXIARO. [26]

Treatment

There is no specific treatment for Japanese encephalitis and treatment is supportive, [27] with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol. [28] There is no transmission from person to person and therefore patients do not need to be isolated.[ citation needed ]

A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapies for Japanese encephalitis. [29] [30]

The effectiveness of intravenous immunoglobulin for the management of encephalitis is unclear due to a lack of evidence. [31] Intravenous immunoglobulin for Japanese encephalitis appeared to have no benefit. [31]

Epidemiology

Disability-adjusted life year for Japanese encephalitis per 100,000 inhabitants in 2002 .mw-parser-output .div-col{margin-top:0.3em;column-width:30em}.mw-parser-output .div-col-small{font-size:90%}.mw-parser-output .div-col-rules{column-rule:1px solid #aaa}.mw-parser-output .div-col dl,.mw-parser-output .div-col ol,.mw-parser-output .div-col ul{margin-top:0}.mw-parser-output .div-col li,.mw-parser-output .div-col dd{page-break-inside:avoid;break-inside:avoid-column} .mw-parser-output .legend{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .legend-color{display:inline-block;min-width:1.25em;height:1.25em;line-height:1.25;margin:1px 0;text-align:center;border:1px solid black;background-color:transparent;color:black}.mw-parser-output .legend-text{} no data less than 1 1-5 5-10 10-15 15-20 20-25 25-30 30-35 35-40 40-45 45-50 more than 50 Japanese encephalitis world map - DALY - WHO2002.svg
Disability-adjusted life year for Japanese encephalitis per 100,000 inhabitants in 2002
  no data
  less than 1
  1–5
  5–10
  10–15
  15–20
  20–25
  25–30
  30–35
  35–40
  40–45
  45–50
  more than 50

Japanese encephalitis (JE) is the leading cause of viral encephalitis in Asia, with up to 70,000 cases reported annually. [32] Case-fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas.[ citation needed ]

Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China, South Korea, Singapore, Japan, Taiwan and Thailand. Other countries that still have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and Malaysia. Japanese encephalitis has been reported in the Torres Strait Islands, and two fatal cases were reported in mainland northern Australia in 1998. There were reported cases in Kachin State, Myanmar in 2013. There were 116 deaths reported in Odisha's Malkangiri district of India in 2016.[ citation needed ]

In 2022, the notable increase in distribution of the virus in Australia due to climate change became a concern to health officials as the population has limited immunity to the disease and the presence of large numbers of farmed and feral pigs could act as reservoirs for the virus. [7] In February 2022, Japanese encephalitis was detected and confirmed in piggeries in Victoria, Queensland and New South Wales. On 4 March, cases were detected in South Australia. By October 2022, the outbreak in eastern mainland Australia had caused 42 symptomatic human cases of the disease, resulting in seven deaths. [33] [34]

Humans, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis. Pigs act as an amplifying host and have a very important role in the epidemiology of the disease. Infection in swine is asymptomatic, except in pregnant sows, when abortion and fetal abnormalities are common sequelae. The most important vector is Culex tritaeniorhynchus , which feeds on cattle in preference to humans. The natural hosts of the Japanese encephalitis virus are birds, not humans, and many believe the virus will therefore never be eliminated. [35] In November 2011, the Japanese encephalitis virus was reported in Culex bitaeniorhynchus in South Korea. [36]

Recently, whole genome microarray research of neurons infected with the Japanese encephalitis virus has shown that neurons play an important role in their own defense against Japanese encephalitis infection. Although this challenges the long-held belief that neurons are immunologically quiescent, an improved understanding of the proinflammatory effects responsible for immune-mediated control of viral infection and neuronal injury during Japanese encephalitis infection is an essential step for developing strategies for limiting the severity of CNS disease. [37]

A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies upon mice. None are currently advocated in treating human patients.

Evolution

It is theorized that the virus may have originated from an ancestral virus in the mid-1500s in the Malay Archipelago region and evolved there into five different genotypes which spread across Asia. [44] The mean evolutionary rate has been estimated to be 4.35×10−4 (range: 3.49×10−4 to 5.30×10−4) nucleotide substitutions per site per year. [44]

Outbreak history

The clinical recognition and recording of Japanese encephalitis (JE) trace back to the 19th century, when recurring encephalitis outbreaks were noted during Japan’s summer months. The first clinical case of JE was documented in 1871 in Japan. However, it wasn’t until 1924, during a major outbreak involving over 6,000 cases, that JE’s severity and potential for widespread impact became apparent. Subsequent outbreaks in Japan were recorded in 1927, 1934, and 1935, each contributing to a deeper understanding of the disease and its transmission patterns. The spread of JE extended beyond Japan over the following decades, impacting numerous countries across Asia. On the Korean Peninsula, the first JE cases were reported in 1933, and mainland China documented its initial cases in 1940. The virus reached the Philippines in the early 1950s and continued its westward spread, with Pakistan recording cases in 1983, marking JE’s furthest westward extension. By 1995, JE cases had reached Papua New Guinea and northern Australia (specifically the Torres Strait), representing the virus's southernmost range. According to the World Health Organization (WHO), JE is also endemic to the Western Pacific Islands, but cases are rare, possibly due to an enzootic cycle that does not sustain continuous viral transmission. Epidemics in these islands likely occur only when the virus is introduced from other JE-endemic regions. [45]

Related Research Articles

<span class="mw-page-title-main">Mumps</span> Human disease caused by paramyxovirus

Mumps is a highly contagious viral disease caused by the mumps virus. Initial symptoms of mumps are non-specific and include fever, headache, malaise, muscle pain, and loss of appetite. These symptoms are usually followed by painful swelling around the side of the face, which is the most common symptom of a mumps infection. Symptoms typically occur 16 to 18 days after exposure to the virus. About one third of people with a mumps infection do not have any symptoms (asymptomatic).

<i>Rotavirus</i> Specific genus of RNA viruses

Rotaviruses are the most common cause of diarrhoeal disease among infants and young children. Nearly every child in the world is infected with a rotavirus at least once by the age of five. Immunity develops with each infection, so subsequent infections are less severe. Adults are rarely affected. Rotavirus is a genus of double-stranded RNA viruses in the family Reoviridae. There are nine species of the genus, referred to as A, B, C, D, F, G, H, I and J. Rotavirus A is the most common species, and these rotaviruses cause more than 90% of rotavirus infections in humans.

<span class="mw-page-title-main">Fifth disease</span> Red rash due to infection with parvovirus B19

Fifth disease, also known as erythema infectiosum and slapped cheek syndrome, is a common and contagious disease caused by infection with parvovirus B19. This virus was discovered in 1975 and can cause other diseases besides fifth disease. Fifth disease typically presents as a rash and is most common in children. While parvovirus B19 can affect people of all ages, only two out of ten individuals will present with symptoms.

<span class="mw-page-title-main">Hepatitis A</span> Acute infectious disease of the liver

Hepatitis A is an infectious disease of the liver caused by Hepatovirus A (HAV); it is a type of viral hepatitis. Many cases have few or no symptoms, especially in the young. The time between infection and symptoms, in those who develop them, is two–six weeks. When symptoms occur, they typically last eight weeks and may include nausea, vomiting, diarrhea, jaundice, fever, and abdominal pain. Around 10–15% of people experience a recurrence of symptoms during the 6 months after the initial infection. Acute liver failure may rarely occur, with this being more common in the elderly.

<span class="mw-page-title-main">Hepatitis E</span> Human disease caused by Orthohepevirus A

Hepatitis E is inflammation of the liver caused by infection with the hepatitis E virus (HEV); it is a type of viral hepatitis. Hepatitis E has mainly a fecal-oral transmission route that is similar to hepatitis A, although the viruses are unrelated. HEV is a positive-sense, single-stranded, nonenveloped, RNA icosahedral virus and one of five known human hepatitis viruses: A, B, C, D, and E.

<i>Flavivirus</i> Genus of viruses

Flavivirus, renamed Orthoflavivirus in 2023, is a genus of positive-strand RNA viruses in the family Flaviviridae. The genus includes the West Nile virus, dengue virus, tick-borne encephalitis virus, yellow fever virus, Zika virus and several other viruses which may cause encephalitis, as well as insect-specific flaviviruses (ISFs) such as cell fusing agent virus (CFAV), Palm Creek virus (PCV), and Parramatta River virus (PaRV). While dual-host flaviviruses can infect vertebrates as well as arthropods, insect-specific flaviviruses are restricted to their competent arthropods. The means by which flaviviruses establish persistent infection in their competent vectors and cause disease in humans depends upon several virus-host interactions, including the intricate interplay between flavivirus-encoded immune antagonists and the host antiviral innate immune effector molecules.

<span class="mw-page-title-main">Microglia</span> Glial cell located throughout the brain and spinal cord

Microglia are a type of glial cell located throughout the brain and spinal cord of the central nervous system (CNS). Microglia account for about 10–15% of cells found within the brain. As the resident macrophage cells, they act as the first and main form of active immune defense in the CNS. Microglia originate in the yolk sac under tightly regulated molecular conditions. These cells are distributed in large non-overlapping regions throughout the CNS. Microglia are key cells in overall brain maintenance – they are constantly scavenging the CNS for plaques, damaged or unnecessary neurons and synapses, and infectious agents. Since these processes must be efficient to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS. This sensitivity is achieved in part by the presence of unique potassium channels that respond to even small changes in extracellular potassium. Recent evidence shows that microglia are also key players in the sustainment of normal brain functions under healthy conditions. Microglia also constantly monitor neuronal functions through direct somatic contacts via their microglial processes, and exert neuroprotective effects when needed.

<span class="mw-page-title-main">Tick-borne encephalitis</span> Medical condition

Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system. The disease most often manifests as meningitis, encephalitis or meningoencephalitis. Myelitis and spinal paralysis also occurs. In about one third of cases sequelae, predominantly cognitive dysfunction, persist for a year or more.

<i>Tick-borne encephalitis virus</i> Species of virus

Tick-borne encephalitis virus (TBEV) is a positive-strand RNA virus associated with tick-borne encephalitis in the genus Flavivirus.

<span class="mw-page-title-main">Viral encephalitis</span> Medical condition

Viral encephalitis is inflammation of the brain parenchyma, called encephalitis, by a virus. The different forms of viral encephalitis are called viral encephalitides. It is the most common type of encephalitis and often occurs with viral meningitis. Encephalitic viruses first cause infection and replicate outside of the central nervous system (CNS), most reaching the CNS through the circulatory system and a minority from nerve endings toward the CNS. Once in the brain, the virus and the host's inflammatory response disrupt neural function, leading to illness and complications, many of which frequently are neurological in nature, such as impaired motor skills and altered behavior.

<span class="mw-page-title-main">Antibody-dependent cellular cytotoxicity</span> Cell-mediated killing of other cells mediated by antibodies

Antibody-dependent cellular cytotoxicity (ADCC), also referred to as antibody-dependent cell-mediated cytotoxicity, is a mechanism of cell-mediated immune defense whereby an effector cell of the immune system kills a target cell, whose membrane-surface antigens have been bound by specific antibodies. It is one of the mechanisms through which antibodies, as part of the humoral immune response, can act to limit and contain infection.

Powassan virus (POWV) is a Flavivirus transmitted by ticks, found in North America and in the Russian Far East. It is named after the town of Powassan, Ontario, where it was identified in a young boy who eventually died from it. It can cause encephalitis, inflammation of the brain. No approved vaccine or antiviral drug exists. Prevention of tick bites is the best precaution.

<span class="mw-page-title-main">Antibody-dependent enhancement</span> Antibodies rarely making an infection worse instead of better

Antibody-dependent enhancement (ADE), sometimes less precisely called immune enhancement or disease enhancement, is a phenomenon in which binding of a virus to suboptimal antibodies enhances its entry into host cells, followed by its replication. The suboptimal antibodies can result from natural infection or from vaccination. ADE may cause enhanced respiratory disease, but is not limited to respiratory disease. It has been observed in HIV, RSV, and Dengue virus and is monitored for in vaccine development.

An attenuated vaccine is a vaccine created by reducing the virulence of a pathogen, but still keeping it viable. Attenuation takes an infectious agent and alters it so that it becomes harmless or less virulent. These vaccines contrast to those produced by "killing" the pathogen.

<span class="mw-page-title-main">Hepatitis B</span> Human viral infection

Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection.

<span class="mw-page-title-main">CLEC5A</span> Protein-coding gene in the species Homo sapiens

C-type lectin domain family 5 member A (CLEC5A), also known as C-type lectin superfamily member 5 (CLECSF5) and myeloid DAP12-associating lectin 1 (MDL-1) is a C-type lectin that in humans is encoded by the CLEC5A gene.

Tahyna orthobunyavirus ("TAHV") is a viral pathogen of humans classified in the California encephalitis virus (CEV) serogroup of the Orthobunyavirus family in the order Bunyavirales, which is endemic to Europe, Asia, Africa and possibly China.

Jamestown Canyon encephalitis is an infectious disease caused by the Jamestown Canyon virus, an orthobunyavirus of the California serogroup. It is mainly spread during the summer by different mosquito species in the United States and Canada.

Microglia are the primary immune cells of the central nervous system, similar to peripheral macrophages. They respond to pathogens and injury by changing morphology and migrating to the site of infection/injury, where they destroy pathogens and remove damaged cells.

Anirban Basu is an Indian neurobiologist, who is primarily interested in neurovirology, a senior scientist at the National Brain Research Centre, a deemed to be university, located in Manesar, Gurgaon, Haryana. He is internationally known for his studies on Japanese encephalitis. Basu is an elected fellow of all the three major Indian science Academies namely the Indian Academy of Sciences, the Indian National Science Academy and the National Academy of Sciences, India as well as of the West Bengal Academy of Science and Technology. The Department of Biotechnology of the Government of India awarded him the National Bioscience Award for Career Development, one of the prominent Indian science awards, for his contributions to biosciences and biotechnology, in 2010.

References

  1. 1 2 3 4 5 6 7 "Symptoms and Treatment". CDC. August 2015. Archived from the original on 17 June 2017. Retrieved 29 October 2017.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 "Japanese encephalitis". World Health Organization. December 2015. Archived from the original on 13 July 2017. Retrieved 29 October 2017.
  3. 1 2 "Japanese Encephalitis". CDC. August 2015. Archived from the original on 24 May 2017. Retrieved 29 October 2017.
  4. ↑ "Japanese encephalitis - Causes". 6 February 2019.
  5. ↑ Moloney, Rachael M.; Kmush, Brittany; Rudolph, Kara E.; Cummings, Derek A. T.; Lessler, Justin (7 May 2014). "Incubation Periods of Mosquito-Borne Viral Infections: A Systematic Review". The American Journal of Tropical Medicine and Hygiene. 90 (5): 882–891. doi:10.4269/ajtmh.13-0403. PMC   4015582 . PMID   24639305.
  6. ↑ Simon, LV; Kruse, B (January 2018). "Japanese Encephalitis". Encephalitis, Japanese. StatPearls. PMID   29262148.
  7. 1 2 Davey, Melissa (8 March 2022). "What is Japanese encephalitis and why is it spreading in Australia?". The Guardian Australia. Retrieved 20 October 2022.
  8. ↑ Mohapatra S, Chakraborty T, Basu A (October 2023). "Japanese Encephalitis virus infection in astrocytes modulate microglial function: Correlation with inflammation and oxidative stress". Cytokine. 170. doi:10.1016/j.cyto.2023.156328. PMID   37567102.
  9. ↑ Ghoshal, A; Das, S; Ghosh, S; Mishra, MK; Sharma, V; Koli, P; Sen, E; Basu, A. (2007). "Proinflammatory mediators released by activated microglia induces neuronal death in Japanese encephalitis". Glia. 55 (5): 483–96. doi: 10.1002/glia.20474 . PMID   17203475. S2CID   13192982.
  10. 1 2 Japanese Encephalitis Virus Archived 18 July 2013 at the Wayback Machine reviewed and published by WikiVet, accessed 11 October 2011.
  11. 1 2 Solomon, T. (2006). "Control of Japanese encephalitis – within our grasp?". New England Journal of Medicine. 355 (9): 869–71. doi:10.1056/NEJMp058263. PMID   16943399.
  12. ↑ Lobigs M, Diamond MS (2012). "Feasibility of cross-protective vaccination against flaviviruses of the Japanese encephalitis serocomplex". Expert Rev Vaccines. 11 (2): 177–87. doi:10.1586/erv.11.180. PMC   3337329 . PMID   22309667.
  13. ↑ He B (March 2006). "Viruses, endoplasmic reticulum stress, and interferon responses". Cell Death Differ. 13 (3): 393–403. doi: 10.1038/sj.cdd.4401833 . PMID   16397582.
  14. ↑ Su HL, Liao CL, Lin YL (May 2002). "Japanese encephalitis virus infection initiates endoplasmic reticulum stress and an unfolded protein response". J. Virol. 76 (9): 4162–71. doi:10.1128/JVI.76.9.4162-4171.2002. PMC   155064 . PMID   11932381.
  15. ↑ Gao, Xiaoyan; Liu, Hong; Li, Minghua; Fu, Shihong; Liang, Guodong (2015). "Insights into the evolutionary history of Japanese encephalitis virus (JEV) based on whole-genome sequences comprising the five genotypes". Virology Journal. 12: 43. doi: 10.1186/s12985-015-0270-z . PMC   4369081 . PMID   25884184.
  16. ↑ "Japanese encephalitis virus complete genome". 2024.
  17. ↑ Shrivastva A, Tripathi NK, Parida M, Dash PK, Jana AM, Lakshmana Rao PV (2008). "Comparison of a dipstick enzyme-linked immunosorbent assay with commercial assays for detection of Japanese encephalitis virus-specific IgM antibodies". J Postgrad Med. 54 (3): 181–5. doi: 10.4103/0022-3859.40959 . hdl: 1807/52179 . PMID   18626163.
  18. ↑ Pham, David; Howard-Jones, Annaleise R.; Hueston, Linda; Jeoffreys, Neisha; Doggett, Stephen; Rockett, Rebecca J.; Eden, John-Sebastian; Sintchenko, Vitali; C-A. Chen, Sharon; O'Sullivan, Matthew V.; Maddocks, Susan; Dwyer, Dominic E.; Kok, Jen (October 2022). "Emergence of Japanese encephalitis in Australia: a diagnostic perspective". Pathology. 54 (6): 669–677. doi: 10.1016/j.pathol.2022.07.001 . PMID   35995617. S2CID   251422417.
  19. ↑ "Jeev an inactivated Japanese Encephalitis vaccine launched in Hyderabad". pharmabiz.com. 15 September 2012. Archived from the original on 23 October 2012. Retrieved 11 January 2013.
  20. ↑ Schiøler KL, Samuel M, Wai KL (2007). "Vaccines for preventing Japanese encephalitis". Cochrane Database Syst Rev. 2007 (3): CD004263. doi:10.1002/14651858.CD004263.pub2. PMC   6532601 . PMID   17636750.
  21. ↑ Jelinek T (July 2008). "Japanese encephalitis vaccine in travelers". Expert Rev Vaccines. 7 (5): 689–93. doi:10.1586/14760584.7.5.689. PMID   18564023. S2CID   34671998.
  22. ↑ EMEA Approval of Vaccine
  23. ↑ Gambel JM, DeFraites R, Hoke C, et al. (1995). "Japanese encephalitis vaccine: persistence of antibody up to 3 years after a three-dose primary series (letter)". J Infect Dis. 171 (4): 1074. doi: 10.1093/infdis/171.4.1074 . PMID   7706798.
  24. ↑ Kurane I, Takashi T (2000). "Immunogenicity and protective efficacy of the current inactivated Japanese encephalitis vaccine against different Japanese encephalitis virus strains". Vaccine. 18 (Suppl): 33–5. doi:10.1016/S0264-410X(00)00041-4. PMID   10821971.
  25. ↑ "Japanese Encephalitis Virus Vaccine (Intramuscular Route)". Mayo Clinic. 2024.
  26. ↑ Grant M. Gallagher (13 January 2020). "Are Japanese Encephalitis Vaccines Interchangeable?".
  27. ↑ Solomon T, Dung NM, Kneen R, Gainsborough M, Vaughn DW, Khanh VT (2000). "Japanese encephalitis". Journal of Neurology, Neurosurgery, and Psychiatry. 68 (9): 405–15. doi:10.1136/jnnp.68.4.405. PMC   1736874 . PMID   10727474.
  28. ↑ Japanese encephalitis~treatment at eMedicine
  29. ↑ Nimesh Gupta; Vinay Lomash; P.V. Lakshmana Rao (September 2010). "Expression profile of Japanese encephalitis virus induced neuroinflammation and its implication in disease severity". Journal of Clinical Virology. 49 (1): 04–10. doi:10.1016/j.jcv.2010.06.009. PMID   20637688.
  30. ↑ Nimesh Gupta; P.V. Lakshmana Rao (March 2011). "Transcriptomic profile of host response in Japanese encephalitis virus infection". Virology Journal. 8 (92): 92. doi: 10.1186/1743-422X-8-92 . PMC   3058095 . PMID   21371334.
  31. 1 2 Iro, Mildred A.; Martin, Natalie G.; Absoud, Michael; Pollard, Andrew J. (2 October 2017). "Intravenous immunoglobulin for the treatment of childhood encephalitis". The Cochrane Database of Systematic Reviews. 2017 (10): CD011367. doi:10.1002/14651858.CD011367.pub2. ISSN   1469-493X. PMC   6485509 . PMID   28967695.
  32. ↑ Campbell GL, Hills SL, Fischer M, Jacobson JA, Hoke CH, Hombach JM, Marfin AA, Solomon T, Tsai TF, Tsu VD, Ginsburg AS (November 2011). "Estimmated global incidence of Japanese encephalitis: a systematic review". Bull World Health Organ. 89 (10): 766–74. doi:10.2471/BLT.10.085233 (inactive 5 December 2024). PMC   3209971 . PMID   22084515.{{cite journal}}: CS1 maint: DOI inactive as of December 2024 (link)
  33. ↑ Australian Government Department of National pest & disease outbreaks (March 2022). "Japanese encephalitis".
  34. ↑ "Japanese encephalitis virus". Australian Government Department of Health and Aged Care. Retrieved 20 October 2022.
  35. ↑ Ghosh D, Basu A (September 2009). Brooker S (ed.). "Japanese encephalitis-a pathological and clinical perspective". PLOS Negl Trop Dis. 3 (9): e437. doi: 10.1371/journal.pntd.0000437 . PMC   2745699 . PMID   19787040.
  36. ↑ Kim, Heung Chul; Terry A. Klein; Ratree Takhampunya; Brian P. Evans; Sirima Mingmongkolchai; Ampornpan Kengluecha; John Grieco; Penny Masuoka; Myung-Soon Kim; Sung-Tae Chong; Jong-Koo Lee & Won-Ja Lee (2011). "Japanese Encephalitis Virus in Culicine Mosquitoes (Diptera: Culicidae) Collected at Daeseongdong, a Village in the Demilitarized Zone of the Republic of Korea". Journal of Medical Entomology . 48 (6): 1250–1256. doi:10.1603/me11091. PMID   22238887. S2CID   23321660.
  37. ↑ Nimesh Gupta; S.R. Santhosh; J. Pradeep Babu; M.M. Parida; P.V. Lakshmana Rao (January 2010). "Chemokine profiling of Japanese encephalitis virus-infected mouse neuroblastoma cells by microarray and real-time RT-PCR: Implication in neuropathogenesis". Virus Research. 147 (1): 107–12. doi:10.1016/j.virusres.2009.10.018. PMC   7126115 . PMID   19896511.
  38. ↑ Swarup V, Ghosh J, Ghosh S, Saxena A, Basu A (September 2007). "Antiviral and anti-inflammatory effects of rosmarinic acid in an experimental murine model of Japanese encephalitis". Antimicrob. Agents Chemother. 51 (9): 3367–70. doi:10.1128/AAC.00041-07. PMC   2043228 . PMID   17576830.
  39. ↑ Swarup V, Ghosh J, Mishra MK, Basu A (March 2008). "Novel strategy for treatment of Japanese encephalitis using arctigenin, a plant lignan". J. Antimicrob. Chemother. 61 (3): 679–88. doi: 10.1093/jac/dkm503 . PMID   18230688.
  40. ↑ Kazłowski B, Chiu YH, Kazłowska K, Pan CL, Wu CJ (August 2012). "Prevention of Japanese encephalitis virus infections by low-degree-polymerisation sulfated saccharides from Gracilaria sp. and Monostroma nitidum". Food Chem. 133 (3): 866–74. doi:10.1016/j.foodchem.2012.01.106.
  41. ↑ Dutta K, Ghosh D, Basu A (May 2009). "Curcumin Protects Neuronal Cells from Japanese Encephalitis Virus-Mediated Cell Death and also Inhibits Infective Viral Particle Formation by Dysregulation of Ubiquitin-Proteasome System". J Neuroimmune Pharmacol. 4 (3): 328–37. doi:10.1007/s11481-009-9158-2. PMID   19434500. S2CID   24691000.
  42. ↑ Mishra MK, Basu A (June 2008). "Minocycline neuroprotects, reduces microglial activation, inhibits caspase 3 induction, and viral replication following Japanese encephalitis". J. Neurochem. 105 (5): 1582–95. doi: 10.1111/j.1471-4159.2008.05238.x . PMID   18208541. S2CID   205618838.
  43. ↑ Mishra MK, Dutta K, Saheb SK, Basu A (December 2009). "Understanding the molecular mechanism of blood–brain barrier damage in an experimental model of Japanese encephalitis: correlation with minocycline administration as a therapeutic agent". Neurochem Int. 55 (8): 717–23. doi:10.1016/j.neuint.2009.07.006. PMID   19628016. S2CID   26964251.
  44. 1 2 Mohammed MA, Galbraith SE, Radford AD, Dove W, Takasaki T, Kurane I, Solomon T (July 2011). "Molecular phylogenetic and evolutionary analyses of Muar strain of Japanese encephalitis virus reveal it is the missing fifth genotype". Infect Genet Evol. 11 (5): 855–62. Bibcode:2011InfGE..11..855M. doi:10.1016/j.meegid.2011.01.020. PMID   21352956.
  45. ↑ Erlanger, Tobias E.; Weiss, Svenja; Keiser, Jennifer; Utzinger, Jürg; Wiedenmayer, Karin (January 2009). "Past, Present, and Future of Japanese Encephalitis". Emerging Infectious Diseases. 15 (1): 1–7. doi:10.3201/eid1501.080311. ISSN   1080-6040. PMC   2660690 . PMID   19116041.

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.