Background: Helicobacter pylori are gram-negative bacteria, which colonize the human
stomach. More than 50% of the world’s population is infected by H. pylori. Based on the high prevalence
of H. pylori, it is very likely that HIV and H. pylori infection may coexist. However, the molecular
events that occur during HIV-H. pylori co-infection remain unclear. Latent HIV reservoirs are
the major obstacle in HIV cure despite effective therapy. Here, we explored the effect of H. pylori
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 H. pylori-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: H. pylori stimulation increased the expression of HIV-1 Gag, both at transcription (p<0.001)
and protein level. H. pylori stimulation also increased the expression of proinflammatory cytokines
IL-1β, CXCL8 and CXCL10 (p<0.0001). Heat-killed H. pylori retained their ability to induce HIV
transcription. RNA-Seq analysis revealed 197 significantly upregulated and 101 significantly downregulated
genes in H. pylori-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: H. pylori 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 in vivo studies elucidating the effect of H. pylori in HIV latency and pathogenesis.