SELEN AY

1 Introduction The human immunodeficiency virus type 1 (HIV-1) is the virus responsible for the global AIDS pandemic [1]. The first cases were reported in 1981 [2], and today, ∼40 million people still live with HIV (http://aidsinfo.unaids.org/). In the past few years, the early steps of the HIV-1 life cycle have been significantly revisited [3-10]. The prevailing view for many years held that HIV-1 reverse transcription was completed entirely in the cytoplasm of infected cells.

eLife Assessment This is a valuable study that presents convincing evidence on the genesis of the CPSF6 condensates that form upon HIV-1 infection and the specific molecular determinants involved in their formation, as well as their interactions with SRRM.

Abstract Viruses rely on host cellular machinery for replication. After entering the nucleus, the HIV genome accumulates in nuclear niches where it undergoes reverse transcription and integrates into neighboring chromatin, promoting high transcription rates and new virus progeny. Despite anti-retroviral treatment, viral genomes can persist in these nuclear niches and reactivate if treatment is interrupted, likely contributing to the formation of viral reservoirs.