resists its self-harming metabolite HGA via secreted factors and collective peroxide scavenging.

Before environmental opportunistic pathogens can infect humans, they must first successfully grow and compete with other microbes in nature, often via secreted antimicrobials. We previously discovered that the bacterium , the causative agent of Legionnaires' disease, can compete with other microbes via a secreted molecule called HGA. Curiously, strains that produce HGA is not wholly immune to its toxicity, making it a mystery how these bacteria can withstand the "friendly fire" of potentially self-targeting antimicrobials during inter-bacterial battles.

Host Cell Redox Alterations Promote Latent HIV-1 Reactivation through Atypical Transcription Factor Cooperativity.

Immune cell state alterations rewire HIV-1 gene expression, thereby influencing viral latency and reactivation, but the mechanisms are still unfolding. Here, using a screen approach on CD4 T cell models of HIV-1 latency, we revealed Small Molecule Reactivators (SMOREs) with unique chemistries altering the CD4 T cell state and consequently promoting latent HIV-1 transcription and reactivation through an unprecedented mechanism of action. SMOREs triggered rapid oxidative stress and activated a redox-responsive program composed of cell-signaling kinases (MEK-ERK axis) and atypical transcription factor (AP-1 and HIF-1α) cooperativity.