Pang Tikki, Cardosa Mary Jane, Guzman Maria G
Department of Research Policy and Cooperation, World Health Organization, Geneva, Switzerland.
Immunol Cell Biol. 2007 Jan;85(1):43-5. doi: 10.1038/sj.icb.7100008. Epub 2006 Nov 28.
The past four decades has witnessed a consolidation of the original observations made in the 1970s that dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) have an immunological basis. Following reinfection with a dengue virus of different serotype, severe disease is linked to high levels of antibody-enhanced viral replication early in illness which is followed by a cascade of memory T-cell activation and a 'storm' of inflammatory cytokines and other chemical mediators. These compounds are released mainly from T cells, monocytes/macrophages and endothelial cells, and ultimately cause an increase in vascular permeability. The consolidation of the evidence has been largely due to several important prospective sero-epidemiological studies in areas endemic for DHF/DSS, which have shown that risk of severe disease is significantly higher in secondary dengue infections. These advances have underscored the fact that DHF/DSS pathogenesis is a complex, multifactorial process involving cocirculation of various dengue virus serotypes and the interplay of host and viral factors that influence disease severity. The continued search to define risk factors in susceptible populations must be combined with the new techniques of molecular virology and innovative approaches in vaccine design to achieve the ultimate objective of developing a safe and effective vaccine.
在过去的四十年里，人们对20世纪70年代的原始观察结果进行了整合，这些观察结果表明登革出血热（DHF）和登革休克综合征（DSS）具有免疫学基础。再次感染不同血清型的登革病毒后，严重疾病与疾病早期高水平的抗体增强病毒复制有关，随后是一系列记忆T细胞激活以及炎症细胞因子和其他化学介质的“风暴”。这些化合物主要从T细胞、单核细胞/巨噬细胞和内皮细胞中释放出来，最终导致血管通透性增加。证据的整合很大程度上归功于在DHF/DSS流行地区进行的几项重要的前瞻性血清流行病学研究，这些研究表明，二次登革热感染中严重疾病的风险显著更高。这些进展强调了这样一个事实，即DHF/DSS的发病机制是一个复杂的多因素过程，涉及各种登革病毒血清型的共同循环以及影响疾病严重程度的宿主和病毒因素的相互作用。在易感人群中持续寻找危险因素的工作必须与分子病毒学的新技术以及疫苗设计的创新方法相结合，以实现开发安全有效疫苗的最终目标。
