Abstract:
The severity of dengue isrnoften ascribed to secondary infection with a virus belonging to a
serotyperndistinct from that of the primary infection. Severe
pathogenicity of DENV might be regulated at the genetic level and mayrnbe associated with unusual mutational and recombination events which are therntwo major reasons behind the extensive genetic diversity of DENV. The possible emergence of undesired genetically novel variant DENV inrnthe near future could create further complexity and subsequent complications inrnthe
pathogenicity of the disease. This review article is an attempt tornunderstand the significance of the extensive genetic diversity of the denguernvirus (DENV) in the development of greater magnitude of the viral
pathogenicityrnas well as in the severity of recurrent outbreaks in the context of changingrnenvironment and epidemiology. DENV antigens have been detected from mononuclearrncells, lymphocytes, Langerhans cells in the skin, neurons, astrocytes,rnendothelial cells and
hepatocytes, heart and skeletal muscle. This alteredrntropism of the dengue virus in humans might indicate the
fitness strategy ofrnthe virus in urban areas since human is the only possible source of
viremicrnvertebrate. Remarkably, the RNA virusrnhas developed the ability to recombine with host
dsDNA genomes. Thernextraordinary abilities of RNA virus like DENV may unlock a new vista in denguernresearch, which encompasses the relevant proposition of a momentousrnplausibility of crucial genetic exchange between DENV (+)
ssRNA genome andrn
dsDNA of the human host and thereby thernpossible emergence of genetically novel DENV variants associated with altered
pathogenicity
Fig. 1: Dengue virus Transmission cycle