Displaying publications 1 - 20 of 23 in total

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  1. Ivan A, Indrei LL
    Rev Med Chir Soc Med Nat Iasi, 2000 Apr-Jun;104(2):51-5.
    PMID: 12089991
    In the interval 1994-1999, in Australia, Malaysia and Singapore, epizootic and epidemiological episodes of meningoencephalitis and severe acute respiratory syndromes were reported. Highly lethal in horses, swine and humans, the episodes were proved to be caused by the "new" viruses Hendra (HeV) and Nipah (NiV). At the same time three "new" viral agents have been isolated: Lyssavirus, Menanglevirus and Tupaia paramyxovirus. The intense contemporary circulation of people, animals and food products together with changes in human ecosystem favor new relations between humans and the "natural reservoirs" of biologic agents with a pathogenic potential for domestic and peridomestic animals and humans.
    Matched MeSH terms: Paramyxoviridae Infections/virology*
  2. Gibbs WW
    Sci. Am., 1999 Aug;281(2):80-7.
    PMID: 10443039
    Matched MeSH terms: Paramyxoviridae Infections/virology
  3. Ozawa Y, Ong BL, An SH
    Rev. - Off. Int. Epizoot., 2001 Aug;20(2):605-13.
    PMID: 11548530
    Traceback systems in most countries of Asia are not well developed, as indicated by responses to a questionnaire by veterinary officials in thirteen countries. Marking of animals for traceback is practised only in a limited number of countries in specific areas or zones and for specific purposes only. In Malaysia, traceback has been undertaken by marking farm code tattoos on pigs. This enables the identification of the farm of origin of pigs found to be infected by Nipah virus in sero-surveillance programmes. The origin of the foot and mouth disease (FMD) virus that surfaced in the Republic of Korea in March 2000 was investigated through several epidemiological studies of suspected sources of contamination such as imported hay, yellow sand, milk collection trucks and feed delivery trucks. None of these studies gave results that indicated the origin of the FMD virus. The origin of the FMD virus that was recorded in Japan in March 2000 was also investigated in epidemiological studies; in this case, imported wheat straw was incriminated as the most likely source of infection. Comparative studies of the pathogenicities of FMD (type O) viruses isolated in Taipei China, the Republic of Korea and Japan, suggest that these viruses might have originated as vaccine strains used in a third country.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  4. Yaiw KC, Ong KC, Chua KB, Bingham J, Wang L, Shamala D, et al.
    J Virol Methods, 2007 Aug;143(2):140-6.
    PMID: 17442409
    Tioman virus is a newly described bat-urine derived paramyxovirus isolated in Tioman Island, Malaysia in 2001. Hitherto, neither human nor animal infection by this virus has been reported. Nonetheless, its close relationship to another paramyxovirus, the Menangle virus which had caused diseases in humans and pigs [Philbey, A.W., Kirkland, P.D., Ross, A.D., Davis, R.J., Gleeson, A.B., Love, R.J., Daniels, P.W., Gould, A.R., Hyatt, A.D., 1998. An apparently new virus (family Paramyxoviridae) infectious for pigs, humans, and fruit bats. Emerg. Infect. Dis. 4, 269-271], raises the possibility that it may be potentially pathogenic. In this study, mice were experimentally infected with Tioman virus by intraperitoneal and intracerebral routes, and the cellular targets and topographical distribution of viral genome and antigens were examined using in situ hybridization and immunohistochemistry, respectively. The possible association between viral infection and apoptosis was also investigated using the TUNEL assay and immunohistochemistry to FasL, Caspase-3, Caspase-8, Caspase-9 and bcl-2. The results showed that Tioman virus inoculated intracerebrally was neurotropic causing plaque-like necrotic areas, and appeared to preferentially replicate in the neocortex and limbic system. Viral infection of inflammatory cells was also demonstrated. TUNEL and Caspase-3 positivity was found in inflammatory cells but not in neurons, while FasL, Caspase-8 and Caspase-9 were consistently negative. This suggests that neuronal infection was associated with necrosis rather than apoptosis. Moreover, the data suggest that there may be an association between viral infection and apoptosis in inflammatory cells, and that it could, at least in part, involve Caspase-independent pathways. Bcl-2 was expressed in some neurons and inflammatory cells indicating its possible role in anti-apoptosis. There was no evidence of central nervous system infection via the intraperitoneal route.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  5. Oong XY, Chook JB, Ng KT, Chow WZ, Chan KG, Hanafi NS, et al.
    Virol J, 2018 05 23;15(1):91.
    PMID: 29792212 DOI: 10.1186/s12985-018-1005-8
    BACKGROUND: Human metapneumovirus (HMPV) is established as one of the causative agents of respiratory tract infections. To date, there are limited reports that describe the effect of HMPV genotypes and/or viral load on disease pathogenesis in adults. This study aims to determine the role of HMPV genetic diversity and nasopharyngeal viral load on symptom severity in outpatient adults with acute respiratory tract infections.
    METHODS: Severity of common cold symptoms of patients from a teaching hospital was assessed by a four-category scale and summed to obtain the total symptom severity score (TSSS). Association between the fusion and glycoprotein genes diversity, viral load (quantified using an improved RT-qPCR assay), and symptom severity were analyzed using bivariate and linear regression analyses.
    RESULTS: Among 81/3706 HMPV-positive patients, there were no significant differences in terms of demographics, number of days elapsed between symptom onset and clinic visit, respiratory symptoms manifestation and severity between different HMPV genotypes/sub-lineages. Surprisingly, elderly patients (≥65 years old) had lower severity of symptoms (indicated by TSSS) than young and middle age adults (p = 0.008). Nasopharyngeal viral load did not correlate with nor predict symptom severity of HMPV infection. Interestingly, at 3-5 days after symptom onset, genotype A-infected patients had higher viral load compared to genotype B (4.4 vs. 3.3 log10 RNA copies/μl) (p = 0.003).
    CONCLUSIONS: Overall, HMPV genetic diversity and viral load did not impact symptom severity in adults with acute respiratory tract infections. Differences in viral load dynamics over time between genotypes may have important implications on viral transmission.
    Study site: Primary Care Clinic, University of Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Paramyxoviridae Infections/virology
  6. Chua KB, Lam SK, Goh KJ, Hooi PS, Ksiazek TG, Kamarulzaman A, et al.
    J Infect, 2001 Jan;42(1):40-3.
    PMID: 11243752
    To study the excretion of Nipah virus in the upper respiratory secretions and urine of infected patients in relation to other clinical features.
    Matched MeSH terms: Paramyxoviridae Infections/virology*
  7. Fieldhouse JK, Toh TH, Lim WH, Ting J, Ha SJ, Hii KC, et al.
    PLoS One, 2018;13(8):e0202147.
    PMID: 30110367 DOI: 10.1371/journal.pone.0202147
    BACKGROUND: Respiratory syncytial virus (RSV) and parainfluenza virus (PIV) are frequent causes of pneumonia and death among children at Sibu and Kapit Hospitals in Sarawak, Malaysia.

    OBJECTIVES: To determine the prevalence and risk factors for RSV subtypes A and B and PIV types 1-4 among patients hospitalized with pneumonia.

    METHODS: In a cross-sectional, pilot study nasopharyngeal swabs were studied with real-time reverse transcription polymerase chain reaction assays. Concurrently, we helped Sibu and Kapit Hospitals adapt their first molecular diagnostics for RSV and PIV.

    RESULTS: Of 129 specimens collected (June to July 2017), 39 tested positive for RSV-A (30.2%), two were positive for RSV B (1.6%), one was positive for PIV-3 (0.8%) and one was positive for PIV-4 (0.8%). No samples were positive for PIV-1 or PIV-2. Of the 39 RSV-A positive specimens, 46.2% were collected from children under one year of age and only 5.1% were from patients over the age of 18. A multivariable analysis found the odds of children <1 year of age testing positive for RSV-A were 32.7 (95% CI: 3.9, 276.2) times larger than >18 years of age, and the odds of patients hospitalized at Kapit Hospital testing positive for RSV-A were 3.2 (95% CI: 1.3, 7.8) times larger than patients hospitalized at Sibu Hospital.

    CONCLUSION: This study found an unusually high prevalence of RSV-A among pneumonia patients admitted to the two hospitals. Subsequently, Sibu Hospital adapted the molecular assays with the goal of providing more directed care for such pneumonia patients.

    Matched MeSH terms: Paramyxoviridae Infections/virology
  8. Nor'e SS, Sam IC, Mohamad Fakri EF, Hooi PS, Nathan AM, de Bruyne JA, et al.
    Trop Biomed, 2014 Sep;31(3):562-6.
    PMID: 25382484 MyJurnal
    Human metapneumovirus (HMPV) is a recently discovered cause of viral respiratory infections. We describe clinical and molecular epidemiology of HMPV cases diagnosed in children with respiratory infection at University of Malaya Medical Centre, Kuala Lumpur, Malaysia. The prevalence rate of HMPV between 2010 and 2012 was 1.1%, and HMPV contributed 6.5% of confirmed viral respiratory infections. The HMPV patients had a median age of 1.6 years, and a median hospital admission of 4 days. The most common clinical presentations were fever, rhinitis, pneumonia, vomiting/diarrhoea, and bronchiolitis. Based on the partial sequences of F fusion gene from 26 HMPV strains, 14 (54%) were subgenotype A2b, which was predominant in 2010; 11 (42%) were subgenotype B1, which was predominant in 2012; and 1 (4%) was subgenotype A2a. Knowledge of the circulating subgenotypes in Malaysia, and the displacement of predominant subgenotypes within 3 years, is useful data for future vaccine planning.
    Matched MeSH terms: Paramyxoviridae Infections/virology*
  9. Chua KB, Bellini WJ, Rota PA, Harcourt BH, Tamin A, Lam SK, et al.
    Science, 2000 May 26;288(5470):1432-5.
    PMID: 10827955
    A paramyxovirus virus termed Nipah virus has been identified as the etiologic agent of an outbreak of severe encephalitis in people with close contact exposure to pigs in Malaysia and Singapore. The outbreak was first noted in late September 1998 and by mid-June 1999, more than 265 encephalitis cases, including 105 deaths, had been reported in Malaysia, and 11 cases of encephalitis or respiratory illness with one death had been reported in Singapore. Electron microscopic, serologic, and genetic studies indicate that this virus belongs to the family Paramyxoviridae and is most closely related to the recently discovered Hendra virus. We suggest that these two viruses are representative of a new genus within the family Paramyxoviridae. Like Hendra virus, Nipah virus is unusual among the paramyxoviruses in its ability to infect and cause potentially fatal disease in a number of host species, including humans.
    Matched MeSH terms: Paramyxoviridae Infections/virology*
  10. Lam SK
    Antiviral Res, 2003 Jan;57(1-2):113-9.
    PMID: 12615307
    Nipah virus, a newly emerging deadly paramyxovirus isolated during a large outbreak of viral encephalitis in Malaysia, has many of the physical attributes to serve as a potential agent of bioterrorism. The outbreak caused widespread panic and fear because of its high mortality and the inability to control the disease initially. There were considerable social disruptions and tremendous economic loss to an important pig-rearing industry. This highly virulent virus, believed to be introduced into pig farms by fruit bats, spread easily among pigs and was transmitted to humans who came into close contact with infected animals. From pigs, the virus was also transmitted to other animals such as dogs, cats, and horses. The Nipah virus has the potential to be considered an agent of bioterrorism.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  11. Chua KB
    J Clin Virol, 2003 Apr;26(3):265-75.
    PMID: 12637075
    Nipah virus, a novel paramyxovirus, closely related to Hendra virus emerged in northern part of Peninsular Malaysia in 1998. The virus caused an outbreak of severe febrile encephalitis in humans with a high mortality rate, whereas, in pigs, encephalitis and respiratory diseases but with a relatively low mortality rate. The outbreak subsequently spread to various regions of the country and Singapore in the south due to the movement of infected pigs. Nipah virus caused systemic infections in humans, pigs and other mammals. Histopathological and radiological findings were characteristic of the disease. Fruitbats of Pteropid species were identified as the natural reservoir hosts. Evidence suggested that climatic and anthropogenic driven ecological changes coupled with the location of piggeries in orchard and the design of pigsties allowed the spill-over of this novel paramyxovirus from its reservoir host into the domestic pigs and ultimately to humans and other animals.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  12. Wong KT, Shieh WJ, Kumar S, Norain K, Abdullah W, Guarner J, et al.
    Am J Pathol, 2002 Dec;161(6):2153-67.
    PMID: 12466131
    In 1998, an outbreak of acute encephalitis with high mortality rates among pig handlers in Malaysia led to the discovery of a novel paramyxovirus named Nipah virus. A multidisciplinary investigation that included epidemiology, microbiology, molecular biology, and pathology was pivotal in the discovery of this new human infection. Clinical and autopsy findings were derived from a series of 32 fatal human cases of Nipah virus infection. Diagnosis was established in all cases by a combination of immunohistochemistry (IHC) and serology. Routine histological stains, IHC, and electron microscopy were used to examine autopsy tissues. The main histopathological findings included a systemic vasculitis with extensive thrombosis and parenchymal necrosis, particularly in the central nervous system. Endothelial cell damage, necrosis, and syncytial giant cell formation were seen in affected vessels. Characteristic viral inclusions were seen by light and electron microscopy. IHC analysis showed widespread presence of Nipah virus antigens in endothelial and smooth muscle cells of blood vessels. Abundant viral antigens were also seen in various parenchymal cells, particularly in neurons. Infection of endothelial cells and neurons as well as vasculitis and thrombosis seem to be critical to the pathogenesis of this new human disease.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  13. Enserink M
    Science, 1999 Apr 16;284(5413):407, 409-10.
    PMID: 10232977 DOI: 10.1126/science.284.5413.407
    Matched MeSH terms: Paramyxoviridae Infections/virology
  14. Chua KB, Koh CL, Hooi PS, Wee KF, Khong JH, Chua BH, et al.
    Microbes Infect., 2002 Feb;4(2):145-51.
    PMID: 11880045
    In late 1998, Nipah virus emerged in peninsular Malaysia and caused fatal disease in domestic pigs and humans and substantial economic loss to the local pig industry. Surveillance of wildlife species during the outbreak showed neutralizing antibodies to Nipah virus mainly in Island flying-foxes (Pteropus hypomelanus) and Malayan flying-foxes (Pteropus vampyrus) but no virus reactive with anti-Nipah virus antibodies was isolated. We adopted a novel approach of collecting urine from these Island flying-foxes and swabs of their partially eaten fruits. Three viral isolates (two from urine and one from a partially eaten fruit swab) that caused Nipah virus-like syncytial cytopathic effect in Vero cells and stained strongly with Nipah- and Hendra-specific antibodies were isolated. Molecular sequencing and analysis of the 11,200-nucleotide fragment representing the beginning of the nucleocapsid gene to the end of the glycoprotein gene of one isolate confirmed the isolate to be Nipah virus with a sequence deviation of five to six nucleotides from Nipah virus isolated from humans. The isolation of Nipah virus from the Island flying-fox corroborates the serological evidence that it is one of the natural hosts of the virus.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  15. Westbury H
    Vet J, 2000 Nov;160(3):165-6.
    PMID: 11061952
    Matched MeSH terms: Paramyxoviridae Infections/virology*
  16. Westbury HA
    Rev. - Off. Int. Epizoot., 2000 Apr;19(1):151-9.
    PMID: 11189712
    The author provides an account of the discovery of a previously undescribed disease of horses and a description of the studies involved in determining the aetiology of the disease. The causative virus, now named Hendra virus (HeV), is the reference virus for a proposed new genus within the virus family Paramyxoviridae. The virus is a lethal zoonotic agent able to cause natural disease in humans and horses and experimentally induced disease in cats, guinea-pigs and mice. The virus also naturally infects species of the family Megachiroptera, mainly subclinically, and such animals are the natural host of HeV. The virus appears to transmit readily between species of Megachiroptera, but not readily between horses under natural and experimental conditions, or from horses to humans. The method of transmission from bats to horses is not known. Three incidents of HeV disease in horses have been recorded in Australia--two in 1994 which caused the death of two humans and fifteen horses and one in 1999 which involved the death of a single horse. Hendra virus is related to Nipah virus, the virus that caused disease and mortality in humans, pigs, dogs and cats in Malaysia during 1998 and 1999.
    Matched MeSH terms: Paramyxoviridae Infections/virology*
  17. Nichol ST, Arikawa J, Kawaoka Y
    Proc Natl Acad Sci U S A, 2000 Nov 07;97(23):12411-2.
    PMID: 11035785
    Matched MeSH terms: Paramyxoviridae Infections/virology
  18. Enserink M
    Science, 2000 Jul 28;289(5479):518-9.
    PMID: 10939954 DOI: 10.1126/science.289.5479.518
    Scientists are a step closer to unraveling a medical mystery that killed 105 people in Malaysia last year and destroyed the country's pig industry. The Nipah virus, which caused the disease, most likely originated in a native fruit bat species, Malaysian researchers reported here at a meeting last week. They say the findings will help Malaysian health authorities prevent future outbreaks of the Nipah virus. Others see the case as an argument for expanding research into infections that can leap the boundary between animals and humans.
    Matched MeSH terms: Paramyxoviridae Infections/virology
  19. 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: Paramyxoviridae Infections/virology*
  20. 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: Paramyxoviridae Infections/virology
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