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Your search keyword '"Nattaya Tangthawornchaikul"' showing total 2 results
Start Over Author "Nattaya Tangthawornchaikul" Journal journal of infectious diseases
2 results on '"Nattaya Tangthawornchaikul"'

1. High Anti–Dengue Virus Activity of theOASGene Family Is Associated With Increased Severity of Dengue

Author

Worachart Lert-itthiporn, Ampaiwan Chuansumrit, Nattaya Tangthawornchaikul, Richard Paul, Prida Malasit, Shyr Yi Lin, Anavaj Sakuntabhai, Han Pang Yu, Etienne Simon-Loriere, Prapat Suriyaphol, Kanchana Tangnararatchakit, Philipe Despres, Wathanee Chaiyaratana, Bi Lan Chang, Sutee Yoksan, Sirijitt Vasanawathana, Ren-Jye Lin, Isabelle Casademont, Yi-Ling Lin, Sita Mint Kalayanarooj, Génétique fonctionnelle des Maladies infectieuses - Functional Genetics of Infectious Diseases, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Mahidol University [Bangkok], Academia Sinica, Siriraj Hospital, Mahidol University, Ramathibodi Hospital, National Science and Technology Development Agency [Bangkok] (NSTDA), Khon Kaen Hospital, Center for Vaccine Development, Mahidol University [Bangkok]-Institute of Science and Technology for Research and Development, Interactions Moléculaires Flavivirus-Hôtes, Institut Pasteur [Paris], Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), and Institut Pasteur [Paris] (IP)

Subjects
Male, [SDV]Life Sciences [q-bio], viruses, MESH: Dengue, Dengue virus, MESH: Dengue Virus, medicine.disease_cause, Dengue fever, Dengue, Interferon, MESH: Child, Genotype, 2',5'-Oligoadenylate Synthetase, Immunology and Allergy, Child, innate immunity, Cells, Cultured, MESH: 2',5'-Oligoadenylate Synthetase, MESH: Genetic Association Studies, MESH: Genetic Predisposition to Disease, virus diseases, interferon, MESH: Infant, 3. Good health, Infectious Diseases, MESH: Young Adult, Child, Preschool, cytokine storm, Female, Viral disease, MESH: Cells, Cultured, medicine.drug, Adult, Adolescent, Biology, Young Adult, Immune system, medicine, Humans, Genetic Predisposition to Disease, Genetic Association Studies, MESH: Adolescent, MESH: Humans, Innate immune system, dengue virus, MESH: Child, Preschool, Infant, MESH: Adult, biochemical phenomena, metabolism, and nutrition, medicine.disease, Virology, MESH: Male, Immunology, Cytokine storm, MESH: Female, genetic susceptibility
Abstract

International audience; Dengue is a mosquito-borne viral disease that afflicts millions of individuals worldwide every year. Infection by any of the 4 dengue virus (DENV) serotypes can result in a spectrum of disease severity. We investigated the impact of variants of interferon-regulated innate immunity genes with a potent antiviral effect on the outcome of DENV infection. We compared the effect of OAS gene family variants on 2 DENV serotypes in cell culture. While both OAS1-p42 and p46 showed antiviral activity against DENV-2, only OAS1-p42 presented anti-DENV-1 activity. Conversely, whereas both OAS3_S381 and R381 variants were able to block DENV-1 infection, the anti-DENV-2 activity observed for OAS3_S381 was largely lost for the R381 variant. By means of an allelic association study of a cohort of 740 patients with dengue, we found a protective effect of OAS3_R381 against shock (odds ratio [OR], 0.37; P < .001). This effect was due to DENV-2 infections (OR, 0.13; P = .007) but was absent for DENV-1, in accordance with the serotype-dependent OAS3 activity found in the functional study. Severe dengue has long been associated with a cytokine storm of unclear origin. This work identifies an early innate immunity process that could lead to the immune overreaction observed in severe dengue and could be triggered by a specific host genotype-pathogen genotype interaction.

Published
2015

2. Vascular Leakage in Severe Dengue Virus Infections: A Potential Role for the Nonstructural Viral Protein NS1 and Complement.

Author

Panisadee Avirutnan, Nuntaya Punyadee, Sansanee Noisakran, Chulaluk Komoltri, Somchai Thiemmeca, Kusuma Auethavornanan, Aroonroong Jairungsri, Rattiyaporn Kanlaya, Nattaya Tangthawornchaikul, Chunya Puttikhunt, Sa-nga Pattanakitsakul, Pa-thai Yenchitsomanus, Juthathip Mongkolsapaya, Watchara Kasinrerk, Nopporn Sittisombut, Husmann, Matthias, Blettner, Maria, Sirijitt Vasanawathana, Bhakdi, Sucharit, and Prida Malasit

Subjects
DENGUE viruses, ENZYME activation, VIRAL proteins, MONOCLONAL antibodies, IMMUNOGLOBULINS, ENZYME regulation, IMMUNITY
Abstract

Background. Vascular leakage and shock are the major causes of death in patients with dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Thirty years ago, complement activation was proposed to be a key underlying event, but the cause of complement activation has remained unknown. Methods. The major nonstructural dengue virus (DV) protein NS1 was tested for its capacity to activate human complement in its membrane-associated and soluble forms. Plasma samples from 163 patients with DV infection and from 19 patients with other febrile illnesses were prospectively analyzed for viral load and for levels of NS1 and complement-activation products. Blood and pleural fluids from 9 patients with DSS were also analyzed. Results. Soluble NS1 activated complement to completion, and activation was enhanced by polyclonal and monoclonal antibodies against NS1. Complement was also activated by cell-associated NS1 in the presence of specific antibodies. Plasma levels of NS1 and terminal SC5b-9 complexes correlated with disease severity. Large amounts of NS1, complement anaphylatoxin C5a, and the terminal complement complex SC5b-9 were present in pleural fluids from patients with DSS. Conclusions. Complement activation mediated by NS1 leads to local and systemic generation of anaphylatoxins and SC5b-9, which may contribute to the pathogenesis of the vascular leakage that occurs in patients with DHF/DSS. [ABSTRACT FROM AUTHOR]

Published
2006
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