Noisakran Sansanee, Perng Guey Chuen
Medical Biotechnology Unit, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathumthani, 12120, Thailand.
Exp Biol Med (Maywood). 2008 Apr;233(4):401-8. doi: 10.3181/0707-MR-198.
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.
登革热由登革病毒感染引起，并非新出现的疾病，但近来因其对健康构成严重的新威胁，以及可能导致包括死亡在内的可怕后果，已引起全球医学界和公共卫生领域的广泛关注。如今，就发病率和死亡率而言，登革热被视为人类最重要的节肢动物传播病毒性疾病之一。据估计，全球每年约有5000万至1亿人感染新型登革病毒。其中，有20万至50万例可能危及生命的登革出血热（DHF）/登革休克综合征（DSS），其特征为血小板减少和血管通透性增加。与更严重的DHF/DSS相关的死亡率约为5%，主要发生在15岁以下的儿童中。尽管已付出巨大努力研究登革热感染的早期临床病理生理学，旨在确定DHF的潜在病因，但目前来自世界不同地区、涉及不同种族群体研究积累的结果或数据，在确定DHF/DSS发病机制的统一假说方面并不一致。因此，DHF和DSS发病机制中涉及的潜在机制仍不明确。本综述的目的是确定其他因素，如先天免疫参数、高温因素、中和抗体的调节、媒介传播概念以及病毒血症患者体内病毒的物理状态，这些因素可能在DHF和DSS的诱发中起作用，而这可能直接或间接导致了迄今文献报道中出现的差异。希望确定DHF/DSS发病机制的另一种解释，将为制定预防这种复杂疾病的新策略铺平道路。
