Displaying publications 1 - 20 of 34 in total

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  1. Yew MMT, Lip JQ, Ling APK
    Trop Biomed, 2021 Sep 01;38(3):435-445.
    PMID: 34608117 DOI: 10.47665/tb.38.3.086
    Ever since the first reported case series on SARS-CoV-2-induced neurological manifestation in Wuhan, China in April 2020, various studies reporting similar as well as diverse symptoms of COVID-19 infection relating to the nervous system were published. Since then, scientists started to uncover the mechanism as well as pathophysiological impacts it has on the current understanding of the disease. SARS-CoV-2 binds to the ACE2 receptor which is present in certain parts of the body which are responsible for regulating blood pressure and inflammation in a healthy system. Presence of the receptor in the nasal and oral cavity, brain, and blood allows entry of the virus into the body and cause neurological complications. The peripheral and central nervous system could also be invaded directly in the neurogenic or hematogenous pathways, or indirectly through overstimulation of the immune system by cytokines which may lead to autoimmune diseases. Other neurological implications such as hypoxia, anosmia, dysgeusia, meningitis, encephalitis, and seizures are important symptoms presented clinically in COVID-19 patients with or without the common symptoms of the disease. Further, patients with higher severity of the SARS-CoV-2 infection are also at risk of retaining some neurological complications in the long-run. Treatment of such severe hyperinflammatory conditions will also be discussed, as well as the risks they may pose to the progression of the disease. For this review, articles pertaining information on the neurological manifestation of SARS-CoV-2 infection were gathered from PubMed and Google Scholar using the search keywords "SARS-CoV-2", "COVID-19", and "neurological dysfunction". The findings of the search were filtered, and relevant information were included.
    Matched MeSH terms: Encephalitis, Viral/virology
  2. Wong KT, Tan CT
    PMID: 22427144 DOI: 10.1007/82_2012_205
    The clinicopathological features of human Nipah virus and Hendra virus infections appear to be similar. The clinical manifestations may be mild, but if severe, includes acute encephalitic and pulmonary syndromes with a high mortality. The pathological features in human acute henipavirus infections comprise vasculopathy (vasculitis, endothelial multinucleated syncytia, thrombosis), microinfarcts and parenchymal cell infection in the central nervous system, lung, kidney and other major organs. Viral inclusions, antigens, nucleocapsids and RNA are readily demonstrated in blood vessel wall and numerous types of parenchymal cells. Relapsing henipavirus encephalitis is a rare complication reported in less than 10% of survivors of the acute infection and appears to be distinct from the acute encephalitic syndrome. Pathological evidence suggests viral recrudescence confined to the central nervous system as the cause.
    Matched MeSH terms: Encephalitis, Viral/virology
  3. Wong KT, Robertson T, Ong BB, Chong JW, Yaiw KC, Wang LF, et al.
    Neuropathol. Appl. Neurobiol., 2009 Jun;35(3):296-305.
    PMID: 19473296 DOI: 10.1111/j.1365-2990.2008.00991.x
    To study the pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis.
    Matched MeSH terms: Encephalitis, Viral/virology
  4. Wong KT
    Neuropathol. Appl. Neurobiol., 2000 Aug;26(4):313-8.
    PMID: 10931364
    Two major epidemics of viral encephalitis occurred in Asia in 1997 and 1998. The first was a re-emergence of neurovirulent strains of enterovirus 71, which caused severe encephalomyelitis in children in Malaysia, Taiwan and Japan, on a background of hand, foot and mouth disease. Necropsy studies of patients who died of enterovirus 71 infection showed severe perivascular cuffing, parenchymal inflammation and neuronophagia in the spinal cord, brainstem and diencephalon, and in focal areas in the cerebellum and cerebrum. Although no viral inclusions were detected, immunohistochemistry showed viral antigen in the neuronal cytoplasm. Inflammation was often more extensive than neuronal infection, suggesting that other factors, in addition to direct viral cytolysis, may be involved in tissue damage. The second epidemic of viral encephalitis was the result of a novel paramyxovirus called Nipah, which mainly involved pig handlers in Malaysia and Singapore. Pathological evidence suggested that the endothelium of small blood vessels in the central nervous system was particularly susceptible to infection. This led to disseminated endothelial damage and syncytium formation, vasculitis, thrombosis, ischaemia and microinfarction. However, there was also evidence of neuronal infection by the virus and this may also have contributed to the neurological dysfunction in Nipah encephalitis. Some patients who seemed to recover from the acute symptoms have been re-admitted with clinical findings suggestive of relapsing encephalitis. As these two epidemics indicate, the emergence and re-emergence of viral encephalitides continue to pose considerable challenges to the neuropathologist, in establishing the diagnosis and unravelling the pathogenesis of the neurological disease.
    Matched MeSH terms: Encephalitis, Viral/virology*
  5. Ternhag A, Penttinen P
    Lakartidningen, 2005 Apr;102(14):1046-7.
    PMID: 15892474
    Matched MeSH terms: Encephalitis, Viral/virology
  6. Tan CT, Wong KT
    Ann Acad Med Singap, 2003 Jan;32(1):112-7.
    PMID: 12625108
    INTRODUCTION: Between September 1998 and June 1999, there was a severe outbreak of viral encephalitis among the pig farm workers in Malaysia.

    METHODS: This is a review of the published literature related to the outbreak with the focus on human diseases.

    RESULTS: The encephalitis was caused by a newly discovered paramyxovirus related to Hendra virus, later named Nipah virus. There were 265 patients with acute encephalitis. The disease is thought to spread from pig to man through close contact. The risk of human-to-human spread is thought to below. The disease affected mainly adult Chinese males, half of whom had affected family members. The disease presented mainly as acute encephalitis with a short incubation period of less than two weeks, with the main symptoms of fever, headache, and giddiness followed by coma. Distinctive clinical signs include segmental myoclonus, areflexia and hypotonia, hypertension, and tachycardia. Initial cerebrospinal fluid was abnormal in 75% of patients. Serology was helpful in confirming the diagnosis. Magnetic resonance imaging showed distinctive changes of multiple, discrete, and small high signal lesions, best seen with fluid-attenuated inversion recovery (FLAIR) sequences. Mortality was high at 40% and death was probably due to severe brainstem involvement. The main necropsy finding in acute encephalitis was that of disseminated microinfarction associated with vasculitis and direct neuronal involvement. Ribavirin was able to reduce the mortality by 36%. Relapse encephalitis was seen in 7.5% of those who recovered from acute encephalitis, and late-onset encephalitis in 3.4% of those with initial non-encephalitic or asymptomatic diseases. The mean interval between initial illness and the onset of the complication was 8.4 months. The relapse and late-onset encephalitis which manifested as focal encephalitis arose from recurrent infection.

    CONCLUSION: Nipah virus, a recently discovered paramyxovirus, causes a unique encephalitis with high mortality as well as relapse and late-onset encephalitis. The infection is mainly spread from pigs to man.

    Matched MeSH terms: Encephalitis, Viral/virology*
  7. Stone R
    Science, 2011 Mar 4;331(6021):1128-31.
    PMID: 21385693 DOI: 10.1126/science.331.6021.1128
    Matched MeSH terms: Encephalitis, Viral/virology
  8. Solomon T
    Curr. Opin. Neurol., 2003 Jun;16(3):411-8.
    PMID: 12858080
    The exotic and emerging viral encephalitides are caused by animal or human viruses and characterised by sudden unexpected outbreaks of neurological disease, usually in tropical and sub-tropical regions, but sometimes spreading to temperate areas. Although a wide range of viruses come within this label, as this review highlights, there are common research questions as to the origin and spread of the viruses, the contribution of viral and host factors to the clinical presentations and outcome, and the possibilities for treatment and vaccination.
    Matched MeSH terms: Encephalitis, Viral/virology*
  9. Parashar UD, Sunn LM, Ong F, Mounts AW, Arif MT, Ksiazek TG, et al.
    J Infect Dis, 2000 May;181(5):1755-9.
    PMID: 10823779
    An outbreak of encephalitis affecting 265 patients (105 fatally) occurred during 1998-1999 in Malaysia and was linked to a new paramyxovirus, Nipah, that infected pigs, humans, dogs, and cats. Most patients were pig farmers. Clinically undetected Nipah infection was noted in 10 (6%) of 166 community-farm controls (persons from farms without reported encephalitis patients) and 20 (11%) of 178 case-farm controls (persons from farms with encephalitis patients). Case patients (persons with Nipah infection) were more likely than community-farm controls to report increased numbers of sick/dying pigs on the farm (59% vs. 24%, P=.001) and were more likely than case-farm controls to perform activities requiring direct contact with pigs (86% vs. 50%, P=.005). Only 8% of case patients reported no contact with pigs. The outbreak stopped after pigs in the affected areas were slaughtered and buried. Direct, close contact with pigs was the primary source of human Nipah infection, but other sources, such as infected dogs and cats, cannot be excluded.
    Matched MeSH terms: Encephalitis, Viral/virology*
  10. Matlani M, Chakravarti A, Rawal A, Kashyap B, Gurtoo A
    Trop Doct, 2009 Apr;39(2):115-6.
    PMID: 19299303 DOI: 10.1258/td.2008.080257
    As well as dengue fever (DF) and dengue haemorrhagic fever-dengue shock syndrome (DHF/DSS), other atypical manifestations of dengue virus infection have also been reported. The frequency of CNS involvement in dengue remains unknown, although isolated cases with neurological manifestations have been reported in Southeast Asia, Malaysia, Burma, Puerto Rico and India. We present two cases of encephalitis associated with DF and DHF from New Delhi, India.
    Matched MeSH terms: Encephalitis, Viral/virology
  11. Maisner A, Neufeld J, Weingartl H
    Thromb. Haemost., 2009 Dec;102(6):1014-23.
    PMID: 19967130 DOI: 10.1160/TH09-05-0310
    Nipah virus (NiV) is a highly pathogenic paramyxovirus that was first isolated in 1999 during an outbreak in Malaysia. In contrast to other paramyxoviruses NiV infects many mammalian species. Because of its zoonotic potential, the high pathogenicity and the lack of therapeutic treatment, NiV was classified as a biosafety level 4 pathogen. In humans NiV causes a severe acute encephalitis whereas in some animal hosts respiratory symptoms are predominantly observed. Despite the differences in the clinical outcome, microvascular endothelial cell damage predominantly underlies the pathological changes in NiV infections in all susceptible host species. NiV generally induces a pronounced vasculitis which is primarily characterised by endothelial cell necrosis and inflammatory cell infiltration. For future developments of specific antiviral therapies or vaccines, a detailed understanding of the molecular basis of NiV pathogenesis is required. This article reviews the current knowledge about natural and experimental infections in different mammals, focusing on the main organ and cell tropism in vivo, and summarises some recent studies in cell culture on the role of ephrin-B2 and -B3 receptors in NiV infection of endothelial cells.
    Matched MeSH terms: Encephalitis, Viral/virology
  12. Mackenzie JS
    J Neurovirol, 2005 Oct;11(5):434-40.
    PMID: 16287684
    The last decade of the 20th Century saw the introduction of an unprecedented number of encephalitic viruses emerge or spread in the Southeast Asian and Western Pacific regions (Mackenzie et al, 2001; Solomon, 2003a). Most of these viruses are zoonotic, either being arthropod-borne viruses or bat-borne viruses. Thus Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, has spread through the Indonesian archipelago to Papua New Guinea (PNG) and to the islands of the Torres Strait of northern Australia, to Pakistan, and to new areas in the Indian subcontinent; a strain of tick-borne encephalitis virus (TBEV) was described for the first time in Hokkaido, Japan; and a novel mosquito-borne alphavirus, Me Tri virus, was described from Vietnam. Three novel bat-borne viruses emerged in Australia and Malaysia; two, Hendra and Nipah viruses, represent the first examples of a new genus in the family Paramyxoviridae, the genus Henipaviruses, and the third, Australian bat lyssavirus (ABLV) is new lyssavirus closely related to classical rabies virus. These viruses will form the body of this brief review.
    Matched MeSH terms: Encephalitis, Viral/virology
  13. Lum LC, Lam SK, Choy YS, George R, Harun F
    Am J Trop Med Hyg, 1996 Mar;54(3):256-9.
    PMID: 8600761 DOI: 10.4269/ajtmh.1996.54.256
    Involvement of the central nervous system in dengue fever and dengue hemorrhagic fever has always been thought to be secondary to vasculitis with resultant fluid extravasation, cerebral edema, hypoperfusion, hyponatremia, liver failure, and/or renal failure. Thus, the condition has been referred to as dengue encephalopathy. Encephalitis or direct involvement of the brain by the virus was thought to be unlikely. This paper reports on six children who were seen over a period of two years presenting on the second or third day of illness with dengue encephalitis. The diagnosis was based upon a clinical picture of encephalitis and confirmed by cerebrospinal fluid (CSF) microscopy and electroencephalography changes. All six cases were confirmed dengue infections. Dengue 3 virus was isolated from the CSF of four cases and in one case, dengue 2 was detected by the polymerase chain reaction in both the CSF and blood. In the sixth case, virologic evidence was negative but dengue immunoglobulin M was detected in the CSF and blood. Since the onset of encephalitis appears early in the course of illness coinciding with the viremic phase, we postulate that the virus crosses the blood-brain barrier and directly invades the brain causing encephalitis. This study provides strong evidence that dengue 2 and 3 viruses have neurovirulent properties and behave similarly to other members of the Flaviviridae.
    Matched MeSH terms: Encephalitis, Viral/virology*
  14. Lu XF, Wang ZG, Wang BY
    Zhonghua Liu Xing Bing Xue Za Zhi, 2004 Jun;25(6):541-3.
    PMID: 15231143
    Matched MeSH terms: Encephalitis, Viral/virology
  15. Lo MK, Rota PA
    J Clin Virol, 2008 Dec;43(4):396-400.
    PMID: 18835214 DOI: 10.1016/j.jcv.2008.08.007
    Nipah virus first emerged in Malaysia and Singapore between 1998 and 1999, causing severe febrile encephalitis in humans with a mortality rate of close to 40%. In addition, a significant portion of those recovering from acute infection had relapse encephalitis and long-term neurological defects. Since its initial outbreak, there have been numerous outbreaks in Bangladesh and India, in which the mortality rate rose to approximately 70%. These subsequent outbreaks were distinct from the initial outbreak, both in their epidemiology and in their clinical presentations. Recent developments in diagnostics may expedite disease diagnosis and outbreak containment, while progress in understanding the molecular biology of Nipah virus could lead to novel therapeutics and vaccines for this deadly pathogen.
    Matched MeSH terms: Encephalitis, Viral/virology
  16. Kono Y, Tsukamoto K, Abd Hamid M, Darus A, Lian TC, Sam LS, et al.
    Am J Trop Med Hyg, 2001 5 19;63(1-2):94-101.
    PMID: 11358004
    A new virus named Sitiawan virus (SV) was isolated from sick broiler chicks in chicken embryos. The virus replicated well with cytopathogenic effect (CPE) in the chicken B-lymphocyte cell line LSCC-BK3. The virus was an enveloped RNA virus of approximately 41 nm in size with hemagglutinating activity (HA) to goose erythrocytes. It was cross-reactive with Japanese encephalitis virus (JEV), a member of flaviviruses by HA inhibition tests but not by cross-virus neutralization tests. The cDNA fragment of NS5 gene was amplified with primers corresponding to NS5 gene of flaviviruses. The nucleotide sequences were 92% homologous to Tembusu virus, a member of the mosquito-borne virus cluster of the genus Flavivirus. In cross-neutralization tests with Tembusu virus, antiserum to SV did not neutralize Tembusu virus, and antiserum to Tembusu virus neutralized more weakly to SV than against homologous virus. These results indicate that SV is a new virus which can be differentiated serologically from Tembusu virus but is otherwise similar with respect to nucleotide sequence. The virus causes encephalitis, growth retardation, and increased blood glucose levels in inoculated chicks.
    Matched MeSH terms: Encephalitis, Viral/virology
  17. Hinson VK, Tyor WR
    Curr. Opin. Neurol., 2001 Jun;14(3):369-74.
    PMID: 11371762
    Over 100 viruses have been associated with acute central nervous system infections. The present review focuses on some of the most common agents of viral encephalitis, as well as important emerging viral encephalitides. In this context, the initial detection of West Nile virus in the Western Hemisphere during the 1999 New York City outbreak, the first description of Nipah virus in Malaysia, and the appearance in Asia of a new neurovirulent enterovirus 71 strain that causes severe neurologic disease are highlighted. In addition, advances regarding diagnosis, neuroimaging and treatment of Japanese and herpes simplex encephalitis are presented.
    Matched MeSH terms: Encephalitis, Viral/virology
  18. Goldsmith CS, Whistler T, Rollin PE, Ksiazek TG, Rota PA, Bellini WJ, et al.
    Virus Res, 2003 Mar;92(1):89-98.
    PMID: 12606080
    Nipah virus, which was first recognized during an outbreak of encephalitis with high mortality in Peninsular Malaysia during 1998-1999, is most closely related to Hendra virus, another emergent paramyxovirus first recognized in Australia in 1994. We have studied the morphologic features of Nipah virus in infected Vero E6 cells and human brain by using standard and immunogold electron microscopy and ultrastructural in situ hybridization. Nipah virions are enveloped particles composed of a tangle of filamentous nucleocapsids and measured as large as 1900 nm in diameter. The nucleocapsids measured up to 1.67 microm in length and had the herringbone structure characteristic for paramyxoviruses. Cellular infection was associated with multinucleation, intracytoplasmic nucleocapsid inclusions (NCIs), and long cytoplasmic tubules. Previously undescribed for other members of the family Paramyxoviridae, infected cells also contained an inclusion formed of reticular structures. Ultrastructural ISH studies suggest these inclusions play an important role in the transcription process.
    Matched MeSH terms: Encephalitis, Viral/virology
  19. Goh KJ, Tan CT, Chew NK, Tan PS, Kamarulzaman A, Sarji SA, et al.
    N Engl J Med, 2000 Apr 27;342(17):1229-35.
    PMID: 10781618 DOI: 10.1056/NEJM200004273421701
    BACKGROUND: Between September 1998 and June 1999, there was an outbreak of severe viral encephalitis due to Nipah virus, a newly discovered paramyxovirus, in Malaysia.
    METHODS: We studied the clinical features of the patients with Nipah virus encephalitis who were admitted to a medical center in Kuala Lumpur. The case definition was based on epidemiologic, clinical, cerebrospinal fluid, and neuroimaging findings.
    RESULTS: Ninety-four patients with Nipah virus infection were seen from February to June 1999 (mean age, 37 years; ratio of male patients to female patients, 4.5 to 1). Ninety-three percent had had direct contact with pigs, usually in the two weeks before the onset of illness, suggesting that there was direct viral transmission from pigs to humans and a short incubation period. The main presenting features were fever, headache, dizziness, and vomiting. Fifty-two patients (55 percent) had a reduced level of consciousness and prominent brain-stem dysfunction. Distinctive clinical signs included segmental myoclonus, areflexia and hypotonia, hypertension, and tachycardia and thus suggest the involvement of the brain stem and the upper cervical spinal cord. The initial cerebrospinal fluid findings were abnormal in 75 percent of patients. Antibodies against Hendra virus were detected in serum or cerebrospinal fluid in 76 percent of 83 patients tested. Thirty patients (32 percent) died after rapid deterioration in their condition. An abnormal doll's-eye reflex and tachycardia were factors associated with a poor prognosis. Death was probably due to severe brain-stem involvement. Neurologic relapse occurred after initially mild disease in three patients. Fifty patients (53 percent) recovered fully, and 14 (15 percent) had persistent neurologic deficits.
    CONCLUSIONS: Nipah virus causes a severe, rapidly progressive encephalitis with a high mortality rate and features that suggest involvement of the brain stem. The infection is associated with recent contact with pigs.
    Matched MeSH terms: Encephalitis, Viral/virology*
  20. Fong MY, Yusup R, Yusof R, Lam SK
    Trans R Soc Trop Med Hyg, 2004 Jun;98(6):379-81.
    PMID: 15099995
    The amino acid sequences of the envelope (E) protein of four encephalitogenic and five non-encephalitogenic dengue 3 virus strains isolated in Malaysia were determined and compared. Multiple sequence alignment revealed a high degree of similarity in the E protein of the strains suggesting that neurovirulence of these four encephalitogenic strains is not attributed to this protein.
    Matched MeSH terms: Encephalitis, Viral/virology*
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