Abstract
The host nucleocytoplasmic trafficking system is often hijacked by viruses to accomplish their replication and to suppress the host immune response. Viruses encode many factors that interact with the host nuclear transport receptors (NTRs) and the nucleoporins of the nuclear pore complex (NPC) to access the host nucleus. In this review, we discuss the viral factors and the host factors involved in the nuclear import and export of viral components. As nucleocytoplasmic shuttling is vital for the replication of many viruses, we also review several drugs that target the host nuclear transport machinery and discuss their feasibility for use in antiviral treatment.
Highlights
Despite advancements in science and technology, humans are still plagued by communicable diseases, and the development and production of effective antiviral drugs and vaccines remains challenging
The host nucleoplasm and cytoplasm are segregated by a nuclear envelope (NE), a lipid bilayer embedded with numerous nano-gates known as nuclear pore complexes (NPCs)
We focus on the various mechanisms used by viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), to hijack the host nucleocytoplasmic trafficking machinery
Summary
Despite advancements in science and technology, humans are still plagued by communicable diseases, and the development and production of effective antiviral drugs and vaccines remains challenging. There have been two severe pandemics, as follows: the 1918 influenza pandemic and the currently ongoing coronavirus disease. As part of their lifecycle, many viruses hijack the host transcription and translation machinery while evading the host immune responses [1]. As exploitation of the host nuclear transport is important for viral replication, the mechanisms that are used by viruses to hijack the host nuclear trafficking are potential targets for antiviral drugs; such drugs might halt viral genome transcription, viral protein synthesis, and viral assembly. We focus on the various mechanisms used by viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), to hijack the host nucleocytoplasmic trafficking machinery.
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