Abstract
The complex nature and structure of the human immunodeficiency virus has rendered the cure for HIV infections elusive. The advances in antiretroviral treatment regimes and the development of highly advanced anti-retroviral therapy, which primarily targets the HIV enzymes, have dramatically changed the face of the HIV epidemic worldwide. Despite this remarkable progress, patients treated with these drugs often witness inadequate efficacy, compound toxicity and non-HIV complications. Considering the limited inventory of druggable HIV proteins and their susceptibility to develop drug resistance, recent attempts are focussed on targeting HIV-host interactomes that are essential for viral reproduction. Noticeably, unlike other viruses, HIV subverts the host nuclear pore complex to enter into and exit through the nucleus. Emerging evidence suggests a crucial role of interactions between HIV-1 proteins and host nucleoporins that underlie the import of the pre-integration complex into the nucleus and export of viral RNAs into the cytoplasm during viral replication. Nevertheless, the interaction of HIV-1 with nucleoporins has been poorly described and the role of nucleoporins during nucleocytoplasmic transport of HIV-1 still remains unclear. In this review, we highlight the advances and challenges in developing a more effective antiviral arsenal by exploring critical host-HIV interactions with a special focus on nuclear pore complex (NPC) and nucleoporins.
Highlights
HIV (Human Immunodeficiency Virus), a major killer worldwide was first recognised in the early 1980s in the United States as a strange retrovirus causing an entirely new disease called AIDS (Acquired Immunodeficiency Syndrome) [1]
While proper nuclear entry and exit is essential for viral replication, the nuclear pore complex can be a key target for virus subversion and may provide the basis for developing antiviral compounds for therapeutic intervention that target viral proteins alone but their interactions with nuclear membrane partners like nucleoporins
They have evolved intrinsically disordered, short protein regions called as eukaryotic linear motifs (ELMs) or short linear motifs (SLiMs) which mediate interactions with their host [50]
Summary
HIV (Human Immunodeficiency Virus), a major killer worldwide was first recognised in the early 1980s in the United States as a strange retrovirus causing an entirely new disease called AIDS (Acquired Immunodeficiency Syndrome) [1]. Focus has been laid on the HIV-1 dependence on different host factors in the nuclear import and export of viral nucleic acids and proteins. Cells 2019, 8, 1155 complete molecular understanding and structural knowledge of the host-viral protein complexes is the most significant limiting factor in the area. The infection with HIV-2 seems to be slowly progressing and less efficiently transmissible These retroviruses are divided into different groups based on their genetic diversity. Nef (negative inhibits host’s defences; pleiotropic regulates the splicing andvirus nuclear export of viral regulatory factor) increase or decrease replication [19]. The viral and host cellular proteins involved in the replication cycle of HIV-1 are highlighted at each step in red and black, respectively
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