Fig. 1: HIV developmental fate upon CD4 + T cell infection.
From: Mathematical modeling and mechanisms of HIV latency for personalized anti latency therapies
a HIV cell infection, proliferation, and latency reversal. Once HIV enters a susceptible cell (i.e., active CD4 + T-lymphocyte), is reverse-transcribed, and integrates within the host genome, forming a provirus. b Transitioning into active-replication. Upon sufficiently-high transactivator of transcription (Tat) production, a provirus enters active replication, forcing the host-cell to fabricate and release virions. c host-cell loss and HIV proliferation. The accumulation of viral products leads to host-cell apoptosis within ~40 h of active replication. d Transitioning into latency. Conversely, upon low Tat concentrations, the provirus remains silent. As opposed to what was initially believed, active replication and latency can be detected both in active and resting lymphocytes, represented by green and purple cells, respectively. e Latency-reversal. Upon increased Tat levels a dormant provirus activates from latency. The shock-and-kill therapy employes latency reversing agents to enhance Tat production and facilitate latency-reversal. [Created in BioRender. Palma, P. (2025) https://BioRender.com/0fw3cwk].
