Interplay Between HIV-1 Replication and Host Transcriptional Machinery

The field of HIV-1 research has made significant strides over the past four decades, yet the virus continues to pose a global health challenge, having infected over 30 million individuals. HIV-1 relies entirely on the host's transcriptional machinery for replication, utilizing its trans-activator Tat to commandeer the host's cellular processes. This dependency has provided a unique window into the mechanisms of eukaryotic transcription regulation, leading to pivotal discoveries such as the role of P-TEFb in elongation control. Despite these advances, the virus's ability to remain dormant in quiescent cells and reactivate later remains a critical area of study. Recent research has highlighted the complex interplay between HIV-1 replication and host transcriptional events, including chromatin modifications, transcription factor dynamics, transcriptional interference, viral RNA export, and RNA interference. While some epigenetic markers have been identified, the detailed mechanisms and potential new markers require further investigation. Additionally, the exact regulatory roles of transcription factors and the contributions of transcriptional interference and RNA interference to viral replication are not fully understood. Addressing these gaps is essential for advancing our understanding of HIV-1's life cycle and its interaction with host cellular machinery.

This research topic aims to elucidate the detailed mechanisms by which host cellular machineries regulate HIV-1 replication. By focusing on these mechanisms, the research will not only enhance our fundamental knowledge of the HIV-1 life cycle but also provide new insights into the balance and dynamics between HIV-1 replication and host transcriptional regulation. Specific questions to be addressed include identifying new transcriptional factors involved in proviral replication, understanding the role of transcriptional interference and RNA interference in viral replication, and exploring the relationship between P-TEFb levels and HIV-1 replication in different cellular states.

To gather further insights into the balance and dynamics between HIV-1 replication and host transcriptional regulation, we welcome articles addressing, but not limited to, the following themes:
- Defining new mechanisms by which host transcription factors regulate proviral replication.
- Exploring how transcriptional interference and RNA interference negatively regulate HIV-1 replication.
- Identifying potential new epigenetic markers correlated with chromatin structures and transcription levels of the provirus.
- Revealing the correlations between dynamic P-TEFb levels in quiescent or proliferating cells and HIV-1 replication levels.