Abstract
Flavivirus replication in host cells requires the formation of replication and assembly complexes on the cytoplasmic side of the endoplasmic reticulum (ER) membrane. These complexes consist of an ER membrane, viral proteins, and host proteins. Genome-wide investigations have identified a number of ER multiprotein complexes as vital factors for flavivirus replication. The detailed mechanisms of the role of ER complexes in flavivirus replication are still largely elusive. This review highlights the fact that the ER multiprotein complexes are crucial for the formation of flavivirus replication and assembly complexes, and the ER complexes could be considered as a target for developing successful broad-spectrum anti-flavivirus drugs.
Highlights
Members of flavivirus genus are the most important arthropod-borne viruses causing disease in humans
DNAJ homolog subfamily C member 14 (DNAJC14) is a vital endoplasmic reticulum (ER)-associated chaperone required for the integration of the flavivirus replication complex to a specific ER membrane location [56,57]
Assembly by transferring the newly synthesized viral RNA to the assembly site through direct binding to the capsid [85]. Other host proteins such as Src Kinases represent crucial factors for dengue virus (DENV) and West Nile virus (WNV) assembly and egress by facilitating virus passing from ER to the Golgi [86]
Summary
Members of flavivirus genus are the most important arthropod-borne viruses causing disease in humans. The lack of specific therapeutics for flavivirus infections imparts a pressing need to identify the viral and host factors in flavivirus replication and disease outcome. Flaviviruses infect the host cells by binding with virus receptors on the cell membrane [4]. RNA binds to the ribosomes by 50 -cap structure, the translation process produces a viral polyprotein anchored to the ER membrane [4]. Viral proteins alter the endoplasmic reticulum (ER) membrane to generate new structures called vesicle packets (VPs), containing viral replication and assembly complexes [12]. Pathogens 2019, 8, 148 targeting the host factors that have important roles in regulating the formation and stabilization of flavivirus replication and assembly complexes represents a new therapeutic approach for developing anti-flavivirus drugs
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