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FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb

DENV causes significantly more human disease than any other abovirus. Annually, an estimated of 50-100 million cases of severe dengue require hospitalization in which 500,000 resulted in DHF/DSS, with more than 20,000 death worldwide (WHO DengueNet report, 2005). Hence, it has now been recognized as...

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Main Authors: Hoh, Boon Peng, Abu Bakar, Sazaly, Hanim Shueb, Rafidah
Format: Research Reports
Language:English
Published: Research Management Institute (RMI) 2011
Online Access:http://ir.uitm.edu.my/id/eprint/17267/1/LP_HOH%20BOON%20PENG%20RMI%2011_5.pdf
http://ir.uitm.edu.my/id/eprint/17267/
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spelling my.uitm.ir.172672019-11-11T04:00:22Z http://ir.uitm.edu.my/id/eprint/17267/ FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb Hoh, Boon Peng Abu Bakar, Sazaly Hanim Shueb, Rafidah DENV causes significantly more human disease than any other abovirus. Annually, an estimated of 50-100 million cases of severe dengue require hospitalization in which 500,000 resulted in DHF/DSS, with more than 20,000 death worldwide (WHO DengueNet report, 2005). Hence, it has now been recognized as a major expanding public health problem of the country. Dengue viruses cause a spectrum of illness ranging from asymptomatic infection or mild febrile illness to severe and fatal hemorrhagic disease. While majority experience uncomplicated Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) can present with severe clinical manifestations including transient vascular permeability resulting in plasma leakage (WHO, 1997). No specific treatment is available to date. Previous studies suggested the involvement of the events in the peripheral blood in association with the DENV disease severity, such as dengue viral replication, cytokine expression, and cellular activation / proliferation and robust host inflammatory immune response (Rothman, 2004). Antibody-dependent enhancement of viral replication is the most widely accepted explanation for the association between DHF and pre-existing antibody. However, it remains considerable uncertainty as to how virus-host interaction triggers the inflammatory response resulting in plasma leakage, the hallmark of DHF/DSS. FcGRII has been reported to play a role in pathogenesis of severe dengue infections (Loke et al., 2002; Littaua et al., 1990). It functions to mediate antibody enhancement in vitro by binding to virus-IgG complexes. A fundamental to any discussion of DENV pathogenesis is the association of secondary infection with heterologous serotypes with DHF/DSS. Antibody Dependent Enhancement (ADE) model during secondary infections, postulates that DENV specific antibodies either cross reactive antibodies, can interact with DENV without neutralizing the virus, and thereby requires FcG receptors to mediate entry of antibody coated DENV into cells (Clyde et al., 2006; Coffey et al, 2009). Therefore, this proposed study investigated and to characterized the CNV of FcGRII gene among the DF and DHF patients. Though association of FcGRII gene SNP polymorphism with dengue has been reported earlier (Loke et al, 2002), none investigated the copy number of this gene and its association to the susceptibility of plasma leakage. Research Management Institute (RMI) 2011 Research Reports NonPeerReviewed text en http://ir.uitm.edu.my/id/eprint/17267/1/LP_HOH%20BOON%20PENG%20RMI%2011_5.pdf Hoh, Boon Peng and Abu Bakar, Sazaly and Hanim Shueb, Rafidah (2011) FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb. [Research Reports] (Unpublished)
institution Universiti Teknologi Mara
building Tun Abdul Razak Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Teknologi Mara
content_source UiTM Institutional Repository
url_provider http://ir.uitm.edu.my/
language English
description DENV causes significantly more human disease than any other abovirus. Annually, an estimated of 50-100 million cases of severe dengue require hospitalization in which 500,000 resulted in DHF/DSS, with more than 20,000 death worldwide (WHO DengueNet report, 2005). Hence, it has now been recognized as a major expanding public health problem of the country. Dengue viruses cause a spectrum of illness ranging from asymptomatic infection or mild febrile illness to severe and fatal hemorrhagic disease. While majority experience uncomplicated Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) can present with severe clinical manifestations including transient vascular permeability resulting in plasma leakage (WHO, 1997). No specific treatment is available to date. Previous studies suggested the involvement of the events in the peripheral blood in association with the DENV disease severity, such as dengue viral replication, cytokine expression, and cellular activation / proliferation and robust host inflammatory immune response (Rothman, 2004). Antibody-dependent enhancement of viral replication is the most widely accepted explanation for the association between DHF and pre-existing antibody. However, it remains considerable uncertainty as to how virus-host interaction triggers the inflammatory response resulting in plasma leakage, the hallmark of DHF/DSS. FcGRII has been reported to play a role in pathogenesis of severe dengue infections (Loke et al., 2002; Littaua et al., 1990). It functions to mediate antibody enhancement in vitro by binding to virus-IgG complexes. A fundamental to any discussion of DENV pathogenesis is the association of secondary infection with heterologous serotypes with DHF/DSS. Antibody Dependent Enhancement (ADE) model during secondary infections, postulates that DENV specific antibodies either cross reactive antibodies, can interact with DENV without neutralizing the virus, and thereby requires FcG receptors to mediate entry of antibody coated DENV into cells (Clyde et al., 2006; Coffey et al, 2009). Therefore, this proposed study investigated and to characterized the CNV of FcGRII gene among the DF and DHF patients. Though association of FcGRII gene SNP polymorphism with dengue has been reported earlier (Loke et al, 2002), none investigated the copy number of this gene and its association to the susceptibility of plasma leakage.
format Research Reports
author Hoh, Boon Peng
Abu Bakar, Sazaly
Hanim Shueb, Rafidah
spellingShingle Hoh, Boon Peng
Abu Bakar, Sazaly
Hanim Shueb, Rafidah
FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb
author_facet Hoh, Boon Peng
Abu Bakar, Sazaly
Hanim Shueb, Rafidah
author_sort Hoh, Boon Peng
title FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb
title_short FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb
title_full FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb
title_fullStr FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb
title_full_unstemmed FCGR3B gene copy number variation and host susceptibility to vascular leakage in Dengue Hemorrhagic Fever / Hoh Boon Peng , Sazaly Abu Bakar and Rafidah Hanim Shueb
title_sort fcgr3b gene copy number variation and host susceptibility to vascular leakage in dengue hemorrhagic fever / hoh boon peng , sazaly abu bakar and rafidah hanim shueb
publisher Research Management Institute (RMI)
publishDate 2011
url http://ir.uitm.edu.my/id/eprint/17267/1/LP_HOH%20BOON%20PENG%20RMI%2011_5.pdf
http://ir.uitm.edu.my/id/eprint/17267/
_version_ 1685648919333175296
score 13.211869

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