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Li-yen Chang - One of the best experts on this subject based on the ideXlab platform.
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Seroprevalence of Nipah Virus Infection in Peninsular Malaysia.
The Journal of infectious diseases, 2020Co-Authors: Ming-yen Yong, Soo-ching Lee, Romano Ngui, Yvonne A. L. Lim, Maude E. Phipps, Li-yen ChangAbstract:Nipah Virus (NiV) outbreak occurred in Malaysia in 1998. The natural host reservoir for NiV is Pteropus bats, which are commonly found throughout Malaysia. Humans become infected when NiV spills over from the reservoir species. In this study, NiV serosurveillance in Peninsular Malaysia, particularly among the indigenous population, was performed. The collected samples were tested for presence of NiV antibodies using a comparative indirect enzyme-linked immunosorbent assay based on the recombinant NiV nucleocapsid (rNiV-N) protein. We found that 10.73% of the participants recruited in this study had antibodies against rNiV-N, suggesting possible exposure to NiV.
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Nipah Virus Infection of immature dendritic cells increases its transendothelial migration across human brain microvascular endothelial cells
Frontiers in Microbiology, 2018Co-Authors: Vunjia Tiong, Sazaly Abubakar, Menghooi Shu, Won Fen Wong, Li-yen ChangAbstract:Nipah Virus (NiV) can infect multiple organs in humans with the central nervous system (CNS) being the most severely affected. Currently, it is not fully understood how NiV spreads throughout the body. NiV has been shown to infect certain leukocyte populations and we hypothesized that these infected cells could cross the blood-brain barrier (BBB), facilitating NiV entry into the CNS. Here, three leukocyte types, primary immature dendritic cells (iDC), primary monocytes (pMO), and monocytic cell line (THP-1), were evaluated for permissiveness to NiV. We found only iDC and THP-1 were permissive to NiV. Transendothelial migration of mock-infected and NiV-infected leukocytes was then evaluated using an in vitro BBB model established with human brain microvascular endothelial cells (HBMEC). There was approximately a three-fold increase in migration of NiV-infected iDC across endothelial monolayer when compared to mock-infected iDC. In contrast, migration rates for pMO and THP-1 did not change upon NiV Infection. Across TNF-α-treated endothelial monolayer, there was significant increase of almost two-fold in migration of NiV-infected iDC and THP-1 over mock-infected cells. Immunofluorescence analysis showed the migrated NiV-infected leukocytes retained their ability to infect other cells. This study demonstrates for the first time that active NiV Infection of iDC and THP-1 increased their transendothelial migration activity across HBMEC and activation of HBMEC by TNF-α further promoted migration. The findings suggest that NiV Infection of leukocytes to disseminate the Virus via the ‘Trojan horse’ mechanism is a viable route of entry into the CNS.
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Nipah Virus Infection
Viral Infections of the Human Nervous System, 2012Co-Authors: Li-yen Chang, Chong Tin TanAbstract:In 1998, a new zoonotic paramyxoVirus emerged and caused an outbreak of severe febrile encephalitis among pig farm workers in Malaysia. The causative agent was named Nipah Virus (NiV), after the village of Sungai Nipah in the state of Negeri Sembilan, Malaysia, which was the residential location from which the first Virus isolate was obtained from cerebrospinal fluid. The disease is spread from the natural reservoir host, Pteropus spp. bats to pigs, and then to humans following close contact with the infected pigs. The mortality rate of NiV Infection in humans is about 40 %. Since then, recurrent outbreaks of NiV encephalitis have been seen once in India and almost annually in Bangladesh. In India and Bangladesh, transmission of the Virus was probably spread directly from bats to humans, with human-to-human spread as an important mode of Infection. Also, there was no evidence of an intermediate animal host. The main pathological features in patients with NiV encephalitis is disseminated microinfarction associated with vasculitis and direct neuronal Infection. Relapse of encephalitis was seen months to years later in 10 % of those who survived the initial illness.
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Late-onset Nipah Virus encephalitis 11 years after the initial outbreak: A case report
2012Co-Authors: Suhailah Abdullah, Khean Jin Goh, Li-yen Chang, Kartini Rahmat, Chong Tin, Kuala LumpurAbstract:Nipah Virus Infection is known to cause late-onset and relapsed encephalitis, in addition to an acute encephalitic illness. This is a report of a 35 years old woman, who had exposure to the Nipah Virus Infection during the 1999 Malaysian outbreak, was positive for Nipah IgG by immunofl uorescence, and had multiple small hyperintense lesions in brain MRI typically seen in acute Nipah encephalitis patients, indicating asymptomatic Nipah Virus Infection. She subsequently developed acute encephalitis after 11 years, manifesting as diplopia, internuclear opthalmoplegia and epileptic seizures with pleocytosis in cerebrospinal fl uid examination. She had another episode of relapsed encephalitis a year later, with seizures, memory impairment, chorea and new lesions in MRI brain. This patient is unusual in the long incubation of 11 years before manifesting with late-onset Nipah encephalitis.
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Human neuronal cell protein responses to Nipah Virus Infection.
Virology journal, 2007Co-Authors: Li-yen Chang, A. R. Mohd Ali, Sharifah Syed Hassan, Sazaly AbubakarAbstract:Nipah Virus (NiV), a recently discovered zoonotic Virus infects and replicates in several human cell types. Its replication in human neuronal cells, however, is less efficient in comparison to other fully susceptible cells. In the present study, the SK-N-MC human neuronal cell protein response to NiV Infection is examined using proteomic approaches. Method for separation of the NiV-infected human neuronal cell proteins using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) was established. At least 800 protein spots were resolved of which seven were unique, six were significantly up-regulated and eight were significantly down-regulated. Six of these altered proteins were identified using mass spectrometry (MS) and confirmed using MS/MS. The heterogenous nuclear ribonucleoprotein (hnRNP) F, guanine nucleotide binding protein (G protein), voltage-dependent anion channel 2 (VDAC2) and cytochrome bc1 were present in abundance in the NiV-infected SK-N-MC cells in contrast to hnRNPs H and H2 that were significantly down-regulated. Several human neuronal cell proteins that are differentially expressed following NiV Infection are identified. The proteins are associated with various cellular functions and their abundance reflects their significance in the cytopathologic responses to the Infection and the regulation of NiV replication. The potential importance of the ratio of hnRNP F, and hnRNPs H and H2 in regulation of NiV replication, the association of the mitochondrial protein with the cytopathologic responses to the Infection and induction of apoptosis are highlighted.
Thomas G. Ksiazek - One of the best experts on this subject based on the ideXlab platform.
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Nipah Virus Infection in dogs, Malaysia, 1999.
Emerging infectious diseases, 2009Co-Authors: James N. Mills, Patrick C. Stockton, Asiah N.m. Alim, Michel L. Bunning, Ong Bee Lee, Kent D. Wagoner, Brian R. Amman, Thomas G. KsiazekAbstract:The 1999 outbreak of Nipah Virus encephalitis in humans and pigs in Peninsular Malaysia ended with the evacuation of humans and culling of pigs in the epidemic area. Serologic screening showed that, in the absence of infected pigs, dogs were not a secondary reservoir for Nipah Virus.
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Histopathologic and Immunohistochemical Characterization of Nipah Virus Infection in the Guinea Pig
Veterinary pathology, 2008Co-Authors: F. J. Torres-velez, Pierre E. Rollin, Wun Ju Shieh, Thomas G. Ksiazek, Timothy Morken, Cathy A. Brown, Sherif R. ZakiAbstract:Mortality rate in humans infected with Nipah Virus (NiV) has been reported as high as 92%. Humans infected with NiV show a widespread multisystemic vasculitis with most severe clinical and pathologic manifestations in the brain, lungs, and spleen. The purpose of this study was to study pathologic and immunohistochemical findings in guinea pigs infected with NiV. Of 28 animals inoculated intraperitoneally, only 2 survived the Infection, and most died between 4 and 8 days postinoculation (dpi). Viral antigen with minimal pathologic changes was first detected 2 dpi in lymph nodes and spleen. More severe changes were noted in these organs 4-8 dpi, where pathologic damage had a vasocentric distribution and viral antigen was abundant in vascular endothelium, tunica media, adventitia, as well as in macrophages lining sinuses. The urinary bladder, uterus, and ovaries were also affected with necrosis and acute inflammation. In these organs, immunohistochemical positive staining was intense in blood vessels, epithe...
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Nipah Virus encephalitis reemergence bangladesh
Emerging Infectious Diseases, 2004Co-Authors: M. J. Hossain, Thomas G. Ksiazek, Umesh D. Parashar, Ivan V Kuzmin, Michael Niezgoda, Charles E Rupprecht, Joseph S Bresee, Robert F BreimanAbstract:We retrospectively investigated two outbreaks of encephalitis in Meherpur and Naogaon, Bangladesh, which occurred in 2001 and 2003. We collected serum samples from persons who were ill, their household contacts, randomly selected residents, hospital workers, and various animals. Cases were classified as laboratory confirmed or probable. We identified 13 cases (4 confirmed, 9 probable) in Meherpur; 7 were in persons in two households. Patients were more likely than nonpatients to have close contact with other patients or have contact with a sick cow. In Naogaon, we identified 12 cases (4 confirmed, 8 probable); 7 were in persons clustered in 2 households. Two Pteropus bats had antibodies for Nipah Virus. Samples from hospital workers were negative for Nipah Virus antibodies. These outbreaks, the first since 1999, suggest that transmission may occur through close contact with other patients or from exposure to a common source. Surveillance and enhancement of diagnostic capacity to detect Nipah Virus Infection are recommended.
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A survey of Nipah Virus Infection among various risk groups in Singapore.
Epidemiology and infection, 2002Co-Authors: Kwai Peng Chan, Kee Tai Goh, Pierre E. Rollin, Thomas G. Ksiazek, Nicholas I Paton, Yee Sin Leo, E. H. Sng, Ai Ee LingAbstract:Following the Nipah Virus (NV) outbreak in March 1999 in Singapore, a serological survey was undertaken to screen individuals potentially exposed to NV. Blood samples were tested for NV IgM, IgG and neutralizing antibodies. Twenty-two (1.5%) of 1469 people tested had antibodies suggesting NV Infection. Although 12 of the 22 infected people (54.6%) were symptomatic, the remaining 10 (45.4%) were clinically well and had no past history of compatible pulmonary or neurological disease. Clinical and serological findings suggested three people had been infected with NV before the outbreak was recognized. All those who were infected were male abattoir workers. None of the people who had contact with horses, and no healthcare workers exposed to infected patients and their specimens had detectable antibodies. This study provides evidence that NV causes asymptomatic Infection. All of the antibody positive individuals had direct contact with pigs and there was no evidence of human to human transmission.
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Nipah Virus Infection among abattoir workers in malaysia 1998 1999
International Journal of Epidemiology, 2001Co-Authors: Mazrura Sahani, Thomas G. Ksiazek, Umesh D. Parashar, Roslinah Ali, Premalatha Das, Munn Sunn Lye, Marzukhi Md. Isa, Mohammad T. Arif, M. Sivamoorthy, A. B. SuleimanAbstract:BACKGROUND An outbreak of encephalitis primarily affecting pig farmers occurred during 1998-1999 in Malaysia and was linked to a new paramyxoVirus, Nipah Virus, which infected pigs, humans, dogs, and cats. Because five abattoir workers were also affected, a survey was conducted to assess the risk of Nipah Infection among abattoir workers. METHODS Workers from all 143 registered abattoirs in 11 of 13 states in Malaysia were invited to participate in this cross-sectional study. Participants were interviewed to ascertain information on illness and activities performed at the abattoir. A serum sample was obtained to test for Nipah Virus antibody. RESULTS Seven (1.6 %) of 435 abattoir workers who slaughtered pigs versus zero (0%) of 233 workers who slaughtered ruminants showed antibody to Nipah Virus (P = 0.05). All antibody-positive workers were from abattoirs in the three states that reported outbreak cases among pig farmers. Workers in these three states were more likely than those in other states to have Nipah antibody (7/144 [4.86%] versus 0/291 [0%], P < 0.001) and report symptoms suggestive of Nipah disease in pigs admitted to the abattoirs (P = 0.001). CONCLUSIONS Nipah Infection was not widespread among abattoir workers in Malaysia and was linked to exposure to pigs. Since it may be difficult to identify Nipah-infected pigs capable of transmitting Virus by clinical symptoms, using personal protective equipment, conducting surveillance for Nipah Infection on pig farms which supply abattoirs, and avoiding handling and processing of potentially infected pigs are presently the best strategies to prevent transmission of Nipah Virus in abattoirs.
Sazaly Abubakar - One of the best experts on this subject based on the ideXlab platform.
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Nipah Virus Infection of immature dendritic cells increases its transendothelial migration across human brain microvascular endothelial cells
Frontiers in Microbiology, 2018Co-Authors: Vunjia Tiong, Sazaly Abubakar, Menghooi Shu, Won Fen Wong, Li-yen ChangAbstract:Nipah Virus (NiV) can infect multiple organs in humans with the central nervous system (CNS) being the most severely affected. Currently, it is not fully understood how NiV spreads throughout the body. NiV has been shown to infect certain leukocyte populations and we hypothesized that these infected cells could cross the blood-brain barrier (BBB), facilitating NiV entry into the CNS. Here, three leukocyte types, primary immature dendritic cells (iDC), primary monocytes (pMO), and monocytic cell line (THP-1), were evaluated for permissiveness to NiV. We found only iDC and THP-1 were permissive to NiV. Transendothelial migration of mock-infected and NiV-infected leukocytes was then evaluated using an in vitro BBB model established with human brain microvascular endothelial cells (HBMEC). There was approximately a three-fold increase in migration of NiV-infected iDC across endothelial monolayer when compared to mock-infected iDC. In contrast, migration rates for pMO and THP-1 did not change upon NiV Infection. Across TNF-α-treated endothelial monolayer, there was significant increase of almost two-fold in migration of NiV-infected iDC and THP-1 over mock-infected cells. Immunofluorescence analysis showed the migrated NiV-infected leukocytes retained their ability to infect other cells. This study demonstrates for the first time that active NiV Infection of iDC and THP-1 increased their transendothelial migration activity across HBMEC and activation of HBMEC by TNF-α further promoted migration. The findings suggest that NiV Infection of leukocytes to disseminate the Virus via the ‘Trojan horse’ mechanism is a viable route of entry into the CNS.
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Human neuronal cell protein responses to Nipah Virus Infection.
Virology journal, 2007Co-Authors: Li-yen Chang, A. R. Mohd Ali, Sharifah Syed Hassan, Sazaly AbubakarAbstract:Nipah Virus (NiV), a recently discovered zoonotic Virus infects and replicates in several human cell types. Its replication in human neuronal cells, however, is less efficient in comparison to other fully susceptible cells. In the present study, the SK-N-MC human neuronal cell protein response to NiV Infection is examined using proteomic approaches. Method for separation of the NiV-infected human neuronal cell proteins using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) was established. At least 800 protein spots were resolved of which seven were unique, six were significantly up-regulated and eight were significantly down-regulated. Six of these altered proteins were identified using mass spectrometry (MS) and confirmed using MS/MS. The heterogenous nuclear ribonucleoprotein (hnRNP) F, guanine nucleotide binding protein (G protein), voltage-dependent anion channel 2 (VDAC2) and cytochrome bc1 were present in abundance in the NiV-infected SK-N-MC cells in contrast to hnRNPs H and H2 that were significantly down-regulated. Several human neuronal cell proteins that are differentially expressed following NiV Infection are identified. The proteins are associated with various cellular functions and their abundance reflects their significance in the cytopathologic responses to the Infection and the regulation of NiV replication. The potential importance of the ratio of hnRNP F, and hnRNPs H and H2 in regulation of NiV replication, the association of the mitochondrial protein with the cytopathologic responses to the Infection and induction of apoptosis are highlighted.
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Quantitative estimation of Nipah Virus replication kinetics in vitro
Virology journal, 2006Co-Authors: Li-yen Chang, A. R. Mohd Ali, Sharifah Syed Hassan, Sazaly AbubakarAbstract:Background Nipah Virus is a zoonotic Virus isolated from an outbreak in Malaysia in 1998. The Virus causes Infections in humans, pigs, and several other domestic animals. It has also been isolated from fruit bats. The pathogenesis of Nipah Virus Infection is still not well described. In the present study, Nipah Virus replication kinetics were estimated from Infection of African green monkey kidney cells (Vero) using the one-step SYBR® Green I-based quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) assay.
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Quantitative estimation of Nipah Virus replication kinetics in vitro
Virology Journal, 2006Co-Authors: Li-yen Chang, Sharifah Syed Hassan, Ar Mohd Ali, Sazaly AbubakarAbstract:Background Nipah Virus is a zoonotic Virus isolated from an outbreak in Malaysia in 1998. The Virus causes Infections in humans, pigs, and several other domestic animals. It has also been isolated from fruit bats. The pathogenesis of Nipah Virus Infection is still not well described. In the present study, Nipah Virus replication kinetics were estimated from Infection of African green monkey kidney cells (Vero) using the one-step SYBR^® Green I-based quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) assay. Results The qRT-PCR had a dynamic range of at least seven orders of magnitude and can detect Nipah Virus from as low as one PFU/μL. Following initiation of Infection, it was estimated that Nipah Virus RNA doubles at every ~40 minutes and attained peak intracellular Virus RNA level of ~8.4 log PFU/μL at about 32 hours post-Infection (PI). Significant extracellular Nipah Virus RNA release occurred only after 8 hours PI and the level peaked at ~7.9 log PFU/μL at 64 hours PI. The estimated rate of Nipah Virus RNA released into the cell culture medium was ~0.07 log PFU/μL per hour and less than 10% of the released Nipah Virus RNA was infectious. Conclusion The SYBR^® Green I-based qRT-PCR assay enabled quantitative assessment of Nipah Virus RNA synthesis in Vero cells. A low rate of Nipah Virus extracellular RNA release and low infectious Virus yield together with extensive syncytial formation during the Infection support a cell-to-cell spread mechanism for Nipah Virus Infection.
Emily S. Gurley - One of the best experts on this subject based on the ideXlab platform.
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Nipah Virus Infection outbreak with nosocomial and corpse-to-human transmission, Bangladesh.
Emerging infectious diseases, 2013Co-Authors: Hossain M. S. Sazzad, M. Jahangir Hossain, Emily S. Gurley, Goutam Podder, Kazi Mohammad Hassan Ameen, Shahana Parveen, M. Saiful Islam, Labib Imran Faruque, S. BanuAbstract:Active Nipah Virus encephalitis surveillance identified an encephalitis cluster and sporadic cases in Faridpur, Bangladesh, in January 2010. We identified 16 case-patients; 14 of these patients died. For 1 case-patient, the only known exposure was hugging a deceased patient with a probable case, while another case-patient’s exposure involved preparing the same corpse for burial by removing oral secretions and anogenital excreta with a cloth and bare hands. Among 7 persons with confirmed sporadic cases, 6 died, including a physician who had physically examined encephalitis patients without gloves or a mask. Nipah Virus–infected patients were more likely than community-based controls to report drinking raw date palm sap and to have had physical contact with an encephalitis patient (29% vs. 4%, matched odds ratio undefined). Efforts to prevent transmission should focus on reducing caregivers’ exposure to infected patients’ bodily secretions during care and traditional burial practices.
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Cluster of Nipah Virus Infection, Kushtia District, Bangladesh, 2007
PloS one, 2010Co-Authors: Nusrat Homaira, M. Jahangir Hossain, Mahmudur Rahman, Nazmun Nahar, Rasheda Khan, Goutam Podder, Kamrun Nahar, Dawlat Khan, Emily S. GurleyAbstract:Objective In March 2007, we investigated a cluster of Nipah encephalitis to identify risk factors for Nipah Infection in Bangladesh. Methods We defined confirmed Nipah cases by the presence of IgM and IgG antibodies against Nipah Virus in serum. Case-patients, who resided in the same village during the outbreak period but died before serum could be collected, were classified as probable cases. Results We identified three confirmed and five probable Nipah cases. There was a single index case. Five of the secondary cases came in close physical contact to the index case when she was ill. Case-patients were more likely to have physical contact with the index case (71% cases versus 0% controls, p =
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cluster of Nipah Virus Infection kushtia district bangladesh 2007
PLOS ONE, 2010Co-Authors: Nusrat Homaira, Mahmudur Rahman, Nazmun Nahar, Rasheda Khan, Goutam Podder, Kamrun Nahar, Dawlat Khan, Jahangir M Hossain, Emily S. GurleyAbstract:Objective In March 2007, we investigated a cluster of Nipah encephalitis to identify risk factors for Nipah Infection in Bangladesh. Methods We defined confirmed Nipah cases by the presence of IgM and IgG antibodies against Nipah Virus in serum. Case-patients, who resided in the same village during the outbreak period but died before serum could be collected, were classified as probable cases. Results We identified three confirmed and five probable Nipah cases. There was a single index case. Five of the secondary cases came in close physical contact to the index case when she was ill. Case-patients were more likely to have physical contact with the index case (71% cases versus 0% controls, p = <0.001). The index case, on her third day of illness, and all the subsequent cases attended the same religious gathering. For three probable cases including the index case, we could not identify any known risk factors for Nipah Infection such as physical contact with Nipah case-patients, consumption of raw date palm juice, or contact with sick animals or fruit bats. Conclusion Though person-to-person transmission remains an important mode of transmission for Nipah Infection, we could not confirm the source of Infection for three of the probable Nipah case-patients. Continued surveillance and outbreak investigations will help better understand the transmission of Nipah Virus and develop preventive strategies.
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Clinical Presentation of Nipah Virus Infection in Bangladesh
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2008Co-Authors: M. Jahangir Hossain, Emily S. Gurley, Joel M. Montgomery, Michael Bell, Darin S. Carroll, Vincent P. Hsu, Pierre Formenty, A. Croisier, Eric Bertherat, M. A. FaizAbstract:BACKGROUND In Bangladesh, 4 outbreaks of Nipah Virus Infection were identified during the period 2001-2004. METHODS We characterized the clinical features of Nipah Virus-infected individuals affected by these outbreaks. We classified patients as having confirmed cases of Nipah Virus Infection if they had antibodies reactive with Nipah Virus antigen. Patients were considered to have probable cases of Nipah Virus Infection if they had symptoms consistent with Nipah Virus Infection during the same time and in the same community as patients with confirmed cases. RESULTS We identified 92 patients with Nipah Virus Infection, 67 (73%) of whom died. Although all age groups were affected, 2 outbreaks principally affected young persons (median age, 12 years); 62% of the affected persons were male. Fever, altered mental status, headache, cough, respiratory difficulty, vomiting, and convulsions were the most common signs and symptoms; clinical and radiographic features of acute respiratory distress syndrome of Nipah illness were identified during the fourth outbreak. Among those who died, death occurred a median of 6 days (range, 2-36 days) after the onset of illness. Patients who died were more likely than survivors to have a temperature >37.8 degrees C, altered mental status, difficulty breathing, and abnormal plantar reflexes. Among patients with Nipah Virus Infection who had well-defined exposure to another patient infected with Nipah Virus, the median incubation period was 9 days (range, 6-11 days). CONCLUSIONS Nipah Virus Infection produced rapidly progressive severe illness affecting the central nervous and respiratory systems. Clinical characteristics of Nipah Virus Infection in Bangladesh, including a severe respiratory component, appear distinct from clinical characteristics reported during earlier outbreaks in other countries.
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Risk of nosocomial transmission of Nipah Virus in a Bangladesh hospital.
Infection control and hospital epidemiology, 2007Co-Authors: Emily S. Gurley, M. Jahangir Hossain, Joel M. Montgomery, M. Rafiqul Islam, M. Abdur Rahim Molla, S. M. Shamsuzzaman, Kazi Akram, Kamruz Zaman, Nima Asgari, James A. ComerAbstract:We conducted a seroprevalence study and exposure survey of healthcare workers to assess the risk of nosocomial transmission of Nipah Virus during an outbreak in Bangladesh in 2004. No evidence of recent Nipah Virus Infection was detected despite substantial exposures and minimal use of personal protective equipment.
Sharifah Syed Hassan - One of the best experts on this subject based on the ideXlab platform.
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Risk Factors for Nipah Virus Infection among Pteropid Bats, Peninsular Malaysia
Emerging infectious diseases, 2013Co-Authors: Sohayati Abdul Rahman, Sharifah Syed Hassan, Hume Field, Latiffah Hassan, Jonathan H. Epstein, Zaini C. Mamat, Aziz M. Yatim, Tom Hughes, Justin Westrum, M.s. NaimAbstract:We conducted cross-sectional and longitudinal studies to determine the distribution of and risk factors for seropositivity to Nipah Virus (NiV) among Pteropus vampyrus and P. hypomelanus bats in Peninsular Malaysia. Neutralizing antibodies against NiV were detected at most locations surveyed. We observed a consistently higher NiV risk (odds ratio 3.9) and seroprevalence (32.8%) for P. vampyrus than P. hypomelanus (11.1%) bats. A 3-year longitudinal study of P. hypomelanus bats indicated nonseasonal temporal variation in seroprevalence, evidence for viral circulation within the study period, and an overall NiV seroprevalence of 9.8%. The seroprevalence fluctuated over the study duration between 1% and 20% and generally decreased during 2004–2006. Adult bats, particularly pregnant, with dependent pup and lactating bats, had a higher prevalence of NiV antibodies than juveniles. Antibodies in juveniles 6 months–2 years of age suggested viral circulation within the study period.
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Human neuronal cell protein responses to Nipah Virus Infection.
Virology journal, 2007Co-Authors: Li-yen Chang, A. R. Mohd Ali, Sharifah Syed Hassan, Sazaly AbubakarAbstract:Nipah Virus (NiV), a recently discovered zoonotic Virus infects and replicates in several human cell types. Its replication in human neuronal cells, however, is less efficient in comparison to other fully susceptible cells. In the present study, the SK-N-MC human neuronal cell protein response to NiV Infection is examined using proteomic approaches. Method for separation of the NiV-infected human neuronal cell proteins using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) was established. At least 800 protein spots were resolved of which seven were unique, six were significantly up-regulated and eight were significantly down-regulated. Six of these altered proteins were identified using mass spectrometry (MS) and confirmed using MS/MS. The heterogenous nuclear ribonucleoprotein (hnRNP) F, guanine nucleotide binding protein (G protein), voltage-dependent anion channel 2 (VDAC2) and cytochrome bc1 were present in abundance in the NiV-infected SK-N-MC cells in contrast to hnRNPs H and H2 that were significantly down-regulated. Several human neuronal cell proteins that are differentially expressed following NiV Infection are identified. The proteins are associated with various cellular functions and their abundance reflects their significance in the cytopathologic responses to the Infection and the regulation of NiV replication. The potential importance of the ratio of hnRNP F, and hnRNPs H and H2 in regulation of NiV replication, the association of the mitochondrial protein with the cytopathologic responses to the Infection and induction of apoptosis are highlighted.
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Quantitative estimation of Nipah Virus replication kinetics in vitro
Virology journal, 2006Co-Authors: Li-yen Chang, A. R. Mohd Ali, Sharifah Syed Hassan, Sazaly AbubakarAbstract:Background Nipah Virus is a zoonotic Virus isolated from an outbreak in Malaysia in 1998. The Virus causes Infections in humans, pigs, and several other domestic animals. It has also been isolated from fruit bats. The pathogenesis of Nipah Virus Infection is still not well described. In the present study, Nipah Virus replication kinetics were estimated from Infection of African green monkey kidney cells (Vero) using the one-step SYBR® Green I-based quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) assay.
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Quantitative estimation of Nipah Virus replication kinetics in vitro
Virology Journal, 2006Co-Authors: Li-yen Chang, Sharifah Syed Hassan, Ar Mohd Ali, Sazaly AbubakarAbstract:Background Nipah Virus is a zoonotic Virus isolated from an outbreak in Malaysia in 1998. The Virus causes Infections in humans, pigs, and several other domestic animals. It has also been isolated from fruit bats. The pathogenesis of Nipah Virus Infection is still not well described. In the present study, Nipah Virus replication kinetics were estimated from Infection of African green monkey kidney cells (Vero) using the one-step SYBR^® Green I-based quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) assay. Results The qRT-PCR had a dynamic range of at least seven orders of magnitude and can detect Nipah Virus from as low as one PFU/μL. Following initiation of Infection, it was estimated that Nipah Virus RNA doubles at every ~40 minutes and attained peak intracellular Virus RNA level of ~8.4 log PFU/μL at about 32 hours post-Infection (PI). Significant extracellular Nipah Virus RNA release occurred only after 8 hours PI and the level peaked at ~7.9 log PFU/μL at 64 hours PI. The estimated rate of Nipah Virus RNA released into the cell culture medium was ~0.07 log PFU/μL per hour and less than 10% of the released Nipah Virus RNA was infectious. Conclusion The SYBR^® Green I-based qRT-PCR assay enabled quantitative assessment of Nipah Virus RNA synthesis in Vero cells. A low rate of Nipah Virus extracellular RNA release and low infectious Virus yield together with extensive syncytial formation during the Infection support a cell-to-cell spread mechanism for Nipah Virus Infection.