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MINIREVIEW

Alternate Hypothesis on the Pathogenesis of Dengue Hemorrhagic Fever (DHF)/Dengue Shock Syndrome (DSS) in Dengue Virus Infection

Sansanee Noisakran^*, and Guey Chuen Perng^,1

^* Medical Biotechnology Unit, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathumthani, 12120, Thailand; Medical Molecular Biology Unit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand; and Department of Pathology and Laboratory Medicine, Emory Vaccine Center, School of Medicine, Emory University, Atlanta, Georgia 30322

To whom requests for reprints should be addressed at ¹ Department of Pathology and Laboratory Medicine, Emory Vaccine Center, School of Medicine, Emory University, Dental Building Room 429, 1462 Clifton Road, Atlanta, GA 30322. E-mail: gperng{at}emory.edu

Dengue fever, caused by infection with dengue virus, is not a new disease, but recently because of its serious emerging health threats, coupled with possible dire consequences including death, it has aroused considerable medical and public health concerns worldwide. Today, dengue is considered one of the most important arthropod-borne viral diseases in humans in terms of morbidity and mortality. Globally, it is estimated that approximate 50 to 100 million new dengue virus infections occur annually. Among these, there are 200,000 to 500,000 cases of potential life-threatening dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS), characterized by thrombocytopenia and increased vascular permeability. The death rate associated with the more severe form DHF/DSS is approximately 5%, predominantly in children under the age of 15. Although intensive efforts have been made to study the early clinical pathophysiology of dengue infection with the objective to identify the potential cause of DHF, results or data that have accumulated from different regions of the world involving studies of different ethnicity groups are inconsistent at present in terms of identifying a unified hypothesis for the pathogenesis of DHF/DSS. Thus, the potential mechanisms involved in the pathogenesis of DHF and DSS remain elusive. The purpose of this review is to identify alternate factors, such as innate immune parameters, hyper-thermal factors, conditioning of neutralizing antibody, concept of vector transmission, and physical status of virus in viremic patients that may play a role in the induction of DHF and DSS, which might have directly or indirectly contributed to the discrepancies that are noted in the literature reported to date. It is the hope that identification of an alternative explanation for the pathogenesis of DHF/DSS will pave the way for the institution of new strategies for the prevention of this complicated disease.

Key Words: Flavivirus • DHF • DSS • emerging infectious disease

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