84 results on '"Maya Williams"'
Search Results
52. Evidence for avian H9N2 influenza virus infections among rural villagers in Cambodia
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Hongxia Shao, Gary L. Heil, Thomas F. Wierzba, Malik Peiris, Whitney S. Krueger, Channimol Chum, Gregory C. Gray, Chadwick Y. Yasuda, Shannon D. Putnam, Maya Williams, Daniel R. Perez, Matthew R. Kasper, Vonthanak Saphonn, John A. Friary, Ana W. Capuano, and Patrick J. Blair
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Male ,Rural Population ,Avian ,Communicable diseases ,Antibodies, Viral ,medicine.disease_cause ,Disease Outbreaks ,Serology ,Surveys and Questionnaires ,Zoonoses ,Influenza A Virus, H9N2 Subtype ,Influenza A virus ,Prospective Studies ,Emerging ,0303 health sciences ,education.field_of_study ,Transmission (medicine) ,lcsh:Public aspects of medicine ,virus diseases ,General Medicine ,Middle Aged ,Occupational exposure ,3. Good health ,Infectious Diseases ,Cohort ,Human mortality from H5N1 ,Cohort studies ,Female ,Cambodia ,Adult ,Population ,Enzyme-Linked Immunosorbent Assay ,Biology ,Article ,Virus ,lcsh:Infectious and parasitic diseases ,Young Adult ,03 medical and health sciences ,Influenza, Human ,medicine ,Animals ,Humans ,lcsh:RC109-216 ,education ,030304 developmental biology ,030306 microbiology ,Public Health, Environmental and Occupational Health ,lcsh:RA1-1270 ,Virology ,Influenza A virus subtype H5N1 ,Immunology - Abstract
Summary: Background: Southeast Asia remains a critical region for the emergence of novel and/or zoonotic influenza, underscoring the importance of extensive sampling in rural areas where early transmission is most likely to occur. Methods: In 2008, 800 adult participants from eight sites were enrolled in a prospective population-based study of avian influenza (AI) virus transmission where highly pathogenic avian influenza (HPAI) H5N1 virus had been reported in humans and poultry from 2006 to 2008. From their enrollment sera and questionnaires, we report risk factor findings for serologic evidence of previous infection with 18 AI virus strains. Results: Serologic assays revealed no evidence of previous infection with 13 different low-pathogenic AI viruses or with HPAI avian-like A/Cambodia/R0404050/2007(H5N1). However, 21 participants had elevated antibodies against avian-like A/Hong Kong/1073/1999(H9N2), validated with a monoclonal antibody blocking ELISA assay specific for avian H9. Conclusions: Although cross-reaction from antibodies against human influenza viruses cannot be completely excluded, the study data suggest that a number of participants were previously infected with the avian-like A/Hong Kong/1073/1999(H9N2) virus, likely due to as yet unidentified environmental exposures. Prospective data from this cohort will help us better understand the serology of zoonotic influenza infection in a rural cohort in SE Asia. Keywords: Influenza A virus, Avian, Zoonoses, Occupational exposure, Communicable diseases, Emerging, Cohort studies
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- 2013
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53. Comparison of the Hemagglutination Inhibition Test and IgG ELISA in Categorizing Primary and Secondary Dengue Infections Based on the Plaque Reduction Neutralization Test
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Maya Williams, Bachti Alisjahbana, Herman Kosasih, Ida Parwati, Nurhayati Lukman, Nugroho Harry Susanto, Silvita Fitri, Susana Widjaja, and Gustiani Salim
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0301 basic medicine ,Adult ,Male ,Hemagglutination Inhibition Tests ,Article Subject ,Adolescent ,Secondary infection ,lcsh:Medicine ,Enzyme-Linked Immunosorbent Assay ,Hemolytic Plaque Technique ,Dengue virus ,medicine.disease_cause ,General Biochemistry, Genetics and Molecular Biology ,Immunoglobulin G ,Dengue fever ,Dengue ,03 medical and health sciences ,Plaque reduction neutralization test ,Neutralization Tests ,medicine ,Humans ,Child ,Hemagglutination assay ,General Immunology and Microbiology ,biology ,business.industry ,Coinfection ,lcsh:R ,General Medicine ,Gold standard (test) ,Dengue Virus ,Middle Aged ,medicine.disease ,Virology ,030104 developmental biology ,Immunology ,biology.protein ,Female ,business ,Research Article - Abstract
Secondary dengue infection by heterotypic serotypes is associated with severe manifestations of disease, that is, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). The World Health Organization (WHO) has recommended criteria based on the hemagglutination inhibition (HI) test to distinguish between primary and secondary dengue infections. Since the HI test has practical limitations and disadvantages, we evaluated the accuracy of WHO HI criteria and compared it with criteria based on an IgG enzyme-linked immunosorbent assay (ELISA) using a plaque reduction neutralization test (PRNT) as the gold standard. Both WHO HI criteria and IgG ELISA criteria performed strongly (16/16) in determining primary infection. However, to determine secondary infection, the IgG ELISA criteria performed better (72/73) compared to the WHO HI criteria (23/73).
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- 2016
54. NK cell degranulation as a marker for measuring antibody-dependent cytotoxicity in neutralizing and non-neutralizing human sera from dengue patients
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Maya Williams, An Li, Peifang Sun, Kevin R. Porter, Charmagne G. Beckett, Brian J. Morrison, Nishith Nagabhushana, and Zhaodong Liang
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0301 basic medicine ,Immunology ,Population ,chemical and pharmacologic phenomena ,Dengue virus ,CD16 ,medicine.disease_cause ,Antibodies, Viral ,GPI-Linked Proteins ,Neutralization ,Cell Degranulation ,Dengue ,03 medical and health sciences ,0302 clinical medicine ,Antigen ,medicine ,Immunology and Allergy ,Humans ,education ,Cytotoxicity ,Antibody-dependent cell-mediated cytotoxicity ,education.field_of_study ,biology ,Chemistry ,Receptors, IgG ,Antibody-Dependent Cell Cytotoxicity ,Dengue Virus ,Virology ,Antibodies, Neutralizing ,Killer Cells, Natural ,030104 developmental biology ,biology.protein ,Antibody ,030215 immunology - Abstract
The study assessed antibody-dependent NK cell degranulation, a biomarker relevant to antibody-dependent cell cytotoxicity (ADCC), to analyze dengue immune sera. We first determined binding intensity of patient sera to the surface of DENV-infected cells and examined the types of antigens expressed on infected cells. Antigens from pre-membrane (PreM) and envelope (E), but not from NS proteins were detected on the surface of infected cells. After adding NK cells to infected target cells previously treated with patient sera, rapid NK cell degranulation was observed. Non-neutralizing patient sera generated comparable NK cell degranulation as that of neutralizing sera, suggesting ADCC may be a protective mechanism apart from Ab neutralization. The level of NK cell degranulation varied dramatically among human individuals and was associated with the level of CD16 expression on NK cells, informing on the complexity of ADCC among human population.
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- 2016
55. Cytokine Analysis and Correlation to Viral Loads in an Otherwise Healthy Population With Influenza Infection
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Michael Rajnik, Peifang Sun, Eugene V. Millar, Michelande Ridore, Michelle S Flores, Mary P. Fairchok, Martin G. Ottolini, Jacqueline Owens Milzman, Wei-Ju Chen, Maya Williams, Patrick Danaher, Erin Hansen, Timothy Burgess, John H. Arnold, and Tahaniyat Lalani
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Correlation ,Infectious Diseases ,Cytokine ,Oncology ,business.industry ,medicine.medical_treatment ,Healthy population ,Immunology ,medicine ,business ,Viral load - Published
- 2016
56. The Epidemiology, Virology and Clinical Findings of Dengue Virus Infections in a Cohort of Indonesian Adults in Western Java
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Hadi Jusuf, Nurhayati, Quirijn de Mast, Herman Kosasih, Patrick J. Blair, Maya Williams, Bachti Alisjahbana, Irani Fianza Rudiman, Susana Widjaja, André J. A. M. van der Ven, Charmagne G. Beckett, Timothy Burgess, Harli Novriani, Kevin R. Porter, Ungke Antonjaya, and Nugroho Harry Susanto
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0301 basic medicine ,myalgia ,Male ,RNA viruses ,Viral Diseases ,Physiology ,lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4] ,Fevers ,Disease ,Dengue virus ,medicine.disease_cause ,Pathology and Laboratory Medicine ,Biochemistry ,Dengue fever ,Dengue Fever ,Dengue ,Geographical Locations ,0302 clinical medicine ,Immune Physiology ,Epidemiology ,Medicine and Health Sciences ,Prospective Studies ,Enzyme-Linked Immunoassays ,Immune System Proteins ,Reverse Transcriptase Polymerase Chain Reaction ,Incidence (epidemiology) ,lcsh:Public aspects of medicine ,Incidence ,Middle Aged ,Infectious Diseases ,Medical Microbiology ,Viral Pathogens ,Cohort ,Viruses ,RNA, Viral ,Female ,medicine.symptom ,Pathogens ,Java ,Research Article ,Neglected Tropical Diseases ,Adult ,medicine.medical_specialty ,lcsh:Arctic medicine. Tropical medicine ,Asia ,Adolescent ,lcsh:RC955-962 ,030231 tropical medicine ,030106 microbiology ,Molecular Sequence Data ,Immunology ,Oceania ,Research and Analysis Methods ,Asymptomatic ,Microbiology ,Antibodies ,03 medical and health sciences ,Young Adult ,Signs and Symptoms ,medicine ,Humans ,Adults ,Immunoassays ,Microbial Pathogens ,Aged ,Biology and life sciences ,Flaviviruses ,business.industry ,Public Health, Environmental and Occupational Health ,Organisms ,Proteins ,lcsh:RA1-1270 ,Sequence Analysis, DNA ,Dengue Virus ,medicine.disease ,Tropical Diseases ,Virology ,lnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4] ,Indonesia ,Age Groups ,People and Places ,Immunologic Techniques ,Population Groupings ,business - Abstract
Background Dengue has emerged as one of the most important infectious diseases in the last five decades. Evidence indicates the expansion of dengue virus endemic areas and consequently the exponential increase of dengue virus infections across the subtropics. The clinical manifestations of dengue virus infection include sudden fever, rash, headache, myalgia and in more serious cases, spontaneous bleeding. These manifestations occur in children as well as in adults. Defining the epidemiology of dengue in a given area is critical to understanding the disease and devising effective public health strategies. Methodology/Principal Findings Here, we report the results from a prospective cohort study of 4380 adults in West Java, Indonesia, from 2000–2004 and 2006–2009. A total of 2167 febrile episodes were documented and dengue virus infections were confirmed by RT-PCR or serology in 268 cases (12.4%). The proportion ranged from 7.6 to 41.8% each year. The overall incidence rate of symptomatic dengue virus infections was 17.3 cases/1,000 person years and between September 2006 and April 2008 asymptomatic infections were 2.6 times more frequent than symptomatic infections. According to the 1997 WHO classification guidelines, there were 210 dengue fever cases, 53 dengue hemorrhagic fever cases (including one dengue shock syndrome case) and five unclassified cases. Evidence for sequential dengue virus infections was seen in six subjects. All four dengue virus serotypes circulated most years. Inapparent dengue virus infections were predominantly associated with DENV-4 infections. Conclusions/Significance Dengue virus was responsible for a significant percentage of febrile illnesses in an adult population in West Java, Indonesia, and this percentage varied from year to year. The observed incidence rate during the study period was 43 times higher than the reported national or provincial rates during the same time period. A wide range of clinical severity was observed with most infections resulting in asymptomatic disease. The circulation of all four serotypes of dengue virus was observed in most years of the study., Author Summary Dengue is the fastest spreading mosquito borne diseases in the world and is endemic in most tropical and sub-tropical countries with an estimated 96 million infections resulting in clinical disease annually. Population-based longitudinal prospective studies are essential for understanding dengue virus in the natural setting and developing prevention strategies to curtail the impact of disease. We present the results of a longitudinal cohort study of adults in West Java, Indonesia that was conducted between 2000–2004 and 2006–2009. We found that in adults, dengue virus was a significant cause of febrile illness. The entire spectrum of clinical severity was observed with most dengue virus infections manifesting as asymptomatic. The incidence of symptomatic dengue virus infections observed in this cohort was much higher than reported national or provincial rates. In addition, we observed all four dengue virus serotypes circulating during most years of the study.
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- 2016
57. Study of viremic profile in febrile specimens of chikungunya in Bandung, Indonesia
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Aditya Perkasa, Bachti Alisjahbana, Frilasita A. Yudhaputri, Ann M. Powers, Chairin Nisa Ma'roef, Ungke Anton Jaya, Herman Kosasih, Jeremy P. Ledermann, Maya Williams, Hofiya Djauhari, A.H.G.S. van der Ven, Silvita Fitri Riswari, Khin Saw Aye Myint, and I.M. Artika
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0301 basic medicine ,Adult ,Male ,Time Factors ,Adolescent ,Viremia ,Enzyme-Linked Immunosorbent Assay ,Biology ,medicine.disease_cause ,Antibodies, Viral ,Real-Time Polymerase Chain Reaction ,Virus ,03 medical and health sciences ,Virology ,medicine ,Dengue transmission ,Humans ,Chikungunya ,Child ,Infection kinetics ,Transmission (medicine) ,Background data ,Outbreak ,virus diseases ,Middle Aged ,Viral Load ,medicine.disease ,Viremia profile ,030104 developmental biology ,Infectious Diseases ,lnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4] ,Immunoglobulin M ,Indonesia ,Immunology ,Vero cell ,Chikungunya Fever ,RNA, Viral ,Female ,Chikungunya virus - Abstract
Contains fulltext : 171554.pdf (Publisher’s version ) (Open Access) BACKGROUND: Data regarding the viremia profile of chikungunya virus (CHIKV) infected patients especially during the pre-febrile period is limited. OBJECTIVE: To obtain virological kinetic data on CHIKV infections. STUDY DESIGN: A two-week community observation for dengue transmission was conducted in Bandung, Indonesia, from 2005 to 2009. Acute specimens from non-dengue febrile patients were screened by pan-alphavirus conventional RT-PCR. The positives were confirmed for CHIKV RNA by a specific RT-PCR followed by sequencing. Simultaneously these specimens were also cultured in Vero cells and tested for anti-CHIK IgM MAC-ELISA. All the available serial specimens,including the pre-febrile specimens, from confirmed CHIK cases, were tested by virus isolation, RT-PCR, qRT-PCR, and CHIK IgM ELISA. RESULTS: There were five laboratory confirmed CHIK cases identified and studied. Among these, viremia was determined to extend from as early as 6 days prior to until 13 days post fever onset. Quantitative RT-PCR showed viremia peaked at or near onset of illness. CONCLUSION: In this study, individuals were identified with viremia prior to fever onset and extending beyond the febrile phase. This extended viremic phase has the potential to impact transmission dynamics and thus the public health response to CHIK outbreaks.
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- 2016
58. Infectious Etiologies of Acute Febrile Illness among Patients Seeking Health Care in South-Central Cambodia
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Chadwick Y. Yasuda, Maya Williams, Patrick J. Blair, Buth Sokhal, Timothy Burgess, Shannon D. Putnam, Matthew R. Kasper, Thomas F. Wierzba, Allen L. Richards, and Sok Touch
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Adult ,Male ,medicine.medical_specialty ,Orthohantavirus ,Adolescent ,Fever ,Developing country ,Dengue fever ,Specimen Handling ,Dengue ,Young Adult ,Virology ,Internal medicine ,Health care ,Influenza, Human ,medicine ,Hepatitis E virus ,Prevalence ,Humans ,Blood culture ,Young adult ,Rickettsia ,Intensive care medicine ,Child ,Developing Countries ,medicine.diagnostic_test ,Bacteria ,business.industry ,Public health ,Articles ,medicine.disease ,Malaria ,Orientia tsutsugamushi ,Infectious Diseases ,Acute Disease ,Etiology ,Parasitology ,Female ,Public Health ,business ,Cambodia - Abstract
The agents of human febrile illness can vary by region and country suggesting that diagnosis, treatment, and control programs need to be based on a methodical evaluation of area-specific etiologies. From December 2006 to December 2009, 9,997 individuals presenting with acute febrile illness at nine health care clinics in south-central Cambodia were enrolled in a study to elucidate the etiologies. Upon enrollment, respiratory specimens, whole blood, and serum were collected. Testing was performed for viral, bacterial, and parasitic pathogens. Etiologies were identified in 38.0% of patients. Influenza was the most frequent pathogen, followed by dengue, malaria, and bacterial pathogens isolated from blood culture. In addition, 3.5% of enrolled patients were infected with more than one pathogen. Our data provide the first systematic assessment of the etiologies of acute febrile illness in south-central Cambodia. Data from syndromic-based surveillance studies can help guide public health responses in developing nations.
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- 2012
59. Rickettsial Infections of Fleas Collected From Small Mammals on Four Islands in Indonesia
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Kathryn A. Barbara, Ungke Antonjaya, Patrick J. Blair, Andre Yunianto, Maya Williams, Ima Nurisa Ibrahim, Arik Farzeli, Dian Perwitasari, Susana Widjaya, Ester, Imelda Winoto, and Allen L. Richards
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Mammals ,General Veterinary ,biology ,Felis ,Zoology ,Rickettsia rickettsii ,biology.organism_classification ,Murine typhus ,medicine.disease ,Virology ,Rickettsia felis ,Spotted fever ,Infectious Diseases ,Rickettsia ,Rickettsiosis ,Indonesia ,Insect Science ,Rickettsia typhi ,medicine ,Animals ,Siphonaptera ,Parasitology - Abstract
Ectoparasites were sampled from small mammals collected in West Java, West Sumatra, North Sulawesi, and East Kalimantan, Indonesia, in 2007-2008 and were screened for evidence of infection from bacteria in the Rickettsaceae family. During eight trap nights at eight sites, 208 fleas were collected from 96 of 507 small mammals trapped from four orders (379 Rodentia; 123 Soricomorpha; two Carnivora; three Scandentia). Two species of fleas were collected: Xenopsylla cheopis (n = 204) and Nosopsyllus spp. (n = 4). Among the 208 fleas collected, 171 X. cheopis were removed from rats (Rattus spp.) and 33 X. cheopis from shrews (Suncus murinus). X. cheopis were pooled and tested for DNA from rickettsial agents Rickettsia typhi, Rickettsia felis, and spotted fever group rickettsiae. R. typhi, the agent of murine typhus, was detected in X. cheopis collected from small mammals in West Java and East Kalimantan. R. felis was detected in X. cheopis collected from small mammals in Manado, North Sulawesi. R. felis and spotted fever group rickettsiae were detected in a pool of X. cheopis collected from an animal in East Kalimantan. Sixteen percent of the X. cheopis pools were found positive for Rickettsia spp.; four (10.8%) R. typhi, one (2.7%) R. felis, and one (2.7%) codetection of R. felis and a spotted fever group rickettsia. These data suggest that rickettsial infections remain a threat to human health across Indonesia.
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- 2010
60. A Novel Trafficking Signal within the HLA-C Cytoplasmic Tail Allows Regulated Expression upon Differentiation of Macrophages
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Kathleen L. Collins, Maya Williams, Pennelope K. Blakely, Deanna A. Kulpa, Malinda Schaefer, and Anna Q. Yaffee
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Cytotoxicity, Immunologic ,Cytoplasm ,media_common.quotation_subject ,Cellular differentiation ,Immunology ,Antigen-Presenting Cells ,Down-Regulation ,chemical and pharmacologic phenomena ,HLA-C Antigens ,CD8-Positive T-Lymphocytes ,Article ,Cross-Priming ,Cell Line, Tumor ,MHC class I ,Humans ,Immunology and Allergy ,Internalization ,Antigen-presenting cell ,media_common ,biology ,U937 cell ,Effector ,Macrophages ,Cell Membrane ,Cell Differentiation ,U937 Cells ,Molecular biology ,Protein Structure, Tertiary ,Cell biology ,Protein Transport ,Gene Expression Regulation ,biology.protein ,Signal transduction ,Lysosomes ,Intracellular ,Signal Transduction - Abstract
Major histocompatibility complex class I molecules (MHC-I) present peptides to cytotoxic T lymphocytes (CTLs). In addition, HLA-C allotypes are recognized by killer cell Ig-like receptors (KIR) found on natural killer (NK) cells and effector CTLs. Compared to other classical MHC-I allotypes, HLA-C has low cell surface expression and an altered intracellular trafficking pattern. We present evidence that this results from effects of both the extracellular domain and the cytoplasmic tail. Notably, we demonstrate that the cytoplasmic tail contains a dihydrophobic (LI) internalization and lysosomal targeting signal that is partially attenuated by an aspartic acid residue (DXSLI). In addition, we provide evidence that this signal is specifically inhibited by hypophosphorylation of the adjacent serine residue upon macrophage differentiation and that this allows high HLA-C expression in this cell type. We propose that tightly regulated HLA-C surface expression facilitates immune surveillance and allows HLA-C to serve a specialized role in macrophages.
- Published
- 2008
61. The Tyrosine Binding Pocket in the Adaptor Protein 1 (AP-1) μ1 Subunit Is Necessary for Nef to Recruit AP-1 to the Major Histocompatibility Complex Class I Cytoplasmic Tail
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Elizabeth R. Wonderlich, Kathleen L. Collins, and Maya Williams
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Cytoplasm ,Protein subunit ,Adaptor Protein Complex 1 ,Amino Acid Motifs ,Molecular Sequence Data ,Plasma protein binding ,Biochemistry ,Clathrin ,Gene Products, nef ,Leucine ,Humans ,Amino Acid Sequence ,Tyrosine ,Binding site ,Molecular Biology ,Tyrosine binding ,Sequence Homology, Amino Acid ,biology ,Histocompatibility Antigens Class I ,Wild type ,virus diseases ,Signal transducing adaptor protein ,Cell Biology ,Virology ,Protein Structure, Tertiary ,Cell biology ,Gene Expression Regulation ,Mutation ,biology.protein ,Protein Binding - Abstract
To evade the anti-human immunodeficiency virus (HIV) immune response, the HIV Nef protein disrupts major histocompatibility complex class I (MHC-I) trafficking by recruiting the clathrin adaptor protein 1 (AP-1) to the MHC-I cytoplasmic tail. Under normal conditions AP-1 binds dileucine and tyrosine signals (YXX phi motifs) via physically separate binding sites. In the case of the Nef-MHC-I complex, a tyrosine in the human leukocyte antigen (HLA)-A2 cytoplasmic tail ((320)YSQA) and a methionine in Nef (Met(20)) are absolutely required for AP-1 binding. Also present in Nef is a dileucine motif, which does not normally affect MHC-I trafficking and is not needed to recruit AP-1 to the Nef-MHC-I-complex. However, evidence is presented here that this dileucine motif can be activated by fusing Nef to the HLA-A2 tail in cis. Thus, the inability of this motif to function in trans likely results from a structural change that occurs when Nef binds to the MHC-I cytoplasmic tail. The physiologically relevant tyrosine-dependent recruitment of AP-1 to MHC-I, which occurs whether Nef is present in cis or trans, was stabilized by the acidic and polyproline domains within Nef. Additionally, amino acids Ala(324) and Asp(327) in the cytoplasmic tails of HLA-A and (but not HLA-C and HLA-E) molecules also stabilized AP-1 binding. Finally, mutation of the tyrosine binding pocket in the mu subunit of AP-1 created a dominant negative inhibitor of Nef-induced down-modulation of HLA-A2 that disrupted binding of wild type AP-1 to the Nef-MHC-I complex. Thus, these data provide evidence that Nef binding to the MHC-I cytoplasmic tail stabilizes the interaction of a tyrosine in the MHC-I cytoplasmic tail with the natural tyrosine binding pocket in AP-1.
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- 2008
62. HIV-1 Nef Disrupts Antigen Presentation Early in the Secretory Pathway
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Kathleen L. Collins, Rebekah I. Fleis, Matthew R. Kasper, Maya Williams, Tracey Filzen, and Jeremiah F. Roeth
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Cytoplasm ,Time Factors ,T-Lymphocytes ,viruses ,Molecular Sequence Data ,Antigen presentation ,Genes, MHC Class I ,Golgi Apparatus ,chemical and pharmacologic phenomena ,Cell Separation ,Major histocompatibility complex ,Biochemistry ,Gene Products, nef ,Adenoviridae ,Phosphates ,symbols.namesake ,HLA-A2 Antigen ,MHC class I ,Humans ,Immunoprecipitation ,Cytotoxic T cell ,Amino Acid Sequence ,Phosphorylation ,Molecular Biology ,Secretory pathway ,Antigen Presentation ,Sequence Homology, Amino Acid ,biology ,Endoplasmic reticulum ,Cell Membrane ,Temperature ,virus diseases ,Signal transducing adaptor protein ,Biological Transport ,Cell Biology ,Golgi apparatus ,Flow Cytometry ,Cell biology ,Microscopy, Fluorescence ,Mutation ,biology.protein ,symbols ,RNA Interference ,Lysosomes ,HeLa Cells ,Protein Binding ,trans-Golgi Network - Abstract
Human immunodeficiency virus, type 1 Nef disrupts viral antigen presentation and promotes viral immune evasion from cytotoxic T lymphocytes. There is evidence that Nef acts early in the secretory pathway to redirect major histocompatibility complex class I (MHC-I) from the trans-Golgi network to the endolysosomal pathway. However, a competing model suggests that Nef acts much later by accelerating MHC-I turnover at the cell surface. Here we demonstrate that Nef targets early forms of MHC-I molecules in the endoplasmic reticulum by preferentially binding hypophosphorylated cytoplasmic tails. The Nef-MHC-I complex migrates normally into the Golgi apparatus but subsequently fails to arrive at the cell surface and become phosphorylated. Cell type-specific differences in the rate of MHC-I transport through the secretory pathway correlate with responsiveness to Nef and co-precipitation of adaptor protein 1 with the Nef.MHC-I complex. We propose that the assembly of a Nef.MHC-I.adaptor protein 1 complex early in the secretory pathway is important for Nef activity.
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- 2005
63. Human Immunodeficiency Virus Type 1 Nef Domains Required for Disruption of Major Histocompatibility Complex Class I Trafficking Are Also Necessary for Coprecipitation of Nef with HLA-A2
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Jeremiah F. Roeth, Tracey Filzen, Kathleen L. Collins, Matthew R. Kasper, and Maya Williams
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T-Lymphocytes ,viruses ,Genetic Vectors ,Immunology ,Protein domain ,Cell ,Major histocompatibility complex ,Microbiology ,Gene Products, nef ,Virus ,Adenoviridae ,Immune system ,Virology ,HLA-A2 Antigen ,medicine ,Humans ,nef Gene Products, Human Immunodeficiency Virus ,Polyproline helix ,biology ,Histocompatibility Antigens Class I ,virus diseases ,biology.organism_classification ,medicine.anatomical_structure ,Insect Science ,Mutation ,Lentivirus ,HIV-1 ,biology.protein ,Pathogenesis and Immunity ,Function (biology) - Abstract
Human immunodeficiency virus type 1 (HIV-1) Nef is a critical protein that is necessary for HIV pathogenesis. Its roles include the disruption of major histocompatibility complex class I (MHC-I) and CD4 trafficking to promote immune evasion and viral spread. Mutational analyses have revealed that separate domains of Nef are required to affect these two molecules. To further elucidate how Nef disrupts MHC-I trafficking in T cells, we examined the role of protein domains that are required for this function (N-terminal alpha helix, polyproline, acidic, and oligomerization domains). We found that each of these regions was required for Nef to disrupt the transport of HLA-A2 to the cell surface and for Nef to coprecipitate with HLA-A2.
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- 2005
64. Direct Binding of Human Immunodeficiency Virus Type 1 Nef to the Major Histocompatibility Complex Class I (MHC-I) Cytoplasmic Tail Disrupts MHC-I Trafficking
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Jeremiah F. Roeth, Matthew R. Kasper, Kathleen L. Collins, Chris G. Przybycin, Rebekah I. Fleis, and Maya Williams
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Recombinant Fusion Proteins ,viruses ,Molecular Sequence Data ,Immunology ,DNA, Recombinant ,chemical and pharmacologic phenomena ,Plasma protein binding ,Human leukocyte antigen ,Major histocompatibility complex ,Models, Biological ,Microbiology ,Gene Products, nef ,Cell Line ,Mice ,HLA Antigens ,Virology ,HLA-A2 Antigen ,MHC class I ,Animals ,Humans ,Cytotoxic T cell ,Amino Acid Sequence ,nef Gene Products, Human Immunodeficiency Virus ,Peptide sequence ,Cell Nucleus ,Binding Sites ,Base Sequence ,biology ,Histocompatibility Antigens Class I ,H-2 Antigens ,CD28 ,In vitro ,Protein Structure, Tertiary ,Virus-Cell Interactions ,Cell biology ,Insect Science ,DNA, Viral ,HIV-1 ,Mutagenesis, Site-Directed ,biology.protein ,HeLa Cells ,Protein Binding - Abstract
Nef, an essential pathogenic determinant for human immunodeficiency virus type 1, has multiple functions that include disruption of major histocompatibility complex class I molecules (MHC-I) and CD4 and CD28 cell surface expression. The effects of Nef on MHC-I have been shown to protect infected cells from cytotoxic T-lymphocyte recognition by downmodulation of a subset of MHC-I (HLA-A and -B). The remaining HLA-C and -E molecules prevent recognition by natural killer (NK) cells, which would otherwise lyse cells expressing small amounts of MHC-I. Specific amino acid residues in the MHC-I cytoplasmic tail confer sensitivity to Nef, but their function is unknown. Here we show that purified Nef binds directly to the HLA-A2 cytoplasmic tail in vitro and that Nef forms complexes with MHC-I that can be isolated from human cells. The interaction between Nef and MHC-I appears to be weak, indicating that it may be transient or stabilized by other factors. Supporting the fact that these molecules interact in vivo, we found that Nef colocalizes with HLA-A2 molecules in a perinuclear distribution inside cells. In addition, we demonstrated that Nef fails to bind the HLA-E tail and also fails to bind HLA-A2 tails with deletions of amino acids necessary for MHC-I downmodulation. These data provide an explanation for differential downmodulation of MHC-I allotypes by Nef. In addition, they provide the first direct evidence indicating that Nef functions as an adaptor molecule able to link MHC-I to cellular trafficking proteins.
- Published
- 2002
65. Lineage II of Southeast Asian/American DENV-2 Is Associated with a Severe Dengue Outbreak in the Peruvian Amazon
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Thomas G. Wood, William Johnson, Kanya C. Long, Sandra V. Mayer, Luis Suarez-Ognio, Maya Williams, Rubing Chen, Steven G. Widen, Kathryn A. Hanley, Evgeniya Volkova, Stalin Vilcarromero, Eric S. Halsey, Nikos Vasilakis, and Amy C. Morrison
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Male ,viruses ,Dengue virus ,medicine.disease_cause ,Dengue fever ,Disease Outbreaks ,Dengue ,Aedes ,Genotype ,Peru ,Child ,Asia, Southeastern ,Phylogeny ,virus diseases ,Articles ,Middle Aged ,Infectious Diseases ,RNA, Viral ,Female ,Adult ,Lineage (genetic) ,Adolescent ,Molecular Sequence Data ,Amazonas ,Aedes aegypti ,Genome, Viral ,Biology ,Southeast asian ,Young Adult ,Species Specificity ,Virology ,medicine ,Animals ,Humans ,Severe Dengue ,Base Sequence ,Sequence Analysis, RNA ,DENV-2 ,Outbreak ,Dengue Virus ,biology.organism_classification ,medicine.disease ,United States ,Insect Vectors ,Amino Acid Substitution ,Parasitology - Abstract
During 2010 and 2011, the Loreto region of Peru experienced a dengue outbreak of unprecedented magnitude and severity for the region. This outbreak coincided with the reappearance of dengue virus-2 (DENV-2) in Loreto after almost 8 years. Whole-genome sequence indicated that DENV-2 from the outbreak belonged to lineage II of the southeast Asian/American genotype and was most closely related to viruses circulating in Brazil during 2007 and 2008, whereas DENV-2 previously circulating in Loreto grouped with lineage I (DENV-2 strains circulating in South America since 1990). One amino acid substitution (NS5 A811V) in the 2010 and 2011 isolates resulted from positive selection. However, the 2010 and 2011 DENV-2 did not replicate to higher titers in monocyte-derived dendritic cells and did not infect or disseminate in a higher proportion of Aedes aegypti than DENV-2 isolates previously circulating in Loreto. These results suggest that factors other than enhanced viral replication played a role in the severity of this outbreak.
- Published
- 2014
66. HIV-1 Nef Blocks Transport of MHC Class I Molecules to the Cell Surface Via a PI 3-Kinase-Dependent Pathway
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Maya Williams, Kevin R. Bobbitt, Rebekah I. Fleis, Craig M. Story, S.A. Swann, and Kathleen L. Collins
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Dynamins ,Morpholines ,Recombinant Fusion Proteins ,Blotting, Western ,Cell ,Down-Regulation ,Golgi Apparatus ,PI 3-kinase ,chemical and pharmacologic phenomena ,Major histocompatibility complex ,Endocytosis ,Transport Pathway ,Gene Products, nef ,GTP Phosphohydrolases ,src Homology Domains ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Virology ,HLA-A2 Antigen ,MHC class I ,Tumor Cells, Cultured ,medicine ,Humans ,Cytotoxic T cell ,nef Gene Products, Human Immunodeficiency Virus ,Phosphoinositide-3 Kinase Inhibitors ,030304 developmental biology ,0303 health sciences ,Nef ,biology ,Cell Membrane ,HIV ,virus diseases ,Flow Cytometry ,CD4 ,3. Good health ,Transport protein ,Cell biology ,Protein Transport ,medicine.anatomical_structure ,Chromones ,030220 oncology & carcinogenesis ,CD4 Antigens ,HIV-1 ,biology.protein - Abstract
HIV causes a chronic infection by evading immune eradication. A key element of HIV immune escape is the HIV-1 Nef protein. Nef causes a reduction in the level of cell surface major histocompatibility complex class I (MHC-I) protein expression, thus protecting HIV-infected cells from anti-HIV cytotoxic T lymphocyte (CTL) recognition and killing. Nef also reduces cell surface levels of the HIV receptor, CD4, by accelerating endocytosis. We show here that endocytosis is not required for Nef-mediated downmodulation of MHC-I molecules. The main effect of Nef is to block transport of MHC-I molecules to the cell surface, leading to accumulation in intracellular organelles. Furthermore, the effect of Nef on MHC-I molecules (but not on CD4) requires phosphoinositide 3-kinase (PI 3-kinase) activity. We propose that Nef diverts MHC-1 proteins into a PI 3-kinase-dependent transport pathway that prevents expression on the cell surface.
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- 2001
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67. Recent advances in understanding the pathogenesis of Huntington's disease
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P. Hemachandra Reddy, Maya Williams, and Danilo A. Tagle
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Huntingtin ,Mice, Transgenic ,In Vitro Techniques ,Biology ,Translocation, Genetic ,Pathogenesis ,Mice ,Degenerative disease ,Trinucleotide Repeats ,Huntington's disease ,Mutant protein ,medicine ,Animals ,Humans ,Protein Isoforms ,Oligochaeta ,Genetics ,Diptera ,General Neuroscience ,Brain ,Chorea ,medicine.disease ,Abnormal involuntary movement ,Disease Models, Animal ,Huntington Disease ,Gene Expression Regulation ,Protein Biosynthesis ,Mutation ,Disease Progression ,medicine.symptom ,Trinucleotide repeat expansion ,Neuroscience - Abstract
Huntington's disease (HD) is an autosomal, dominantly inherited neurodegenerative disorder that is characterized by abnormal involuntary movements (chorea), intellectual impairment and selective neuronal loss. The expansion of a polymorphic trinucleotide repeat (the sequence CAG that codes for glutamine) to a length that exceeds 40 repeat units in exon 1 of the gene, HD, correlates with the onset and progression of the disease. The protein encoded by HD, huntingtin, is normally localized in the cytoplasm, whereas the mutant protein is also found in the nucleus, suggesting that its translocation to this site is important for the pathogenesis of HD. Although several proteins that interact with huntingtin have been identified in vitro, the significance of these interactions with the mutant protein in the pathogenesis of HD has yet to be determined. Recent progress in the development of cellular and animal models for the disease have provided invaluable insights and resources for studying the disease mechanisms underlying HD, and will be useful for screening and evaluating possible therapeutic strategies.
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- 1999
68. The diagnostic and prognostic value of dengue non-structural 1 antigen detection in a hyper-endemic region in Indonesia
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Timothy Burgess, Herman Kosasih, André J. A. M. van der Ven, Nurhayati, Maya Williams, Bachti Alisjahbana, Ida Parwati, Susana Widjaja, Patrick J. Blair, and Quirijn de Mast
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Serotype ,Adult ,Male ,Adolescent ,Fever ,Secondary infection ,viruses ,lcsh:Medicine ,Dengue virus ,Viral Nonstructural Proteins ,medicine.disease_cause ,Antibodies, Viral ,Sensitivity and Specificity ,Virus ,Dengue fever ,Dengue ,Diagnosis, Differential ,Antigen ,medicine ,Humans ,lcsh:Science ,Child ,Antigens, Viral ,Multidisciplinary ,biology ,business.industry ,lcsh:R ,virus diseases ,biochemical phenomena, metabolism, and nutrition ,Dengue Virus ,Middle Aged ,medicine.disease ,Prognosis ,Virology ,Antibodies, Neutralizing ,Titer ,Early Diagnosis ,Immunoglobulin M ,Indonesia ,Child, Preschool ,Immunology ,biology.protein ,lcsh:Q ,Female ,Reagent Kits, Diagnostic ,Antibody ,business ,Poverty-related infectious diseases Infectious diseases and international health [N4i 3] ,Research Article - Abstract
Contains fulltext : 126079.pdf (Publisher’s version ) (Open Access) As dengue fever is undifferentiated from other febrile illnesses in the tropics and the clinical course is unpredictable, early diagnosis is important. Several commercial assays to detect dengue NS1 antigen have been developed; however, their performances vary and data is lacking from hyper-endemic areas where all four serotypes of dengue are equally represented. To assess the sensitivity of the Bio-Rad platelia Dengue NS1 antigen assay according to virus serotype, immune status, gender, and parameters of severe disease, acute sera from 220 individuals with confirmed dengue and 55 individuals with a non-dengue febrile illness were tested using the Bio-Rad platelia Dengue NS1 antigen assay. The overall sensitivity of the NS1 ELISA was 46.8% and the specificity was 100%. The sensitivity in primary infections was significantly higher than in secondary infections (100% vs. 35.7%). In secondary infections, the sensitivity of NS1 detection was highest in DENV-3 (47.1%), followed by DENV-1 (40.9%), DENV-2 (30%) and DENV-4 (27%) infections. NS1 was less frequently detected in sera with high titers of HI antibodies or in acute samples from patients whose pre-illness sera showed neutralizing antibodies to more than one serotype. The detection of NS1 was higher in females, severe cases, and individuals with lower platelet counts (
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- 2013
69. Characterization of a novel flavivirus isolated from Culex (Melanoconion) ocossa mosquitoes from Iquitos, Peru
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Eric S. Halsey, Brett M. Forshey, Amy C. Morrison, Julio Evangelista, Carolina Guevara, Cristhopher Cruz, Maya Williams, Cristiam Carey, Tadeusz J. Kochel, and Helvio Astete
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Male ,Culex ,viruses ,Molecular Sequence Data ,Virus ,Cell Line ,Flavivirus Infections ,Mice ,Viral Proteins ,Dogs ,Phylogenetics ,Virology ,Cricetinae ,Peru ,medicine ,Animals ,Humans ,Amino Acid Sequence ,Phylogeny ,Phylogenetic tree ,biology ,Flavivirus ,Yellow fever ,virus diseases ,medicine.disease ,biology.organism_classification ,Insect Vectors ,biology.protein ,Female ,Antibody ,Sequence Alignment ,Encephalitis - Abstract
We describe the isolation and characterization of a novel flavivirus, isolated from a pool of Culex (Melanoconion) ocossa Dyar and Knab mosquitoes collected in 2009 in an urban area of the Amazon basin city of Iquitos, Peru. Flavivirus infection was detected by indirect immunofluorescent assay of inoculated C6/36 cells using polyclonal flavivirus antibodies (St. Louis encephalitis virus, yellow fever virus and dengue virus type 1) and confirmed by RT-PCR. Based on partial sequencing of the E and NS5 gene regions, the virus isolate was most closely related to the mosquito-borne flaviviruses but divergent from known species, with less than 45 and 71 % pairwise amino acid identity in the E and NS5 gene products, respectively. Phylogenetic analysis of E and NS5 amino acid sequences demonstrated that this flavivirus grouped with mosquito-borne flaviviruses, forming a clade with Nounané virus (NOUV). Like NOUV, no replication was detected in a variety of mammalian cells (Vero-76, Vero-E6, BHK, LLCMK, MDCK, A549 and RD) or in intracerebrally inoculated newborn mice. We tentatively designate this genetically distinct flavivirus as representing a novel species, Nanay virus, after the river near where it was first detected.
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- 2013
70. Epidemiological characteristics, clinical presentation and diagnosis at point-of-care during the first wave of the H1N1 influenza pandemic in Cambodia
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Chadwick, Yasuda, Ly, Sovann, Matthew, Kasper, Maya, Williams, and Thomas F, Wierzba
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Adult ,Male ,Adolescent ,Incidence ,Point-of-Care Systems ,Infant ,Real-Time Polymerase Chain Reaction ,Disease Outbreaks ,Influenza A Virus, H1N1 Subtype ,Child, Preschool ,Population Surveillance ,Influenza, Human ,Prevalence ,Humans ,Female ,Cambodia ,Child - Abstract
We conducted clinic-based surveillance for influenza virus among cases with acute febrile illness at 9 medical clinics in south-central Cambodia during 2006-2009. Patients greater than or equal to 24 months old presenting with acute fever (38 degrees C) were enrolled. In late July 2009, the study identified its first case of pandemic H1N1 (pH1N1) influenza virus infection. The prevalence of pH1N1 infections increased rapidly during August and September and by October, pH1N1 infections had peaked replacing H3N2 as the dominant subtype. The incidence of pH1N1 subsequently decreased, with only one case identified in late December. From late July through December 2009, 42.4% of all influenza cases were caused by pH1N1. Except for headache, less frequently reported among pH1N1-infected patients, patients infected with the pH1N1 reported symptoms (eg, cough, diarrhea, vomiting and nausea) similar to seasonal H3N2 and B virus infections. Among children 6 to 12 years old, there was a higher number of hospitalizations campared to other age groups. Identification of influenza virus types A and B using the QuickVue rapid diagnostic test was found to be equally sensitive for pH1N1 (50.4%), H3N2 (51.7%) and influenza B (53.9%) viruses, although the sensitivity was low among all subtypes. The pH1N1 virus rapidly became the dominant virus subtype in 2009 in Cambodia, but no symptoms consistently distinguished the pandemic strain from other influenza virus subtypes. The QuickVue test was as sensitive for detecting pH1N1 viral as well as other circulating seasonal influenza viruses.
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- 2012
71. Population-based active surveillance cohort studies for influenza: lessons from Peru
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Ernesto J. Ortiz, Andrew J. Bennett, Yeny Tinoco, Jorge Gomez, J.S. Bresee, Erik J. Reaves, Joel M. Montgomery, Victor Alberto Laguna-Torres, Timothy M. Uyeki, Marc-Alain Widdowson, Maya Williams, Maria Claudia Guezala, Eric S. Halsey, Maria Silva, Candice Romero, Eduardo Azziz-Baumgartner, Hugo Razuri, Ann Moen, and Daniel G. Bausch
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Disease surveillance ,medicine.medical_specialty ,Case detection ,business.industry ,Public health ,Public Health, Environmental and Occupational Health ,Population based ,World Health Organization ,Risk Assessment ,World health ,Cohort Studies ,Influenza A Virus, H1N1 Subtype ,Environmental health ,Pandemic ,Influenza, Human ,Peru ,Medicine ,Humans ,Risk assessment ,business ,Pandemics ,Sentinel Surveillance ,Cohort study ,Perspectives - Abstract
Disease surveillance, essential for guid -ing the public health response to influ-enza and other respiratory diseases, al-lows for early case detection and for the implementation of preventive measures. The World Health Organization (WHO) recommends passive health-provider based surveillance, or “sentinel surveil -lance”, for influenza-like illness (ILI)
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- 2012
72. Emergent 2009 influenza A(H1N1) viruses containing HA D222N mutation associated with severe clinical outcomes in the Americas
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Jose L. Sanchez, Richard W. Douce, Wilson Chicaiza, Yanfei Zhou, Patrick J. Blair, Gregory Deye, Maya Williams, Christopher A. Myers, Huo-Shu H. Houng, Kristina St. Clair, Arthur Lyons, Eric S. Halsey, Jason Garner, Robert A. Kuschner, and Ronald L Burke
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Adult ,Male ,Virulence ,Influenza season ,Hemagglutinin Glycoproteins, Influenza Virus ,Acute respiratory distress ,Biology ,Receptor binding site ,Communicable Diseases, Emerging ,Influenza A Virus, H1N1 Subtype ,Virology ,Influenza, Human ,Humans ,Mexico ,Respiratory Tract Infections ,Phylogeny ,Binding Sites ,Outbreak ,Influenza a ,Pneumonia ,Middle Aged ,Infectious Diseases ,Amino Acid Substitution ,District of Columbia ,Mutation ,Amino acid change ,Severe morbidity ,Receptors, Virus ,Female ,Ecuador - Abstract
Background During the 2010–2011 influenza season, a small sub-group of 2009 influenza A(H1N1) viruses (hereafter referred to as 2009 A(H1N1)) emerged that was associated with more severe clinical outcomes in Ecuador and North America. Genetically, the haemagglutinin (HA) of this sub-clade was distinct from HAs found in viruses associated with severe outbreaks in 2010 from the United Kingdom and from other global specimens isolated earlier in the season. Objective We report the emergence of a novel 2009 A(H1N1) variant possessing a re-emergent HA D222N mutation obtained from patients with severe respiratory illnesses and phylogenetically characterise these D222N mutants with other severe disease-causing variants clustering within a common emerging sub-clade. Case reports In early 2011, three cases of 2009 A(H1N1) infection, two from Quito, Ecuador, and one from Washington, DC, USA, were complicated by severe pneumonia requiring mechanical ventilation, resulting in one fatality. These cases were selected due to the reported nature of the acute respiratory distress (ARD) that were captured in Department of Defence (DoD)-sponsored global influenza surveillance nets. Results Genetically, the 2009 A(H1N1) strains isolated from two of the three severe cases carried a prominent amino acid change at position 222 (D222N) within the primary HA receptor binding site. Furthermore, these cases represent an emerging sub-clade of viruses defined by amino acid changes within HA: N31D, S162N, A186T and V272I. Phylogenetically, these viruses share a high degree of homology with strains associated with recent fatal cases in Chihuahua, Mexico. Discussion Previously, enhanced virulence associated with the change, D222G, has been clinically linked to severe morbidity and mortality. Initial observations of the prevalence of a novel sub-clade of strains in the Americas suggest that viruses with a re-emergent D222N mutation may too correlate with severe clinical manifestations. These findings warrant heightened vigilance for emerging sub-clades of 2009 A(H1N1) and presumptive clinical implications.
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- 2011
73. Evidence of human hantavirus infection and zoonotic investigation of hantavirus prevalence in rodents in western Java, Indonesia
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Bachti Alisjahbana, Patrick J. Blair, Susana Widjaja, Iing H. Yo, Yumilia Hoo, Herman Kosasih, Ima Nurisa Ibrahim, Rudi Wicaksana, Ungke Antonjaya, Maya Williams, and Imelda Winoto
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Adult ,Male ,Java ,Hantavirus Infections ,information science ,Rodentia ,Biology ,Antibodies, Viral ,Microbiology ,Virology ,Zoonoses ,Prevalence ,Animals ,Humans ,natural sciences ,computer.programming_language ,Hantavirus ,virus diseases ,humanities ,Infectious Diseases ,Immunoglobulin M ,Indonesia ,Immunoglobulin G ,Population Surveillance ,Immunology ,Hantavirus Infection ,computer - Abstract
During febrile surveillance in the western Java City of Bandung, Indonesia, a patient with clinical symptoms consistent with hantavirus infection was found to have elevated titers of hantavirus-specific immunoglobulin M (IgM) and IgG antibodies. A subsequent epizoological investigation demonstrated a higher prevalence of hantavirus IgG antibodies in rodents trapped in the vicinity of the patient's home compared with rodents from a control area (13.2% vs. 4.7%, p = 0.036). The Old World Seoul hantavirus was detected by reverse transcriptase-polymerase chain reaction in the organs of 71% of the seropositive rodents tested. This is the first report of a Seoul virus infection in Indonesia supported by clinical, serological, and epizoological evidences. These findings suggest that hantavirus infection should be on the clinical differential diagnosis when acutely ill febrile patients report for care in western Java.
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- 2010
74. H5N1 surveillance in migratory birds in Java, Indonesia
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Patrick J. Blair, Ima Nurisa Ibrahim, Arik Farzeli, Shannon D. Putnam, N. Hidayatullah, Maya Williams, Mochamad Indrawan, Ige Kristanto, S. Purnama, A.M. Tampubolon, Arthur C. Stoops, Timothy Burgess, Lim W. Sin, Ungke Antonjaya, Katie A. Barbara, Steve Tobias, Susan Wijaya, Adam Supriatna, and Wicaksana B. Petrus
- Subjects
Sandpiper ,Hemagglutination ,Zoology ,Enzyme-Linked Immunosorbent Assay ,Biology ,medicine.disease_cause ,Antibodies, Viral ,Microbiology ,law.invention ,Serology ,Birds ,Cloaca ,law ,Virology ,biology.animal ,medicine ,Prevalence ,Animals ,Polymerase chain reaction ,Phylogeny ,Hemagglutination assay ,Influenza A Virus, H5N1 Subtype ,Reverse Transcriptase Polymerase Chain Reaction ,Zoonosis ,medicine.disease ,biology.organism_classification ,Influenza A virus subtype H5N1 ,Infectious Diseases ,Indonesia ,Influenza in Birds ,Population Surveillance ,Pharynx ,Animal Migration ,Heron ,Databases, Nucleic Acid - Abstract
We sought to elucidate the role of migratory birds in transmission of H5N1 in an enzoonotic area. Resident, captive, and migratory birds were sampled at five sites in Java, Indonesia. Mist nets were used to trap birds. Birds were identified to species. RNA was extracted from swabs and reverse transcriptase polymerase chain reaction (RT-PCR) conducted for the HA and M genes of H5N1. Antibodies were detected by enzyme-linked immunosorbent assay and hemagglutination inhibition test. Between October 2006 and September 2007, a total of 4,067 captive, resident, and migratory birds comprising 98 species in 23 genera were sampled. The most commonly collected birds were the common sandpiper (6% of total), striated heron (3%), and the domestic chicken (14%). The overall prevalence of H5N1 antibodies was 5.3%. A significantly higher percentage of captive birds (16.1%) showed antibody evidence of H5N1 exposure when compared to migratory or resident birds. The greatest number of seropositive birds in each category were Muschovy duck (captive), striated heron (resident), and the Pacific golden plover (migratory). Seven apparently well captive birds yielded molecular evidence of H5N1 infection. Following amplification, the HA, NA, and M genes were analyzed. Phylogenetic analysis of the HA gene showed that the isolates were 97% similar to EU124153.1 A/chicken/West Java/Garut May 2006, an isolate obtained in a similar region of West Java. While no known markers of neuraminidase inhibitor resistance were found within the NA gene, M segment analysis revealed the V27A mutation known to confer resistance to adamantanes. Our results demonstrate moderate serologic evidence of H5N1 infection in captive birds, sampled in five sites in Java, Indonesia, but only occasional infection in resident and migratory birds. These data imply that in an enzoonotic region of Indonesia the role of migratory birds in transmission of H5N1 is limited.
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- 2009
75. Microglial activation is not prevented by tacrolimus but dopamine neuron damage is reduced in a rat model of Parkinson's disease progression
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Ann K. Wright, Maya Williams, Gordon W. Arbuthnott, and Clare E. Miller
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medicine.medical_specialty ,Parkinson's disease ,Time Factors ,Dopamine ,Substantia nigra ,Biology ,Globus Pallidus ,Neuroprotection ,Tacrolimus ,Lesion ,chemistry.chemical_compound ,Internal medicine ,medicine ,Animals ,Gliosis ,Molecular Biology ,Neurons ,Cell Death ,General Neuroscience ,MPTP ,Dopaminergic ,Parkinson Disease ,medicine.disease ,Rats ,Substantia Nigra ,Disease Models, Animal ,Globus pallidus ,Endocrinology ,Neuroprotective Agents ,nervous system ,chemistry ,Disease Progression ,Neurology (clinical) ,Microglia ,medicine.symptom ,Developmental Biology ,medicine.drug - Abstract
A progressive model of Parkinson's disease has been recently developed in the rat where a unilateral excitotoxic injection into the globus pallidus leads to a gradual loss of dopaminergic neurons in the ipsilateral substantia nigra over a period of at least 6 weeks. In this model microglial activation is observed in the ipsilateral substantia nigra 3 weeks after the lesion and could contribute to neuronal death at this time. The immunosuppressant drug tacrolimus (FK506) reduces dopamine cell death at 3 weeks following a globus pallidus lesion, but not thereafter. Tacrolimus-mediated neuroprotection could result from suppression of microglial activation but the microglial activation at three weeks post-lesion was not much reduced. Microglial activation was observed even in the apparent absence of neuronal death, prompting the suggestion that tacrolimus may prevent, or at least delay, the release of toxic cytokines from activated microglia. By 6 weeks after the GP lesion, even this mechanism fails to protect the dopamine cells from damage.
- Published
- 2008
76. HIV-1 Nef disrupts MHC-I trafficking by recruiting AP-1 to the MHC-I cytoplasmic tail
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Kathleen L. Collins, Jeremiah F. Roeth, Maya Williams, Matthew R. Kasper, and Tracey Filzen
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Cytoplasm ,Protein subunit ,T-Lymphocytes ,Antigen presentation ,Adaptor Protein Complex 1 ,chemical and pharmacologic phenomena ,HIV Infections ,Major histocompatibility complex ,Models, Biological ,Gene Products, nef ,Article ,Cell Line ,03 medical and health sciences ,MHC class I ,Cytotoxic T cell ,Humans ,nef Gene Products, Human Immunodeficiency Virus ,Binding site ,Research Articles ,030304 developmental biology ,0303 health sciences ,Antigen Presentation ,Binding Sites ,biology ,030302 biochemistry & molecular biology ,Cell Membrane ,Histocompatibility Antigens Class I ,Signal transducing adaptor protein ,virus diseases ,Cell Biology ,3. Good health ,Transport protein ,Cell biology ,Adaptor Protein Complex mu Subunits ,Protein Structure, Tertiary ,Protein Transport ,biology.protein ,HIV-1 ,Lysosomes ,trans-Golgi Network - Abstract
To avoid immune recognition by cytotoxic T lymphocytes (CTLs), human immunodeficiency virus (HIV)-1 Nef disrupts the transport of major histocompatibility complex class I molecules (MHC-I) to the cell surface in HIV-infected T cells. However, the mechanism by which Nef does this is unknown. We report that Nef disrupts MHC-I trafficking by rerouting newly synthesized MHC-I from the trans-Golgi network (TGN) to lysosomal compartments for degradation. The ability of Nef to target MHC-I from the TGN to lysosomes is dependent on expression of the μ1 subunit of adaptor protein (AP) AP-1A, a cellular protein complex implicated in TGN to endolysosomal pathways. We demonstrate that in HIV-infected primary T cells, Nef promotes a physical interaction between endogenous AP-1 and MHC-I. Moreover, we present data that this interaction uses a novel AP-1 binding site that requires amino acids in the MHC-I cytoplasmic tail. In sum, our evidence suggests that binding of AP-1 to the Nef–MHC-I complex is an important step required for inhibition of antigen presentation by HIV.
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- 2004
77. Little Evidence of Subclinical Avian Influenza Virus Infections among Rural Villagers in Cambodia
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Thomas F. Wierzba, Chadwick Y. Yasuda, Shannon D. Putnam, Gary L. Heil, Maya Williams, Channimol Chum, Whitney S. Krueger, Patrick J. Blair, Gregory C. Gray, Benjamin Anderson, Matthew R. Kasper, and Vonthanak Saphonn
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Rural Population ,Viral Diseases ,Epidemiology ,lcsh:Medicine ,Global Health ,medicine.disease_cause ,Cohort Studies ,0302 clinical medicine ,Zoonoses ,Influenza A Virus, H9N2 Subtype ,Medicine and Health Sciences ,Influenza A virus ,Public and Occupational Health ,030212 general & internal medicine ,lcsh:Science ,Prospective cohort study ,Avian influenza A viruses ,Subclinical infection ,0303 health sciences ,Multidisciplinary ,Antibody titer ,virus diseases ,Medical microbiology ,3. Good health ,Infectious Diseases ,Veterinary Diseases ,Cohort ,Human mortality from H5N1 ,Cambodia ,Research Article ,Cohort study ,Adult ,Microbiology ,Infectious Disease Epidemiology ,Animal Influenza ,03 medical and health sciences ,Influenza, Human ,medicine ,Humans ,Influenza viruses ,Influenza A Virus, H5N1 Subtype ,Biology and life sciences ,Population Biology ,030306 microbiology ,business.industry ,lcsh:R ,Viral pathogens ,Veterinary Virology ,Virology ,Influenza ,Influenza A virus subtype H5N1 ,Microbial pathogens ,lcsh:Q ,Veterinary Science ,business ,Orthomyxoviruses - Abstract
In 2008, 800 adults living within rural Kampong Cham Province, Cambodia were enrolled in a prospective cohort study of zoonotic influenza transmission. After enrollment, participants were contacted weekly for 24 months to identify acute influenza-like illnesses (ILI). Follow-up sera were collected at 12 and 24 months. A transmission substudy was also conducted among the family contacts of cohort members reporting ILI who were influenza A positive. Samples were assessed using serological or molecular techniques looking for evidence of infection with human and avian influenza viruses. Over 24 months, 438 ILI investigations among 284 cohort members were conducted. One cohort member was hospitalized with a H5N1 highly pathogenic avian influenza (HPAI) virus infection and withdrew from the study. Ninety-seven ILI cases (22.1%) were identified as influenza A virus infections by real-time RT-PCR; none yielded evidence for AIV. During the 2 years of follow-up, 21 participants (3.0%) had detectable antibody titers (≥ 1:10) against the studied AIVs: 1 against an avian-like A/Migratory duck/Hong Kong/MPS180/2003(H4N6), 3 against an avian-like A/Teal/Hong Kong/w312/97(H6N1), 9 (3 of which had detectible antibody titers at both 12- and 24-month follow-up) against an avian-like A/Hong Kong/1073/1999(H9N2), 6 (1 detected at both 12- and 24-month follow-up) against an avian-like A/Duck/Memphis/546/74(H11N9), and 2 against an avian-like A/Duck/Alberta/60/76(H12N5). With the exception of the one hospitalized cohort member with H5N1 infection, no other symptomatic avian influenza infections were detected among the cohort. Serological evidence for subclinical infections was sparse with only one subject showing a 4-fold rise in microneutralization titer over time against AvH12N5. In summary, despite conducting this closely monitored cohort study in a region enzootic for H5N1 HPAI, we were unable to detect subclinical avian influenza infections, suggesting either that these infections are rare or that our assays are insensitive at detecting them.
- Published
- 2014
78. Transgenic mice expressing mutated full-length HD cDNA: a paradigm for locomotor changes and selective neuronal loss in Huntington's disease
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Danilo A. Tagle, William O. Whetsell, Vinod Charles, Maya Williams, P. Hemachandra Reddy, and Georgina F. Miller
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Genetically modified mouse ,Huntingtin ,DNA, Complementary ,Transgene ,Mice, Transgenic ,Nerve Tissue Proteins ,Biology ,Motor Activity ,General Biochemistry, Genetics and Molecular Biology ,Mice ,Huntington's disease ,medicine ,Animals ,Humans ,Gliosis ,Neurons ,Huntingtin Protein ,Neurodegeneration ,Brain ,Nuclear Proteins ,Exons ,Trinucleotide repeat disorder ,medicine.disease ,Cell biology ,medicine.anatomical_structure ,Huntington Disease ,Phenotype ,Cerebral cortex ,General Agricultural and Biological Sciences ,Trinucleotide repeat expansion ,Peptides ,Trinucleotide Repeat Expansion ,Neuroscience ,Research Article - Abstract
Huntington's disease (HD) is a progressive neurodegenerative disorder characterized clinically by motor and psychiatric disturbances and pathologically by neuronal loss and gliosis (reactive astrocytosis) particularly in the striatum and cerebral cortex. We have recently created HD full-length cDNA transgenic mouse models that may serve as a paradigm for HD. A more detailed characterization of these models is presented here. The transgene encoding normal huntingtin consists of 9417 bp of the huntingtin coding sequences including 16 tandem CAGs coding for polyglutamines as part of exon 1. The transgene is driven by a heterologous cytomegalovirus promoter. Five independent transgenic mouse lines were obtained using this construct. An additional six transgenic lines were obtained using full-length HD constructs that have been modified to include either 48 or 89 CAG repeat expansions. Southern blot and densitometric analyses indicated unique integration sites for the transgene in each of the lines with a copy number ranging from two to 22 copies. Widespread expression of the transgene in brain, heart, spleen, kidney, lung, liver and gonads from each line was determined by Western blot analyses. In the brain, transgene expression was found in cerebral cortex, striatum, hippocampus and cerebellum. Expression of the transgene was as much as five times the endogenous mouse huntingtin level. Phenotypically, only mice expressing 48 or 89 CAG repeats manifested progressive behavioural and motor dysfunction. Early behavioural abnormalities were characterized by trunk curling and clasping of both fore- and hindlimbs when the animals were suspended by their tails. Subsequently, these mice exhibited hyperkinetic movements, including heightened exploratory activities, unidirectional rotational behaviour, backflipping and excessive grooming that lasted for several weeks. Eventually, the animals progressed to a hypokinetic phase consisting of slowed movements and lack of response to sensory stimuli. Urine retention or incontinence was also a prominent feature of the hypokinetic phase. At the end stage of the disease process, HD48(B,D) and HD89(A-C) mice became akinetic just prior to death. Neuropathological examination of mice at various stages indicated that it was only during the hypokinetic phase and thereafter when selective neuronal loss was most apparent. Regions of neurodegeneration and loss included the striatum, cerebral cortex, thalamus and hippocampus. TUNEL staining indicated an apoptotic mode of cell death in these brain regions. Comparative neuronal counts after Nissl staining showed as much as 20% loss of small and medium neurons in the striatum in mice at the hypokinetic and akinetic stages. Reactive astrocytosis accompanied the areas of neurodegeneration and loss. Polyglutamine aggregates in the form of neuronal intranuclear inclusions and diffuse nuclear and perinuclear aggregations were found in a small percentage of neurons, including those in brain regions that are typically spared in HD. This observation suggests that polyglutamine aggregates may not be sufficient to cause neuronal loss in HD. In both behavioural and neuropathological analyses, wild-type and transgenic animals with 16 CAG repeats were indistinguishable from each other and do not exhibit the changes observed for mice carrying the 48 and 89 CAG repeat mutations. Thus, animals expressing the CAG repeat expansions appear to represent clinically analogous models for HD pathogenesis, and may also provide insights into the underlying pathophysiological mechanisms of other triplet repeat disorders.
- Published
- 1999
79. Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA
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Maya Williams, William O. Whetsell, P. Hemachandra Reddy, Vinod Charles, Georgina F. Miller, Danilo A. Tagle, Lisa Pike-Buchanan, and Lisa Garrett
- Subjects
Huntingtin ,DNA, Complementary ,Thalamus ,Restriction Mapping ,Hippocampus ,Apoptosis ,Mice, Transgenic ,Nerve Tissue Proteins ,Striatum ,Biology ,Mice ,Degenerative disease ,Trinucleotide Repeats ,Genetics ,medicine ,Animals ,Humans ,Ubiquitins ,Neurons ,Huntingtin Protein ,Behavior, Animal ,Subthalamus ,Nuclear Proteins ,medicine.disease ,Corpus Striatum ,medicine.anatomical_structure ,Huntington Disease ,Gliosis ,Cerebral cortex ,medicine.symptom ,Neuroscience - Abstract
Huntington disease (HD) is an adult-onset, autosomal dominant inherited human neurodegenerative disorder characterized by hyperkinetic involuntary movements, including motor restlessness and chorea, slowing of voluntary movements and cognitive impairment. Selective regional neuron loss and gliosis in striatum, cerebral cortex, thalamus, subthalamus and hippocampus 1,2,3,4 are well recognized as neuropathological correlates for the clinical manifestations of HD. The underlying genetic mutation is the expansion of CAG trinucleotide repeats (coding for polyglutamines) to 36-121 copies in exon 1 of the HD gene 5,6,7,8. The HD mRNA and protein product (huntingtin) show widespread distribution9,10,11, and thus much remains to be understood about the selective and progressive neurodegeneration in HD. To create an experimental animal model for HD, transgenic mice were generated showing widespread expression of full-length human HD cDNA with either 16, 48 or 89 CAG repeats. Only mice with 48 or 89 CAG repeats manifested progressive behavioural and motor dysfunction with neuron loss and gliosis in striatum, cerebral cortex, thalamus and hippocampus. These animals represent clinically relevant models for HD pathogenesis, and may provide insights into the underlying pathophysiological mechanisms of other triplet repeat disorders.
- Published
- 1998
80. Evidence for Endemic Chikungunya Virus Infections in Bandung, Indonesia
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Timothy Burgess, Ungke Antonjaya, Bachti Alisjahbana, Herman Kosasih, Primal Sudjana, Chairin Nisa Ma'roef, Silvita Fitri Riswari, André J. A. M. van der Ven, Kevin R. Porter, Susana Widjaja, Maya Williams, and Quirijn de Mast
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Adult ,Male ,medicine.medical_specialty ,lcsh:Arctic medicine. Tropical medicine ,Adolescent ,Endemic Diseases ,lcsh:RC955-962 ,Molecular Sequence Data ,Antibodies, Viral ,medicine.disease_cause ,Dengue fever ,Cohort Studies ,Young Adult ,Epidemiology ,medicine ,Humans ,Prospective Studies ,Chikungunya ,Alphavirus infection ,Aged ,biology ,Alphavirus Infections ,Reverse Transcriptase Polymerase Chain Reaction ,Transmission (medicine) ,business.industry ,lcsh:Public aspects of medicine ,Incidence ,Incidence (epidemiology) ,Public Health, Environmental and Occupational Health ,virus diseases ,Outbreak ,lcsh:RA1-1270 ,Sequence Analysis, DNA ,Middle Aged ,medicine.disease ,Virology ,Infectious Diseases ,Immunoglobulin M ,Indonesia ,Immunoglobulin G ,biology.protein ,RNA, Viral ,Female ,Poverty-related infectious diseases Infectious diseases and international health [N4i 3] ,business ,Chikungunya virus ,Research Article - Abstract
Chikungunya virus (CHIKV) is known to cause sporadic or explosive outbreaks. However, little is known about the endemic transmission of CHIKV. To ascertain the endemic occurrence of CHIKV transmission, we tested blood samples from patients with a non-dengue febrile illness who participated in a prospective cohort study of factory workers in Bandung, Indonesia. From August 2000 to June 2004, and September 2006 to April 2008, 1901 febrile episodes occurred and 231 (12.2%) dengue cases were identified. The remaining febrile cases were evaluated for possible CHIKV infection by measuring anti-CHIKV IgM and IgG antibodies in acute and convalescent samples. Acute samples of serologically positive cases were subsequently tested for the presence of CHIKV RNA by RT-PCR and/or virus isolation. A total of 135 (7.1%) CHIKV infections were identified, providing an incidence rate of 10.1/1,000 person years. CHIKV infections were identified all year round and tended to increase during the rainy season (January to March). Severe illness was not found and severe arthralgia was not a prominently reported symptom. Serial post-illness samples from nine cases were tested to obtain a kinetic picture of IgM and IgG anti-CHIKV antibodies. Anti-CHIKV IgM antibodies were persistently detected in high titers for approximately one year. Three patients demonstrated evidence of possible sequential CHIKV infections. The high incidence rate and continuous chikungunya cases in this adult cohort suggests that CHIKV is endemically transmitted in Bandung. Further characterization of the circulating strains and surveillance in larger areas are needed to better understand CHIKV epidemiology in Indonesia., Author Summary Chikungunya is one of the neglected diseases. It has only attracted attention during outbreaks, in particular, the large epidemics in the Indian Ocean in 2005–2006. To our knowledge, there has never been any surveillance to determine the transmission of this virus among humans in non-outbreak settings. Such surveillance is particularly important because it will provide a better estimate of the disease burden and valuable information on how this virus is maintained outside outbreaks. Our study, conducted between 2000 and 2008 in Bandung, West Java, Indonesia, yielded several important findings: 1. Chikungunya is an important cause of fever among adults in Bandung, Indonesia. 2. The clinical symptoms are mostly mild and short lasting. 3. In addition to previously described epidemiological features involving episodic outbreaks, it is also continuously transmitted throughout the year. 4. A few patients may have experienced more than one chikungunya virus infection. 5. Only the Asian genotype was found and not the East Central South African genotype that was responsible for the 2005 outbreak in the Indian Ocean. 6. The persistence of IgM for a long period after illness may complicate the interpretation of laboratory results.
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- 2013
81. A growing global network’s role in outbreak response: AFHSC-GEIS 2008-2009
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Matthew C, Johns, Ronald L, Burke, Kelly G, Vest, Mark, Fukuda, Julie A, Pavlin, Sanjaya K, Shrestha, David C, Schnabel, Steven, Tobias, Jeffrey A, Tjaden, Joel M, Montgomery, Dennis J, Faix, Mark R, Duffy, Michael J, Cooper, Jose L, Sanchez, David L, Blazes, Sonam, Wangchuk, Tandin, Dorji, Robert, Gibbons, Sopon, Iamsirithaworn, Jason, Richardson, Rome, Buathong, Richard, Jarman, In-Kyu, Yoon, Geeta, Shakya, Victor, Ofula, Rodney, Coldren, Wallace, Bulimo, Rosemary, Sang, Duke, Omariba, Beryl, Obura, Dennis, Mwala, Matthew, Kasper, Gary, Brice, Maya, Williams, Chad, Yasuda, Robert V, Barthel, Guillermo, Pimentel, Chris, Meyers, Peter, Kammerer, Darcie E, Baynes, David, Metzgar, Anthony, Hawksworth, Patrick, Blair, Melody, Ellorin, Robert, Coon, Victor, Macintosh, Kristen, Burwell, Elizabeth, Macias, Thomas, Palys, and Kurt, Jerke
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Outbreak response ,medicine.medical_specialty ,Economic growth ,International Cooperation ,Review ,Disease ,Global Health ,World Health Organization ,Communicable Diseases, Emerging ,International Health Regulations ,Disease Outbreaks ,Government Agencies ,Environmental health ,Global network ,Humans ,Medicine ,Disease surveillance ,business.industry ,Public health ,Public Health, Environmental and Occupational Health ,Outbreak ,United States ,Military Personnel ,Communicable Disease Control ,Emerging infectious disease ,business ,Sentinel Surveillance - Abstract
A cornerstone of effective disease surveillance programs comprises the early identification of infectious threats and the subsequent rapid response to prevent further spread. Effectively identifying, tracking and responding to these threats is often difficult and requires international cooperation due to the rapidity with which diseases cross national borders and spread throughout the global community as a result of travel and migration by humans and animals. From Oct.1, 2008 to Sept. 30, 2009, the United States Department of Defense’s (DoD) Armed Forces Health Surveillance Center Global Emerging Infections Surveillance and Response System (AFHSC-GEIS) identified 76 outbreaks in 53 countries. Emerging infectious disease outbreaks were identified by the global network and included a wide spectrum of support activities in collaboration with host country partners, several of which were in direct support of the World Health Organization’s (WHO) International Health Regulations (IHR) (2005). The network also supported military forces around the world affected by the novel influenza A/H1N1 pandemic of 2009. With IHR (2005) as the guiding framework for action, the AFHSC-GEIS network of international partners and overseas research laboratories continues to develop into a far-reaching system for identifying, analyzing and responding to emerging disease threats.
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- 2011
82. H5N1 Surveillance in Migratory Birds in Java, Indonesia.
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Arthur C. Stoops, Katie A. Barbara, Mochamad Indrawan, Ima N. Ibrahim, Wicaksana B. Petrus, Susan Wijaya, Arik Farzeli, Ungke Antonjaya, Lim W. Sin, N. Hidayatullah, Ige Kristanto, A.M. Tampubolon, S. Purnama, Adam Supriatna, Timothy H. Burgess, Maya Williams, Shannon D. Putnam, Steve Tobias, and Patrick J. Blair
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H5N1 Influenza ,MIGRATORY birds ,INFLUENZA transmission ,REVERSE transcriptase polymerase chain reaction ,IDENTIFICATION of birds ,SANDPIPERS ,NEURAMINIDASE ,ADAMANTANE ,MOLECULAR phylogeny - Abstract
AbstractWe sought to elucidate the role of migratory birds in transmission of H5N1 in an enzoonotic area. Resident, captive, and migratory birds were sampled at five sites in Java, Indonesia. Mist nets were used to trap birds. Birds were identified to species. RNA was extracted from swabs and reverse transcriptase polymerase chain reaction (RT-PCR) conducted for the HA and M genes of H5N1. Antibodies were detected by enzyme-linked immunosorbent assay and hemagglutination inhibition test. Between October 2006 and September 2007, a total of 4,067 captive, resident, and migratory birds comprising 98 species in 23 genera were sampled. The most commonly collected birds were the common sandpiper (6% of total), striated heron (3%), and the domestic chicken (14%). The overall prevalence of H5N1 antibodies was 5.3%. A significantly higher percentage of captive birds (16.1%) showed antibody evidence of H5N1 exposure when compared to migratory or resident birds. The greatest number of seropositive birds in each category were Muschovy duck (captive), striated heron (resident), and the Pacific golden plover (migratory). Seven apparently well captive birds yielded molecular evidence of H5N1 infection. Following amplification, the HA, NA, and M genes were analyzed. Phylogenetic analysis of the HA gene showed that the isolates were 97% similar to EU124153.1 A/chicken/West Java/Garut May 2006, an isolate obtained in a similar region of West Java. While no known markers of neuraminidase inhibitor resistance were found within the NA gene, M segment analysis revealed the V27A mutation known to confer resistance to adamantanes. Our results demonstrate moderate serologic evidence of H5N1 infection in captive birds, sampled in five sites in Java, Indonesia, but only occasional infection in resident and migratory birds. These data imply that in an enzoonotic region of Indonesia the role of migratory birds in transmission of H5N1 is limited. [ABSTRACT FROM AUTHOR]
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- 2009
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83. Frequency of influenza H3N2 intra-subtype reassortment: attributes and implications of reassortant spread
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Patrick J. Blair, Tao Li, Melanie C. Melendrez, Richard G. Jarman, Leslie D. Edwards, Gary T. Brice, Irina Maljkovic Berry, Stephen J. Thomas, Anthony W. Hawksworth, In-Kyu Yoon, Robert A. Kuschner, Stefan Fernandez, Eric S. Halsey, Maya Williams, and Xiaoxu Lin
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0301 basic medicine ,Physiology ,Spread ,Reassortment ,Population ,Genome, Viral ,Plant Science ,Biology ,Genome ,General Biochemistry, Genetics and Molecular Biology ,Virus ,Evolution, Molecular ,03 medical and health sciences ,Structural Biology ,Influenza, Human ,Pandemic ,Humans ,Clade ,education ,Phylogeny ,Ecology, Evolution, Behavior and Systematics ,Genetics ,education.field_of_study ,Phylogenetic tree ,Agricultural and Biological Sciences(all) ,Biochemistry, Genetics and Molecular Biology(all) ,Influenza A Virus, H3N2 Subtype ,Cell Biology ,H3N2 ,Vaccine efficacy ,Influenza ,030104 developmental biology ,General Agricultural and Biological Sciences ,Research Article ,Developmental Biology ,Biotechnology - Abstract
Background Increasing evidence suggests that influenza reassortment not only contributes to the emergence of new human pandemics but also plays an important role in seasonal influenza epidemics, disease severity, evolution, and vaccine efficacy. We studied this process within 2091 H3N2 full genomes utilizing a combination of the latest reassortment detection tools and more conventional phylogenetic analyses. Results We found that the amount of H3N2 intra-subtype reassortment depended on the number of sampled genomes, occurred with a steady frequency of 3.35%, and was not affected by the geographical origins, evolutionary patterns, or previous reassortment history of the virus. We identified both single reassortant genomes and reassortant clades, each clade representing one reassortment event followed by successful spread of the reassorted variant in the human population. It was this spread that was mainly responsible for the observed high presence of H3N2 intra-subtype reassortant genomes. The successfully spread variants were generally sampled within one year of their formation, highlighting the risk of their rapid spread but also presenting an opportunity for their rapid detection. Simultaneous spread of several different reassortant lineages was observed, and despite their limited average lifetime, second and third generation reassortment was detected, as well as reassortment between viruses belonging to different vaccine-associated clades, likely displaying differing antigenic properties. Some of the spreading reassortants remained confined to certain geographical regions, while others, sharing common properties in amino acid positions of the HA, NA, and PB2 segments, were found throughout the world. Conclusions Detailed surveillance of seasonal influenza reassortment patterns and variant properties may provide unique information needed for prediction of spread and construction of future influenza vaccines. Electronic supplementary material The online version of this article (doi:10.1186/s12915-016-0337-3) contains supplementary material, which is available to authorized users.
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84. Department of Defense influenza and other respiratory disease surveillance during the 2009 pandemic
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Ronald L, Burke, Kelly G, Vest, Angelia A, Eick, Jose L, Sanchez, Matthew C, Johns, Julie A, Pavlin, Richard G, Jarman, Jerry L, Mothershead, Miguel, Quintana, Thomas, Palys, Michael J, Cooper, Jian, Guan, David, Schnabel, John, Waitumbi, Alisa, Wilma, Candelaria, Daniels, Matthew L, Brown, Steven, Tobias, Matthew R, Kasper, Maya, Williams, Jeffrey A, Tjaden, Buhari, Oyofo, Timothy, Styles, Patrick J, Blair, Anthony, Hawksworth, Joel M, Montgomery, Hugo, Razuri, Alberto, Laguna-Torres, Randal J, Schoepp, David A, Norwood, Victor H, Macintosh, Thomas, Gibbons, Gregory C, Gray, David L, Blazes, Kevin L, Russell, Jennifer, Rubenstein, Kyle, Hathaway, Robert, Gibbons, In-Kyu, Yoon, David, Saunders, Jariyanart, Gaywee, Mikal, Stoner, Ans, Timmermans, Sanjaya K, Shrestha, John Mark S, Velasco, Maria T, Alera, Darunee, Tannitisupawong, Khin Saw, Myint, Sathit, Pichyangkul, Ben, Woods, Kurt H, Jerke, Michael G, Koenig, Denis K, Byarugaba, Fred Wabwire, Mangen, Berhane, Assefa, Gary, Brice, Moustafa, Mansour, Guillermo, Pimentel, Peter, Sebeny, Maha, Talaat, Tamer, Saeed, Ben, Espinosa, Dennis, Faix, Ryan, Maves, Tadeusz, Kochel, James, Smith, Alicia, Guerrero, Gen, Maupin, Paul, Sjoberg, Mark, Duffy, Jason, Garner, Linda, Canas, Elizabeth, Macias, Robert A, Kuschner, Dennis, Shanks, Sheri, Lewis, Gosia, Nowak, Lucy M, Ndip, Nathan, Wolfe, and Karen, Saylors
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medicine.medical_specialty ,Respiratory Tract Diseases ,Disease ,Review ,medicine.disease_cause ,Global Health ,Military medicine ,Influenza A Virus, H1N1 Subtype ,Pandemic ,Global network ,Influenza, Human ,medicine ,Global health ,Influenza A virus ,Humans ,Military Medicine ,Pandemics ,business.industry ,Public health ,Public Health, Environmental and Occupational Health ,Capacity building ,virus diseases ,medicine.disease ,United States Department of Defense ,Virology ,United States ,Medical emergency ,business ,Sentinel Surveillance - Abstract
The Armed Forces Health Surveillance Center’s Division of Global Emerging Infections Surveillance and Response System (AFHSC-GEIS) supports and oversees surveillance for emerging infectious diseases, including respiratory diseases, of importance to the U.S. Department of Defense (DoD). AFHSC-GEIS accomplishes this mission by providing funding and oversight to a global network of partners for respiratory disease surveillance. This report details the system’s surveillance activities during 2009, with a focus on efforts in responding to the novel H1N1 Influenza A (A/H1N1) pandemic and contributions to global public health. Active surveillance networks established by AFHSC-GEIS partners resulted in the initial detection of novel A/H1N1 influenza in the U.S. and several other countries, and viruses isolated from these activities were used as seed strains for the 2009 pandemic influenza vaccine. Partners also provided diagnostic laboratory training and capacity building to host nations to assist with the novel A/H1N1 pandemic global response, adapted a Food and Drug Administration-approved assay for use on a ruggedized polymerase chain reaction platform for diagnosing novel A/H1N1 in remote settings, and provided estimates of seasonal vaccine effectiveness against novel A/H1N1 illness. Regular reporting of the system’s worldwide surveillance findings to the global public health community enabled leaders to make informed decisions on disease mitigation measures and controls for the 2009 A/H1N1 influenza pandemic. AFHSC-GEIS’s support of a global network contributes to DoD’s force health protection, while supporting global public health.
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