NF-κB sub-pathways and HIV cure: A revisit.
review · Level V
Where this comes from
- Record sourced from PubMed, PMID 33340992.
- Also identified by DOI 10.1016/j.ebiom.2020.103159 and PMC identifier 7750564.
- Licence recorded as CC BY-NC-ND.
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Abstract
HIV cure is thwarted by the presence of quiescent yet replication competent HIV-1 (HIV). Antiretroviral therapy (ART) is unable to eradicate reservoirs, and upon cessation of ART, HIV will rebound. This review encompasses the curative strategies of HIV in the context of NF-κB sub-pathways that are currently exploited and demonstrate promise in the disruption of latent HIV. Canonical NF-κB signaling has long been established to drive HIV proviral expression while noncanonical NF-κB signaling, a novel and perhaps more desirable mechanism of latency reversal due to its unique characteristics, has recently been shown to also promote HIV expression from latency. Furthermore, we discuss the previously unrecognized upstream signaling of NF-κB as a new avenue for exploration of a functional cure of HIV.
Medical subject headings
- HIV
- HIV Infections
- Host-Pathogen Interactions
- NF-kappa B
- Signal Transduction