Panpimon Luangtrakool1, Sasijit Vejbaesya1, Komon Luangtrakool1, Somporn Ngamhawornwong1, Kusuma Apisawes1, Siripen Kalayanarooj2, Louis R Macareo3, Stefan Fernandez3, Richard G Jarman4, Robert W M Collins5, Steven T Cox6, Anon Srikiatkhachorn7,8, Alan L Rothman7, Henry A F Stephens1,9. 1. Department of Transfusion Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand. 2. Queen Sirikit National Institute of Child Health, Bangkok, Thailand. 3. Department of Virology, Armed Forces Research Institute of Medical Science, Bangkok, Thailand. 4. Viral Diseases Branch, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA. 5. Clinical Science Laboratory, Guy's Hospital, London, United Kingdom. 6. Anthony Nolan Research Institute, Royal Free Hospital, London, United Kingdom. 7. Institute for Immunology and Informatics and Department of Cell and Molecular Biology, University of Rhode Island, Providence, Rhode Island, USA. 8. Faculty of Medicine, King Mongkut's Institute of Technology Ladkrabang, Bangkok, Thailand. 9. UCL Department of Renal Medicine and Anthony Nolan Laboratories, Royal Free NHS Foundation Trust, Royal Free Hospital, London, United Kingdom.
Abstract
BACKGROUND: Major histocompatibility complex class I chain-related (MIC) A and B (MICA and MICB) are polymorphic stress molecules recognized by natural killer cells. This study was performed to analyze MIC gene profiles in hospitalized Thai children with acute dengue illness. METHODS: MIC allele profiles were determined in a discovery cohort of patients with dengue fever or dengue hemorrhagic fever (DHF) (n = 166) and controls (n = 149). A replication cohort of patients with dengue (n = 222) was used to confirm specific MICB associations with disease. RESULTS: MICA*045 and MICB*004 associated with susceptibility to DHF in secondary dengue virus (DENV) infections (odds ratio [OR], 3.22; [95% confidence interval (CI), 1.18-8.84] and 1.99 [1.07-2.13], respectively), and MICB*002 with protection from DHF in secondary DENV infections (OR, 0.41; 95% CI, .21-.68). The protective effect of MICB*002 against secondary DHF was confirmed in the replication cohort (OR, 0.43; 95% CI, .22-.82) and was stronger when MICB*002 is present in individuals also carrying HLA-B*18, B*40, and B*44 alleles which form the B44 supertype of functionally related alleles (0.29, 95% CI, .14-.60). CONCLUSIONS: Given that MICB*002 is a low expresser of soluble proteins, these data indicate that surface expression of MICB*002 with B44 supertype alleles on DENV-infected cells confer a protective advantage in controlling DENV infection using natural killer cells.
BACKGROUND:Major histocompatibility complex class I chain-related (MIC) A and B (MICA and MICB) are polymorphic stress molecules recognized by natural killer cells. This study was performed to analyze MIC gene profiles in hospitalized Thai children with acute dengue illness. METHODS: MIC allele profiles were determined in a discovery cohort of patients with dengue fever or dengue hemorrhagic fever (DHF) (n = 166) and controls (n = 149). A replication cohort of patients with dengue (n = 222) was used to confirm specific MICB associations with disease. RESULTS:MICA*045 and MICB*004 associated with susceptibility to DHF in secondary dengue virus (DENV) infections (odds ratio [OR], 3.22; [95% confidence interval (CI), 1.18-8.84] and 1.99 [1.07-2.13], respectively), and MICB*002 with protection from DHF in secondary DENVinfections (OR, 0.41; 95% CI, .21-.68). The protective effect of MICB*002 against secondary DHF was confirmed in the replication cohort (OR, 0.43; 95% CI, .22-.82) and was stronger when MICB*002 is present in individuals also carrying HLA-B*18, B*40, and B*44 alleles which form the B44 supertype of functionally related alleles (0.29, 95% CI, .14-.60). CONCLUSIONS: Given that MICB*002 is a low expresser of soluble proteins, these data indicate that surface expression of MICB*002 with B44 supertype alleles on DENV-infected cells confer a protective advantage in controlling DENVinfection using natural killer cells.
Authors: Sasijit Vejbaesya; Rungrot Thongpradit; Siripen Kalayanarooj; Komon Luangtrakool; Panpimon Luangtrakool; Robert V Gibbons; Duangporn Srinak; Somporn Ngammthaworn; Kusuma Apisawes; In-Kyu Yoon; Stephen J Thomas; Richard G Jarman; Anon Srikiakthachorn; Sharone Green; Dasnayanee Chandanayingyong; Sangshin Park; Jennifer Friedman; Alan L Rothman; Henry A F Stephens Journal: J Infect Dis Date: 2015-03-04 Impact factor: 5.226
Authors: D W Vaughn; S Green; S Kalayanarooj; B L Innis; S Nimmannitya; S Suntayakorn; T P Endy; B Raengsakulrach; A L Rothman; F A Ennis; A Nisalak Journal: J Infect Dis Date: 2000-01 Impact factor: 5.226
Authors: Sasijit Vejbaesya; Panpimon Luangtrakool; Komon Luangtrakool; Siripen Kalayanarooj; David W Vaughn; Timothy P Endy; Mammen P Mammen; Sharone Green; Daniel H Libraty; Francis A Ennis; Alan L Rothman; Henry A F Stephens Journal: J Infect Dis Date: 2009-05-15 Impact factor: 5.226