Abstract
Flaviviruses, as critically important pathogens, are still major public health problems all over the world. For instance, the evolution of ZIKV led to large-scale outbreaks in the Yap island in 2007. DENV was considered by the World Health Organization (WHO) as one of the 10 threats to global health in 2019. Enveloped viruses hijack a variety of host factors to complete its replication cycle. Phosphatidylserine (PS) receptor, AXL, is considered to be a candidate receptor for flavivirus invasion. In this review, we discuss the molecular structure of ZIKV and DENV, and how they interact with AXL to successfully invade host cells. A more comprehensive understanding of the molecular mechanisms of flavivirus-AXL interaction will provide crucial insights into the virus infection process and the development of anti-flavivirus therapeutics.
Highlights
The Flaviviridae family includes three viral genera, namely Flavivirus, Pestivirus, and Hepatitis C virus, with a total of more than 70 viruses
By constructing a pseudotyped virus, Bhattacharyya discovered that enveloped viruses suppressed innate immune responses by activating TAM receptors, which may explain that why AXL intracellular domain deletion or ATP binding site mutant cannot promote dengue virus (DENV) replication (Bhattacharyya et al, 2013)
There is no significant difference in the brain and placental tissue of fetal WT and AXL−/− mice (Hastings et al, 2017). These results prove that AXL is not essential for the vertical propagation of Zika virus (ZIKV)
Summary
Flaviviruses, as critically important pathogens, are still major public health problems all over the world. The evolution of ZIKV led to large-scale outbreaks in the Yap island in 2007. DENV was considered by the World Health Organization (WHO) as one of the 10 threats to global health in 2019. Enveloped viruses hijack a variety of host factors to complete its replication cycle. Phosphatidylserine (PS) receptor, AXL, is considered to be a candidate receptor for flavivirus invasion. We discuss the molecular structure of ZIKV and DENV, and how they interact with AXL to successfully invade host cells. A more comprehensive understanding of the molecular mechanisms of flavivirusAXL interaction will provide crucial insights into the virus infection process and the development of anti-flavivirus therapeutics
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