Reactivates Human Immunodeficiency Virus-1 in Latently Infected Monocytes with Increased Expression of IL-1β and CXCL8.

Background: are gram-negative bacteria, which colonize the human stomach. More than 50% of the world's population is infected by . Based on the high prevalence of , it is very likely that HIV and infection may coexist. However, the molecular events that occur during HIV- co-infection remain unclear. Latent HIV reservoirs are the major obstacle in HIV cure despite effective therapy. Here, we explored the effect of stimulation on latently HIV-infected monocytic cell line U1.

Methods: High throughput RNA-Seq using Illumina platform was performed to analyse the change in transcriptome between unstimulated and -stimulated latently HIV-infected U1 cells. Transcriptome analysis identified potential genes and pathways involved in the reversal of HIV latency using bioinformatic tools that were validated by real-time PCR.

Results: stimulation increased the expression of HIV-1 Gag, both at transcription (p<0.001) and protein level. stimulation also increased the expression of proinflammatory cytokines IL-1β, CXCL8 and CXCL10 (p<0.0001). Heat-killed retained their ability to induce HIV transcription. RNA-Seq analysis revealed 197 significantly upregulated and 101 significantly downregulated genes in -stimulated U1 cells. IL-1β and CXCL8 were found to be significantly upregulated using transcriptome analysis, which was consistent with real-time PCR data.

Conclusion: reactivate HIV-1 in latently infected monocytes with the upregulation of IL-1β and CXCL8, which are prominent cytokines involved in the majority of inflammatory pathways. Our results warrant future studies elucidating the effect of in HIV latency and pathogenesis.