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Journal articles on the topic 'Virus encephalitis'

Author: Grafiati

Published: 24 April 2022

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1

Shindo, Atsuhiko, Genko Oyama, Noriko Nishikawa, and Nobutaka Hattori. "Varicella-zoster virus encephalitis resembling herpes simplex virus encephalitis." BMJ Case Reports 14, no. 12 (December 2021): e247602. http://dx.doi.org/10.1136/bcr-2021-247602.

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2

Vergara Centeno, J. L., L. González Zambrano, and J. M. Jáuregui Solórzano. "Zika virus encephalitis." Medicina Intensiva (English Edition) 43, no. 1 (January 2019): 59. http://dx.doi.org/10.1016/j.medine.2018.10.005.

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3

Chittick, Paul, John C. Williamson, and Christopher A. Ohl. "BK Virus Encephalitis." Annals of Pharmacotherapy 47, no. 9 (September 2013): 1229–33. http://dx.doi.org/10.1177/1060028013500646.

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4

Tan, Chong-Tin, and Kaw-Bing Chua. "Nipah virus encephalitis." Current Infectious Disease Reports 10, no. 4 (July 2008): 315–20. http://dx.doi.org/10.1007/s11908-008-0051-6.

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5

Jhan, Ming-Kai, Chia-Ling Chen, Ting-Jing Shen, Po-Chun Tseng, Yung-Ting Wang, Rahmat Dani Satria, Chia-Yi Yu, and Chiou-Feng Lin. "Polarization of Type 1 Macrophages Is Associated with the Severity of Viral Encephalitis Caused by Japanese Encephalitis Virus and Dengue Virus." Cells 10, no. 11 (November 15, 2021): 3181. http://dx.doi.org/10.3390/cells10113181.

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Infection with flaviviruses causes mild to severe diseases, including viral hemorrhagic fever, vascular shock syndrome, and viral encephalitis. Several animal models explore the pathogenesis of viral encephalitis, as shown by neuron destruction due to neurotoxicity after viral infection. While neuronal cells are injuries caused by inflammatory cytokine production following microglial/macrophage activation, the blockade of inflammatory cytokines can reduce neurotoxicity to improve the survival rate. This study investigated the involvement of macrophage phenotypes in facilitating CNS inflammation and neurotoxicity during flavivirus infection, including the Japanese encephalitis virus, dengue virus (DENV), and Zika virus. Mice infected with different flaviviruses presented encephalitis-like symptoms, including limbic seizure and paralysis. Histology indicated that brain lesions were identified in the hippocampus and surrounded by mononuclear cells. In those regions, both the infiltrated macrophages and resident microglia were significantly increased. RNA-seq analysis showed the gene profile shifting toward type 1 macrophage (M1) polarization, while M1 markers validated this phenomenon. Pharmacologically blocking C-C chemokine receptor 2 and tumor necrosis factor-α partly retarded DENV-induced M1 polarization. In summary, flavivirus infection, such as JEV and DENV, promoted type 1 macrophage polarization in the brain associated with encephalitic severity.

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6

Bondre, Vijay P., Gajanan N. Sapkal, Prasanna N. Yergolkar, Pradip V. Fulmali, Vasudha Sankararaman, Vijay M. Ayachit, Akhilesh C. Mishra, and Milind M. Gore. "Genetic characterization of Bagaza virus (BAGV) isolated in India and evidence of anti-BAGV antibodies in sera collected from encephalitis patients." Journal of General Virology 90, no. 11 (November 1, 2009): 2644–49. http://dx.doi.org/10.1099/vir.0.012336-0.

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During investigations into the outbreak of encephalitis in 1996 in the Kerala state in India, an arbovirus was isolated from a Culex tritaeniorhynchus mosquito pool. It was characterized as a Japanese encephalitis and West Nile virus cross-reactive arbovirus by complement fixation test. A plaque reduction–neutralization test was performed using hyperimmune sera raised against the plaque-purified arbovirus isolate. The sera did not show reactivity with Japanese encephalitis virus and were weakly reactive with West Nile virus. Complete open reading frame sequence analysis characterized the arbovirus as Bagaza virus (BAGV), with 94.80 % nucleotide identity with African BAGV strain DakAr B209. Sera collected from the encephalitic patients during the acute phase of illness showed 15 % (8/53) positivity for anti-BAGV neutralizing antibodies. This is the first report of the isolation of BAGV from India. The presence of anti-BAGV neutralizing antibodies suggests that the human population has been exposed to BAGV.

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7

Lobigs, Mario, Maximilian Larena, Mohammed Alsharifi, Eva Lee, and Megan Pavy. "Live Chimeric and Inactivated Japanese Encephalitis Virus Vaccines Differ in Their Cross-Protective Values against Murray Valley Encephalitis Virus." Journal of Virology 83, no. 6 (December 24, 2008): 2436–45. http://dx.doi.org/10.1128/jvi.02273-08.

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ABSTRACT The Japanese encephalitis virus (JEV) serocomplex, which also includes Murray Valley encephalitis virus (MVEV), is a group of antigenically closely related, mosquito-borne flaviviruses that are responsible for severe encephalitic disease in humans. While vaccines against the prominent members of this serocomplex are available or under development, it is unlikely that they will be produced specifically against those viruses which cause less-frequent disease, such as MVEV. Here we have evaluated the cross-protective values of an inactivated JEV vaccine (JE-VAX) and a live chimeric JEV vaccine (ChimeriVax-JE) against MVEV in two mouse models of flaviviral encephalitis. We show that (i) a three-dose vaccination schedule with JE-VAX provides cross-protective immunity, albeit only partial in the more severe challenge model; (ii) a single dose of ChimeriVax-JE gives complete protection in both challenge models; (iii) the cross-protective immunity elicited with ChimeriVax-JE is durable (≥5 months) and broad (also giving protection against West Nile virus); (iv) humoral and cellular immunities elicited with ChimeriVax-JE contribute to protection against lethal challenge with MVEV; (v) ChimeriVax-JE remains fully attenuated in immunodeficient mice lacking type I and type II interferon responses; and (vi) immunization with JE-VAX, but not ChimeriVax-JE, can prime heterologous infection enhancement in recipients of vaccination on a low-dose schedule, designed to mimic vaccine failure or waning of vaccine-induced immunity. Our results suggest that the live chimeric JEV vaccine will protect against other viruses belonging to the JEV serocomplex, consistent with the observation of cross-protection following live virus infections.

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8

Ahn, Seon-Jae, Jangsup Moon, Jun-Sang Sunwoo, Jin-Sun Jun, Soon-Tae Lee, Kyung-Il Park, Keun-Hwa Jung, et al. "Respiratory virus-related meningoencephalitis in adults." encephalitis 1, no. 1 (January 10, 2020): 14–19. http://dx.doi.org/10.47936/encephalitis.2020.00052.

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9

Millichap, J. Gordon. "Herpes Simplex Virus Encephalitis." Pediatric Neurology Briefs 6, no. 4 (April 1, 1992): 27. http://dx.doi.org/10.15844/pedneurbriefs-6-4-3.

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10

Lee Fanning, W. "Japanese Encephalitis Virus Vaccine." Journal of Travel Medicine 3, no. 1 (March 1, 1996): 57–59. http://dx.doi.org/10.1111/j.1708-8305.1996.tb00698.x.

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11

Latronico, N., and A. Candiani. "BRAINSTEM HERPES VIRUS ENCEPHALITIS." Lancet 330, no. 8560 (September 1987): 690–91. http://dx.doi.org/10.1016/s0140-6736(87)92483-4.

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12

Sinha, Nitin, Sahil Sareen, AshwiniKumar Malhotra, and Sanchit Singh. "Human immunodeficiency virus encephalitis." Indian Journal of Sexually Transmitted Diseases and AIDS 41, no. 1 (2020): 108. http://dx.doi.org/10.4103/ijstd.ijstd_112_16.

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13

Lizzi, Jared, Tyler Hill, and Julian Jakubowski. "Varicella Zoster Virus Encephalitis." Clinical Practice and Cases in Emergency Medicine 3, no. 4 (October 14, 2019): 380–82. http://dx.doi.org/10.5811/cpcem.2019.8.43010.

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Varicella zoster virus in the adult patient most commonly presents as shingles. Shingles is a painful vesicular eruption localized to a specific dermatome of the body. One of the potential complications of this infection is involvement of the central nervous system causing encephalitis. An increased risk of this complication is associated with the immunocompromised patient. In this case report, we review the history and physical exam findings that should raise clinical suspicion for varicella zoster encephalitis, as well as the epidemiology, risk factors, treatment, and prognosis of this type of infection.

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14

Kleinschmidt-DeMasters, B. K. "Herpes Simplex Virus Encephalitis." Pathology Case Reviews 9, no. 1 (January 2004): 7–10. http://dx.doi.org/10.1097/01.pcr.0000109250.14446.eb.

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15

Gérardin, Patrick, Thérèse Couderc, Marc Bintner, Patrice Tournebize, Michel Renouil, Jérome Lémant, Véronique Boisson, et al. "Chikungunya virus–associated encephalitis." Neurology 86, no. 1 (November 25, 2015): 94–102. http://dx.doi.org/10.1212/wnl.0000000000002234.

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16

McCullers, Jonathan A., Sergio Facchini, P. Joan Chesney, and Robert G. Webster. "Influenza B Virus Encephalitis." Clinical Infectious Diseases 28, no. 4 (April 1999): 898–900. http://dx.doi.org/10.1086/515214.

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17

Padwell, A. "Herpes Simplex Virus Encephalitis." Journal of the Royal Army Medical Corps 139, no. 2 (June 1, 1993): 69–72. http://dx.doi.org/10.1136/jramc-139-02-11.

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18

Petersen, Lyle R., John T. Roehrig, and James M. Hughes. "West Nile Virus Encephalitis." New England Journal of Medicine 347, no. 16 (October 17, 2002): 1225–26. http://dx.doi.org/10.1056/nejmo020128.

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19

Egdell, R., D. Egdell, and T. Solomon. "Herpes simplex virus encephalitis." BMJ 344, jun13 2 (June 13, 2012): e3630-e3630. http://dx.doi.org/10.1136/bmj.e3630.

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20

Neeley, S. P., A. J. Cross, T. J. Crow, J. A. Johnson, and G. R. Taylor. "Herpes simplex virus encephalitis." Journal of the Neurological Sciences 71, no. 2-3 (December 1985): 325–37. http://dx.doi.org/10.1016/0022-510x(85)90071-1.

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21

Dean, James L., and Brandon J. Palermo. "West nile virus encephalitis." Current Infectious Disease Reports 7, no. 4 (July 2005): 292–96. http://dx.doi.org/10.1007/s11908-005-0062-5.

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22

Ito, Masatoshi, Tohshin Go, Takehiko Okuno, and Haruki Mikawa. "Chronic mumps virus encephalitis." Pediatric Neurology 7, no. 6 (November 1991): 467–70. http://dx.doi.org/10.1016/0887-8994(91)90033-h.

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23

Sanyal, D., G. Kudesia, and M. Young. "Epstein-Barr virus encephalitis." Journal of Infection 22, no. 1 (January 1991): 101–2. http://dx.doi.org/10.1016/0163-4453(91)91290-e.

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24

Batalis, Nick I., Luis Galup, Sherif R. Zaki, and Joseph A. Prahlow. "West Nile Virus Encephalitis." American Journal of Forensic Medicine & Pathology 26, no. 2 (June 2005): 192–96. http://dx.doi.org/10.1097/01.paf.0000163826.56278.da.

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25

Solomon, T. "Flavivirus encephalitis and other neurological syndromes (Japanese encephalitis, WNV, Tick borne encephalits, Dengue, Zika virus)." International Journal of Infectious Diseases 45 (April 2016): 24. http://dx.doi.org/10.1016/j.ijid.2016.02.086.

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26

McCarthy, Micheline. "St. Louis encephalitis and West nile virus encephalitis." Current Treatment Options in Neurology 3, no. 5 (September 2001): 433–38. http://dx.doi.org/10.1007/s11940-001-0031-8.

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27

Suri, Vinit, Swapnil Jain, Mohit Kalangi Venkata Naga, Sudheer Tyagi, Aditendraditya Singh Bhati, and Kanika Suri. "Decompressive craniectomy in herpes simplex encephalitis: a case report." International Journal of Research in Medical Sciences 8, no. 7 (June 26, 2020): 2705. http://dx.doi.org/10.18203/2320-6012.ijrms20202923.

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Herpes Simplex Encephalitis is the commonest form of sporadic encephalitis. Availability of effective antiviral therapy viz Acyclovir has significantly reduced the mortality of Herpes Simplex Encephalitis. Elevated intracranial pressure resulting in herniation syndromes continues to be an important cause of mortality. Antiviral therapy and medical measures for managing raised intracranial pressure including osmotic diuretics, careful usage of steroids and controlled hyperventilation continue to be the cornerstones in management of these patients. Authors present a 38-year-old male patient with Cerebrospinal fluid Meningo-encephalitic panel positivity for herpes simplex virus 1 and bilateral temporal lobe lesions with secondary decline due to impending herniation syndrome despite osmotic diuretics and steroids with patient survival and complete recovery following decompressive hemicraniectomy.

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28

Licon Luna, Rosa M., Eva Lee, Arno Müllbacher, Robert V. Blanden, Rod Langman, and Mario Lobigs. "Lack of both Fas Ligand and Perforin Protects from Flavivirus-Mediated Encephalitis in Mice." Journal of Virology 76, no. 7 (April 1, 2002): 3202–11. http://dx.doi.org/10.1128/jvi.76.7.3202-3211.2002.

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ABSTRACT The mechanism by which encephalitic flaviviruses enter the brain to inflict a life-threatening encephalomyelitis in a small percentage of infected individuals is obscure. We investigated this issue in a mouse model for flavivirus encephalitis in which the virus was administered to 6-week-old animals by the intravenous route, analogous to the portal of entry in natural infections, using a virus dose in the range experienced following the bite of an infectious mosquito. In this model, infection with 0.1 to 105 PFU of virus gave mortality in ∼50% of animals despite low or undetectable virus growth in extraneural tissues. We show that the cytolytic effector functions play a crucial role in invasion of the encephalitic flavivirus into the brain. Mice deficient in either the granule exocytosis- or Fas-mediated pathway of cytotoxicity showed delayed and reduced mortality. Mice deficient in both cytotoxic effector functions were resistant to a low-dose peripheral infection with the neurotropic virus.

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29

Landers, V. Douglas, Daniel W. Wilkey, Michael L. Merchant, Thomas C. Mitchell, and Kevin J. Sokoloski. "The Alphaviral Capsid Protein Inhibits IRAK1-Dependent TLR Signaling." Viruses 13, no. 3 (February 27, 2021): 377. http://dx.doi.org/10.3390/v13030377.

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Alphaviruses are arthropod-borne RNA viruses which can cause either mild to severe febrile arthritis which may persist for months, or encephalitis which can lead to death or lifelong cognitive impairments. The non-assembly molecular role(s), functions, and protein–protein interactions of the alphavirus capsid proteins have been largely overlooked. Here we detail the use of a BioID2 biotin ligase system to identify the protein–protein interactions of the Sindbis virus capsid protein. These efforts led to the discovery of a series of novel host–pathogen interactions, including the identification of an interaction between the alphaviral capsid protein and the host IRAK1 protein. Importantly, this capsid–IRAK1 interaction is conserved across multiple alphavirus species, including arthritogenic alphaviruses SINV, Ross River virus, and Chikungunya virus; and encephalitic alphaviruses Eastern Equine Encephalitis virus, and Venezuelan Equine Encephalitis virus. The impact of the capsid–IRAK1 interaction was evaluated using a robust set of cellular model systems, leading to the realization that the alphaviral capsid protein specifically inhibits IRAK1-dependent signaling. This inhibition represents a means by which alphaviruses may evade innate immune detection and activation prior to viral gene expression. Altogether, these data identify novel capsid protein–protein interactions, establish the capsid–IRAK1 interaction as a common alphavirus host–pathogen interface, and delineate the molecular consequences of the capsid–IRAK1 interaction on IRAK1-dependent signaling.

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30

Wangchuk, Sonam, Tshewang Dorji Tamang, Jit Bahadur Darnal, Sonam Pelden, Karma Lhazeen, Mimi Lhamu Mynak, G. William Letson, et al. "Japanese Encephalitis Virus as Cause of Acute Encephalitis, Bhutan." Emerging Infectious Diseases 26, no. 9 (September 2020): 2239–42. http://dx.doi.org/10.3201/eid2609.200620.

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31

Zheng, Yayun, Minghua Li, Huanyu Wang, and Guodong Liang. "Japanese encephalitis and Japanese encephalitis virus in mainland China." Reviews in Medical Virology 22, no. 5 (March 8, 2012): 301–22. http://dx.doi.org/10.1002/rmv.1710.

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32

Qureshi, Muhammad Salman Haider, Bakhtawar Wajeeha Qureshi, and Ramsha Khan. "Zika virus infection: a public health emergency!" International Journal of Scientific Reports 3, no. 3 (February 25, 2017): 68. http://dx.doi.org/10.18203/issn.2454-2156.intjscirep20170884.

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<p class="abstract"><em>Zika virus</em> belongs to the family of Flaviviridae. The Flaviviridae family also includes other human pathogens like <em>West Nile virus</em> (WNV), <em>Yellow fever virus</em> (YFV), mosquito transmitted <em>Dengue virus</em> (DENV), <em>Tick borne encephalitic virus</em> (TBEV) and <em>Japanese encephalitis virus</em> (JEV). <em>Zika virus</em> is a mosquito-borne disease and is transmitted by <em>Aedes aegypti</em> mosquito<span lang="EN-IN">. </span></p>

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33

Kumar, Rashmi. "Understanding and managing acute encephalitis." F1000Research 9 (January 29, 2020): 60. http://dx.doi.org/10.12688/f1000research.20634.1.

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Encephalitis is an important cause of morbidity, mortality, and permanent neurologic sequelae globally. Causes are diverse and include viral and non-viral infections of the brain as well as autoimmune processes. In the West, the autoimmune encephalitides are now more common than any single infectious cause, but, in Asia, infectious causes are still more common. In 2006, the World Health Organization coined the term “acute encephalitis syndrome”, which simply means acute onset of fever with convulsions or altered consciousness or both. In 2013, the International Encephalitis Consortium set criteria for diagnosis of encephalitis on basis of clinical and laboratory features. The most important infectious cause in the West is herpes simplex virus, but globally Japanese encephalitis (JE) remains the single largest cause. Etiologic diagnosis is difficult because of the large number of agents that can cause encephalitis. Also, the responsible virus may be detectable only in the brain and is either absent or transiently found in blood or cerebrospinal fluid (CSF). Virological diagnosis is complex, expensive, and time-consuming. Different centres could make their own algorithms for investigation in accordance with the local etiologic scenarios. Magnetic resonance imaging (MRI) and electroencephalography are specific for few agents. Clinically, severity may vary widely. A severe case may manifest with fever, convulsions, coma, neurologic deficits, and death. Autoimmune encephalitis (AIE) includes two major categories: (i) classic paraneoplastic limbic encephalitis (LE) with autoantibodies against intracellular neuronal antigens (Eg: Hu and Ma2) and (ii) new-type AIE with autoantibodies to neuronal surface or synaptic antigens (Eg: anti-N-methyl-D-aspartate receptor). AIE has prominent psychiatric manifestations: psychosis, aggression, mutism, memory loss, euphoria, or fear. Seizures, cognitive decline, coma, and abnormal movements are common. Symptoms may fluctuate rapidly. Treatment is largely supportive. Specific treatment is available for herpesvirus group and non-viral infections. Various forms of immunotherapy are used for AIE.

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34

Agha, Rabia. "Arbovirus Infections." Pediatrics In Review 16, no. 9 (September 1, 1995): 353. http://dx.doi.org/10.1542/pir.16.9.353.

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Arbovirus infections are viral diseases transmitted by insect vectors—that is, they are arthropod borne. Clinically significant arboviruses in the United States include western equine encephalitis virus (WEE), eastern equine encephalitis virus (EEE), St. Louis encephalitis virus (SLE), the La Crosse (LAC) strain of the California encephalitis group, Powassan virus (POW), and Colorado tick fever virus (CTF). The four encephalitis viruses are spread by mosquitoes, whereas POW and CTF are tick borne. Not surprisingly, given that transmission depends on mosquito and tick vectors, arbovirus infections are most common in the US during the late spring and summer months. The geographic distribution of these viruses (see Table) is helpful to diagnosis because their clinical manifestations are not distinctive enough in individual patients to be diagnostic.

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35

Jones, Clinton, Melissa Inman, Weiping Peng, Gail Henderson, Alan Doster, Guey-Chuen Perng, and Anisa Kaenjak Angeletti. "The Herpes Simplex Virus Type 1 Locus That Encodes the Latency-Associated Transcript Enhances the Frequency of Encephalitis in Male BALB/c Mice." Journal of Virology 79, no. 22 (November 15, 2005): 14465–69. http://dx.doi.org/10.1128/jvi.79.22.14465-14469.2005.

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ABSTRACT Herpes simplex virus type 1 (HSV-1) is the leading cause of virus-induced encephalitis; however, the viral genes that regulate encephalitis have not been well characterized. In this study, we tested whether the LAT (latency-associated transcript) locus regulates the frequency of encephalitis in male or female mice. Male BALB/c mice are more susceptible to HSV-1-induced encephalitis than age-matched female BALB/c mice. Deletion of LAT coding sequences reduced the frequency of encephalitis. A recombinant virus containing the first 1.5 kb of the LAT coding sequence induces levels of encephalitis in male BALB/c mice similar to those induced by wild-type HSV-1.

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36

Storset, A. K., Ø. Evensen, and E. Rimstad. "Immunohistochemical Identification of Caprine Arthritis-Encephalitis Virus in Paraffin-embedded Specimens from Naturally Infected Goats." Veterinary Pathology 34, no. 3 (May 1997): 180–88. http://dx.doi.org/10.1177/030098589703400302.

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The expression of caprine arthritis-encephalitis virus capsid protein was studied in seropositive naturally infected asymptomatic goats (10), seropositive naturally infected encephalitic kids (12) and goats (4), and noninfected control goats (3). Rabbit antiserum to recombinant viral capsid and matrix proteins were used in a biotin-streptavidin-alkaline phosphatase complex immunohistochemical method on sections of formalin-and ethanol-fixed tissue specimens. Macrophages in inflamed areas of the lung (8/12), in the brain (5/16), and in the spinal cord (4/16) from encephalitic animals harbored viral antigens, as revealed by immunohistochemistry and use of a capsid protein-specific antiserum. Altogether 12/16 encephalitic animals tested positive for viral antigen. Viral antigens were found in 5/10 seropositive asymptomatic goats in macrophages located in the lung (3), the udder (1), and the medulla of lymph nodes (4). None of the control animals tested positive for viral antigen. Ethanol fixation showed highest sensitivity, and the lowest antigen concentration that revealed a positive signal discernible from background was twofold higher in ethanol-fixed specimens than in formalin-fixed specimens. The evaluation was performed on artificial antigen substrates embedded with defined concentrations of recombinant viral capsid protein. Immunohistochemistry is a valuable supplement to the methods presently available for diagnosis in cases suspicious of caprine arthritis-encephalitis.

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37

Sapkal, Gajanan N., Pradeep M. Sawant, and Devendra T. Mourya. "Chandipura Viral Encephalitis: A Brief Review." Open Virology Journal 12, no. 1 (August 31, 2018): 44–51. http://dx.doi.org/10.2174/1874357901812010044.

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Introduction:In recent years, the Chandipura virus (CHPV) has emerged as an encephalitic pathogen and found associated with a number of outbreaks in different parts of India. Children under 15 years of age are most susceptible to natural infection. CHPV is emerging as a significant encephalitis, causing virus in the Indian subcontinent. Severe outbreaks caused by the virus have been reported from several parts of India.Expalanation:In the recent past, the noticeable association of CHPV with pediatric sporadic encephalitis cases as well as a number of outbreaks in Andhra Pradesh (2004, 2005, 2007 and 2008), Gujarat in (2005, 2009-12) and Vidarbha region of Maharashtra (2007, 2009-12) have been documented. Prevalence and seasonal activity of the virus in these regions are established by NIV through outbreak investigations, sero-survey and diagnosis of the referred clinical specimens. Recently CHPV has been isolated from pools of sand flies collected during outbreak investigations in Vidarbha region of Maharashtra. Since its discovery from India and above-mentioned activity of CHPV, it was suspected to be restricted only to India.Conclusion:However, CHPV has also been isolated from human cases during 1971-72 in Nigeria, and hedgehogs (Atelerix spiculus) during entomological surveillance in Senegal, Africa (1990-96) and recently referred samples from Bhutan and Nepal and from wild toque macaques (Macaca sinica) at Polonnaruwa, Sri Lanka during 1993 suggest its circulation in many tropical countries. Based on the limited study on vector related report, it appears that sandflies may be the principle vector.

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38

Ma’roef, Chairin Nisa, Rama Dhenni, Dewi Megawati, Araniy Fadhilah, Anton Lucanus, I. Made Artika, Sri Masyeni, et al. "Japanese encephalitis virus infection in non-encephalitic acute febrile illness patients." PLOS Neglected Tropical Diseases 14, no. 7 (July 14, 2020): e0008454. http://dx.doi.org/10.1371/journal.pntd.0008454.

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39

Anam, Ahmad Mursel, Jamia Ahmad, Shihan Mahmud Redwanul Huq, and Raihan Rabbani. "Nipah virus encephalitis: MRI findings." Journal of the Royal College of Physicians of Edinburgh 49, no. 3 (2019): 227–28. http://dx.doi.org/10.4997/jrcpe.2019.312.

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40

Birge, Justin, and Steven Sonnesyn. "Powassan Virus Encephalitis, Minnesota, USA." Emerging Infectious Diseases 18, no. 10 (October 2012): 1669–71. http://dx.doi.org/10.3201/eid1810.120621.

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41

Neitzel, David F., Ruth Lynfield, and Kirk Smith. "Powassan Virus Encephalitis, Minnesota, USA." Emerging Infectious Diseases 19, no. 4 (April 2013): 686. http://dx.doi.org/10.3201/eid1904.121651.

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42

Briggs, Benjamin J., Barry Atkinson, Donna M. Czechowski, Peter A. Larsen, Heather N. Meeks, Juan P. Carrera, Ryan M. Duplechin, et al. "Tick-Borne Encephalitis Virus, Kyrgyzstan." Emerging Infectious Diseases 17, no. 5 (May 2011): 876–79. http://dx.doi.org/10.3201/eid1705.101183.

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43

Bowman, C. A., P. D. Woolley, and G. R. Kinghorn. "HERPES SIMPLEX VIRUS NEONATAL ENCEPHALITIS." Lancet 331, no. 8586 (March 1988): 646. http://dx.doi.org/10.1016/s0140-6736(88)91443-2.

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44

Kelly, Teresa, and Saurabh Guleria. "Human herpes virus-6 encephalitis." Journal of Pediatric Neuroradiology 01, no. 02 (July 28, 2015): 143–44. http://dx.doi.org/10.3233/pnr-2012-022.

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Rabinstein, Alejandro A. "Herpes Virus Encephalitis in Adults." Neurologic Clinics 35, no. 4 (November 2017): 695–705. http://dx.doi.org/10.1016/j.ncl.2017.06.006.

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Chai, Wanxing, and Michael Gong-Ruey Ho. "Disseminated varicella zoster virus encephalitis." Lancet 384, no. 9955 (November 2014): 1698. http://dx.doi.org/10.1016/s0140-6736(14)60755-8.

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Stahl, Jean Paul, and Alexandra Mailles. "Herpes simplex virus encephalitis update." Current Opinion in Infectious Diseases 32, no. 3 (June 2019): 239–43. http://dx.doi.org/10.1097/qco.0000000000000554.

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Schleede, Lena, Wolfgang Bueter, Sara Baumgartner-Sigl, Thomas Opladen, Katharina Weigt-Usinger, Susanne Stephan, Martin Smitka, et al. "Pediatric Herpes Simplex Virus Encephalitis." Journal of Child Neurology 28, no. 3 (January 16, 2013): 321–31. http://dx.doi.org/10.1177/0883073812471428.

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Hsu, Vincent P., Mohammed Jahangir Hossain, Umesh D. Parashar, Mohammed Monsur Ali, Thomas G. Ksiazek, Ivan Kuzmin, Michael Niezgoda, Charles Rupprecht, Joseph Bresee, and Robert F. Breiman. "Nipah Virus Encephalitis Reemergence, Bangladesh." Emerging Infectious Diseases 10, no. 12 (December 2004): 2082–87. http://dx.doi.org/10.3201/eid1012.040701.

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Beltrame, Anna, Maurizio Ruscio, Barbara Cruciatti, Angela Londero, Vito Di Piazza, Roberto Copetti, Valentino Moretti, et al. "Tickborne Encephalitis Virus, Northeastern Italy." Emerging Infectious Diseases 12, no. 10 (October 2006): 1617–19. http://dx.doi.org/10.3201/eid1210.060395.

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