Dengue encephalopathy in children in Northern India: Clinical features and comparison with non dengue

Kumar, Rashmi; Tripathi, Shweta; Tambe, Joshua; Arora, Vanita; Srivastava, Amit; Nag, Vijaya Lakshmi

doi:10.1016/j.jns.2007.12.018

Cited by 70 publications

(52 citation statements)

References 16 publications

(24 reference statements)

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“…A large proportion of AES patients were found to be positive for DV. Unusual manifestations of dengue including encephalopathy, have been reported earlier from North India, although the prevalence of DV as a causative agent of AES in this study (8.92z) is lesser than that in the previous study (23.4z) (12). The pathogenesis of dengue encephalopathy has been attributed to multisystem derangement, including liver failure, shock, and coagulopathy, that accompanies severe infections; however, direct viral encephalitis resulting from dengue viral neurotropism has also been suggested (13).…”

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confidence: 67%

Epidemiology and Etiology of Acute Encephalitis Syndrome in North India

et al. 2014

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Section: Discussioncontrasting

confidence: 67%

Epidemiology and Etiology of Acute Encephalitis Syndrome in North India

et al. 2014

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“…Additionally, DENV-induced paralysis has been reported in numerous mouse models (4, 49), but only a few studies have investigated this phenomenon (1,18,20). Presently, whether DENV infects the CNS in natural human infections continues to be a subject of debate (25,30,32).Mice lacking the alpha/beta interferon and gamma interferon receptors (IFN-␣/␤R and IFN-␥R) in the 129/Sv genetic background (AG129) are highly susceptible to disease resembling human DHF/DSS, as well as paralysis, following infection with mouse-passaged variants of DENV2 clinical isolate PL046 (5,35,40,51). In contrast, congenic mice lacking only IFN-␣/␤R (A129) are largely protected from DENV-induced paralysis (39).…”

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confidence: 99%

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confidence: 99%

Gamma Interferon (IFN-γ) Receptor Restricts Systemic Dengue Virus Replication and Prevents Paralysis in IFN-α/β Receptor-Deficient Mice

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Zellweger

et al. 2012

J Virol

108

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T he four serotypes of dengue virus (DENV1 to -4) belong to the Flaviviridae family, which also includes West Nile virus (WNV), St. Louis encephalitis virus (SLEV), Japanese encephalitis virus (JEV), and yellow fever virus (YFV). More than 2.5 billion people live in areas where DENV is endemic, and approximately 50 million people are infected each year (17). DENV generally manifests as an acute systemic infection that is cleared within 14 days (46). In most cases, infected individuals develop a febrile illness (dengue fever [DF]) characterized by flu-like symptoms, often accompanied by retro-orbital pain, ostealgia, and maculopapular rash. In nearly 500,000 cases per year, patients develop severe vascular leakage, which may result in hypovolemic shock (dengue hemorrhagic fever/dengue shock syndrome [DHF/ DSS]), ultimately leading to fatality rates as high as 10 to 15% in some countries or more than 25,000 deaths worldwide each year (15,17). In a subset of both DF and DHF/DSS cases (16), DENV infection was linked to encephalitis and signs of encephalopathy, including lethargy, confusion, seizure, and coma, as well as delayed neurological symptoms, such as paralysis of extremities, loss of sensation, and psychosis (2,21,23,30,36,38,43). DENVinduced neurological disease is being increasingly recognized as an important component of dengue disease in humans independent of DF and DHF/DSS (24). The prevalence of DENV-induced neurological disease has been estimated to be 4.2% of DENV cases (44) and as high as 18% of undiagnosed suspected viral central nervous system (CNS) infections in regions where DENV is endemic (21, 23).In the last decade, DENV has increasingly been linked to neurological disease in both the presence and absence of DF. Viruses of the Flaviviridae family generally cluster in a phylogenetic pattern that mirrors the typical disease manifestations they cause (13); for example, encephalitic flaviviruses cluster together. DENV, however, usually causes hemorrhagic illness but is genetically more homologous to the encephalitic viruses, including WNV, SLEV, and JEV, than it is to other hemorrhagic flaviviruses, such as YFV, based on several analyses of the nonstructural (NS) proteins NS3 and NS5 (11, 13). The close relationship of DENV to encephalitic flaviviruses may help explain the capacity of DENV to cause neurological disease and, possibly, infection of the CNS in humans (6, 37). Additionally, DENV-induced paralysis has been reported in numerous mouse models (4, 49), but only a few studies have investigated this phenomenon (1,18,20). Presently, whether DENV infects the CNS in natural human infections continues to be a subject of debate (25,30,32).Mice lacking the alpha/beta interferon and gamma interferon receptors (IFN-␣/␤R and IFN-␥R) in the 129/Sv genetic background (AG129) are highly susceptible to disease resembling human DHF/DSS, as well as paralysis, following infection with mouse-passaged variants of DENV2 clinical isolate PL046 (5,35,40,51). In contrast, congenic mice lacking only IFN-␣/␤R (A12...

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“…Japanese encephalitis virus (JEV), dengue virus, chikungunya virus, and EV have been reported in encephalitis cases from India (12,13,16,20,21,27). Due to the large number of EV serotypes and their diverse clinical presentations (19), it is difficult to distinguish EV in encephalitis cases from other viruses, which is necessary for timely supportive therapy to avoid neurological sequelae (7).…”

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confidence: 99%