Abstract
HIV-1 employs a rich arsenal of viral factors throughout its life cycle and co-opts intracellular trafficking pathways. This exquisitely coordinated process requires precise manipulation of the host microenvironment, most often within defined subcellular compartments. The virus capitalizes on the host by modulating cell-surface proteins and cleverly exploiting nuclear import pathways for post entry events, among other key processes. Successful virus–cell interactions are indeed crucial in determining the extent of infection. By evolving defenses against host restriction factors, while simultaneously exploiting host dependency factors, the life cycle of HIV-1 presents a fascinating montage of an ongoing host–virus arms race. Herein, we provide an overview of how HIV-1 exploits native functions of the host cell and discuss recent findings that fundamentally change our understanding of the post-entry replication events.
Highlights
Human immunodeficiency virus (HIV)-1 is a complex retrovirus known to infect humans and diminish the immune system leading to acquired immunodeficiency syndrome (AIDS)
HIV-1 depends on the host
This dependency also portrays the interaction with diverse cellular organelles
Summary
Human immunodeficiency virus (HIV)-1 is a complex retrovirus known to infect humans and diminish the immune system leading to acquired immunodeficiency syndrome (AIDS). The process commences by recruiting host RNA polymerase (pol) II at 5 -LTR and several other transcriptional regulators such as NF-κB, NFAT, AP-1, and SP-1 at their respective binding sites upstream to the LTR promoter These regulators work synergistically to ensure the viral gene expression while minimizing the host’s antiviral gene activity (reviewed in Ruelas and Greene, 2013; Van Lint et al, 2013; Röling et al, 2016). For further understanding of the molecular mechanism of translation initiation, elongation, and completion, readers are encouraged to follow the articles by Ohlmann et al (2014) and Guerrero et al (2015) These studies show that apart from using host cellular factors and plasma membrane for viral entry and budding, the virus tricks the host machinery and makes the host environment favorable for viral replication. HIV1 accessory proteins, during binding, fusion, and budding, extensively remodel the plasma membrane and manipulate the host intracellular environment for productive infection and immune evasion
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