Expanded Dengue Syndrome by Tauqeer Hussain Mallhi & Yusra Habib Khan & Azreen Syazril Adnan & Nida Tanveer & Raja Ahsan Aftab

Author:Tauqeer Hussain Mallhi & Yusra Habib Khan & Azreen Syazril Adnan & Nida Tanveer & Raja Ahsan Aftab
Language: eng
Format: epub
ISBN: 9789811573378
Publisher: Springer Singapore

The mechanisms of neurological involvements during the course of DVI are assumed to be related to the specific type of neurological disease. However, viral and host factors play a pivotal role in the pathogenesis of disease. As described earlier, neuropathogenesis might be attributed to the direct viral invasion of the CNS [17], autoimmune reactions, and metabolic disturbances or alterations [18, 19]. Previously, dengue virus (DENV) was not considered as non-neurotropic. However, growing body of evidences has changed the concept and established neurotropic feature of DENV. The evidence of DENV in the CNS has already been described around 25 years ago [20, 21]. Moreover, it has been demonstrated that DENV damages blood–brain barrier (BBB) during infection in experimental animal models, indicating viral invasion [22]. Neurological complications according to the pathogenesis are described in Table 6.1. Initially DENV neurotropism in the human host was considered as opportunistic feature [24]. However, recent data establishes the notion that dengue virus is highly neurotropic in Aedes aegypti and is direct neurovirulent in humans [8, 25]. The neurological examinations of the CNS have detected viral proteins, ribonucleic acid (RNA), and immunoglobulins [26], indicating the DENV can actively enter the CNS [27]. Immunoreactive neurons, astrocytes, microglia, and endothelial cells have also been detected in cerebral tissues of a fatal case with dengue hemorrhagic fever [24]. Existing literature indicate that DENV-2 and DENV-3 are two common serotypes predominantly involved in the neurological complications [28, 29].Table 6.1Neurological complications in dengue according to pathogenesis

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