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.

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Background: Hand, foot, and mouth disease (HFMD) is a common illness in infants and children. It can be caused by many different human enteroviruses. Of these human enteroviruses, human enterovirus 71 (EV71) infection is more frequently associated with serious neurological complications and fatalities. The emergence of this virus emphasized the need for surveillance study and identification of EV71 to provide early warning of potential EV71 encephalitis outbreaks and assist in directing public health interventions as well as inform clinical decisions. This surveillance study was aimed to examine the prevalence of enteroviruses and EV71 in suspected clinical specimens.