Abstract
Dengue virus (DENV) is an arboviral human pathogen transmitted through mosquito bite that infects an estimated ~400 million humans (~5% of the global population) annually. To date, no specific therapeutics have been developed that can prevent or treat infections resulting from this pathogen. DENV utilizes numerous host molecules and factors for transcribing the single-stranded ~11 kb positive-sense RNA genome. For example, the glycosylation machinery of the host is required for viral particles to assemble in the endoplasmic reticulum. Since a variety of host factors seem to be utilized by the pathogens, targeting these factors may result in DENV inhibitors, and will play an important role in attenuating the rapid emergence of other flaviviruses. Many experimental studies have yielded findings indicating that host factors facilitate infection, indicating that the focus should be given to targeting the processes contributing to pathogenesis along with many other immune responses. Here, we provide an extensive literature review in order to elucidate the progress made in the development of host-based approaches for DENV viral infections, focusing on host cellular mechanisms and factors responsible for viral replication, aiming to aid the potential development of host-dependent antiviral therapeutics.
Highlights
Dengue is an important arthropod-borne viral infectious disease caused by any one of the four-dengue virus (DENV-1 to -4) viral serotypes
Several remarkable points arise in the way of host inhibition processes that interrupt Dengue virus (DENV) replication along with infections
Host metabolic pathways serve as a source of energy, and molecular building blocks are required for the multiplication of DENV
Summary
Dengue is an important arthropod-borne viral infectious disease caused by any one of the four-dengue virus (DENV-1 to -4) viral serotypes. The antigenically distinct but closely related serotypes of DENV belong to the genus Flavivirus, family Flaviviridae. The genus includes more than 70 small-enveloped viruses related to Japanese encephalitis (JEV), Zika viruses (ZIKV), West Nile (WNV), yellow fever virus (YFV), DENV, or tick-borne encephalitis (TBEV), and other medically-important arboviruses [3]. Thereafter, patients suffering from dengue hemorrhagic fever (DHF) may develop petechiae, bruising, thrombocytopenia, and shock. Ultimate disease signs include rapid or weak pulse, manifestations of hypotension and clammy skin, and cold and restlessness in dengue shock syndrome (DSS) [6]. Specific therapeutics are presently not available for DENV infections [7], necessitating an improved approach for re-mediating this global burden. We will explore the host factors or targets that influence DENV replication, focusing on the factors that can potentially be utilized in a new process that may help alleviate this global burden
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