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Host factors required for parechovirus entry are not well understood. Here, the authors identify MYADM as an essential host entry factor that directly binds human parechovirus 1 and that is required for PeV-A infection in cell lines and human gastrointestinal epithelial organoids.
IFITM1 can compete with EBV glycoproteins for EphA2 binding and prevent virus entry into epithelial cells, in vitro and in vivo. YTHDF3 suppresses IFITM1 via the degradation-related protein DDX5.
The VP53 protein, which is expressed from RNA2 of broad bean wilt virus 2 (genus Fabavirus, family Secoviridae) through ribosomal leaky scanning, is essential for the successful systemic infection of the virus.
In this Journal Club, Ricardo Soto-Rifo discusses a study on intron-containing HIV-1 RNA, revealing its role as a pathogen-associated molecular pattern in myeloid cells, which has implications for immune activation, inflammation and clinical outcomes.
This study shows that a single-stranded RNA phage binds to the Pseudomonas aeruginosa type IV pilus, leading to phage entry into the cell and the detachment of the pilus, which impairs bacterial motility.
A participatory research initiative generates actionable data on avian diseases in New York City, showcases how a community-based approach can tackle misinformation, and actively engages students from historically underrepresented communities in science, technology, engineering and maths.
We find that people with non-suppressible human immunodeficiency virus (HIV) viremia despite antiretroviral therapy (ART) exhibit several distinguishing features. These include expanded CD4+ T cell clones containing HIV proviruses integrated into transcriptionally permissive regions, the presence of certain proviral defects or human leukocyte antigen (HLA)-escape mutations, enhanced survival signatures, and muted interferon and cytotoxic CD8+ T cell responses.
This study reports the identification of an archaeal virus Acr protein that blocks the dissociation of the target RNA from the type III-B CRISPR–Cas effector complex, which prevents the recycling of the complex.