Abstract
Flaviviruses comprise a genus of viruses that pose a significant burden on human health worldwide. Transmission by both mosquito and tick vectors, and broad host tropism contribute to the presence of flaviviruses globally. Like all viruses, they require utilization of host molecular machinery to facilitate their replication through physical interactions. Their RNA genomes are translated using host ribosomes, synthesizing viral proteins that cooperate with each other and host proteins to reshape the host cell into a factory for virus replication. Thus, dissecting the physical interactions between viral proteins and their host protein targets is essential in our comprehension of how flaviviruses replicate and how they alter host cell behavior. Beyond replication, even single interactions can contribute to immune evasion and pathogenesis, providing potential avenues for therapeutic intervention. Here, we review protein interactions between flavivirus and host proteins that contribute to virus replication, immune evasion, and disease.
Highlights
Flavivirus is a genus of positive-sense, single-stranded RNA, arthropod-transmitted viruses within the family Flaviviridae
Flaviviruses are arthropod-borne viruses that cause significant human disease worldwide. Their limited genome requires them to co-opt host proteins through physical interactions during infection to properly replicate
Some of these interactions appear to be broadly conserved among flaviviruses, while other unique interactions contribute to observed differences in host tropism and pathogenesis
Summary
Flavivirus is a genus of positive-sense, single-stranded RNA (ssRNA+), arthropod-transmitted viruses within the family Flaviviridae. Flaviviruses have a conserved replication cycle, which includes viral entry, virion fusion with the endosome and release of viral RNA, genome replication and protein production in the ER, virion packaging and processing through the secretory pathway, and viral release via exocytosis (Figure 1). At each of these stages, flaviviruses are dependent on host machinery to perform necessary functions. This review will focus on virus-host protein–protein interactions (PPIs) emerging from both targeted and comprehensive studies that directly facilitate flavivirus replication, dampen host immune response, or disrupt cellular processes to cause disease. We review the data emerging from both comprehensive and targeted studies of flavivirus-host PPIs as they relate to various stages of flavivirus replication
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