Pathogens adapt through cellular aging and linker DNA as Salmonella resistance rises
Invasive Salmonella shows increasing azithromycin resistance despite poor sampling, a lung bacterium evades immunity by aging host cells, and HIV targets the exposed DNA connecting nucleosomes.
Science··Midday
Azithromycin resistance is rising in invasive Salmonella
Azithromycin resistance is rising in invasive strains of Salmonella, complicating clinical treatments for the severe infections it triggers. Despite the increasing global health burden and the urgent need for updated treatment protocols, researchers found that genomic sampling remains extremely sparse across two major continents. This profound lack of data leaves deep gaps in tracking the pathogen's actual geographic spread, masking the true scale of its evolutionary shifts.[1]
A lung pathogen ages its host cells, and a senolytic drug clears them
In a separate mechanism of immune evasion, a lung pathogen ensures its long-term survival by inducing senescence in the specific host cells where it hides. The bacterium actively shifts its host cells into an aged, inactive biological state, successfully shielding itself from the body's natural immune responses. Researchers demonstrated in the laboratory that applying a targeted senolytic drug clears these aged cells, effectively eliminating the pathogen's protective safe haven without damaging surrounding healthy tissue.[2]
HIV's integration machinery works in the linker DNA between nucleosomes
At the structural level, the human immunodeficiency virus secures its permanent hold on the host by exploiting specific architectural regions of the human genome. The virus's integration machinery operates directly in the linker DNA, which are the relatively exposed genetic strands that connect densely packed nucleosomes. This precise and targeted mechanical behavior allows the viral genetic material to successfully splice into the host's DNA sequence, ensuring ongoing replication.[3]
