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A transposon-based screen identifies a family of outer membrane proteins — named surface lipoprotein assembly modulator (Slam) — that are important for the surface display of lipoprotein virulence factors in Neisseria spp.
Inhibition of BCL-XL eliminates Legionella infection, suggesting that host-directed BH3-mimetic therapy may be effective against intracellular pathogens that inhibit host cell protein synthesis.
Infection with HIV-1 triggers an increase in N6-methyladenosine (m6A) modification of both viral and host mRNAs, which impacts viral replication and nuclear export of viral RNA.
Renal infection with Middle East respiratory syndrome coronavirus (MERS-CoV) leads to both the induction of apoptosis through upregulation of Smad7 and FGF2 and to renal failure.
The HigBA toxin–antitoxin system of Caulobacter crescentus can act as a switch between promoting and inhibiting bacterial growth, depending on the dosage of HigA antitoxin, HigB toxin and its mRNA target.
Genomic reconstruction from hot spring sediment metagenomes show that 'Hadesarchaea' have streamlined yet metabolically versatile genomes, with genes involved in CO and H2 oxidation, with potential coupling to nitrite reduction to ammonia.
T. gondii crosses biological barriers using transcellular migration or within an infected migrating cell. Here, infection and lysis of endothelial cells in the brain vasculature is identified as a new route of access to the central nervous system.
Whole genome sequencing of vancomycin-resistant Enterococcus faecalis isolates from the UK and Ireland reveal a population with three predominant lineages, two of which have acquired and lost resistance multiple times.
Significant gaps in our characterization of microbial diversity remain; this meta-analysis of amplicon-based rRNA studies shows that they miss approximately 10% of environmental microbial sequences, most belonging to the candidate phyla radiation.
Deletions in amino acid biosynthetic pathways (auxotrophy) are widely used as selection markers, but induce major alterations of the Saccharomyces transcriptome, proteome and metabolome, representing a confounding factor in the use of auxotrophs.
The microenvironment of injured intestinal mucosa induces the rapid emergence of microbiota constituents that contribute to repair of the mucosal wounds.
pks5-recombination-mediated cell surface remodelling increased virulence of Mycobacterium canettii, driving evolution from a putative generalist mycobacteria towards a professional pathogen of mammalian hosts.
Analysis of microbial cell and virus abundance estimates from 25 distinct marine surveys reveals that virus-to-microbial cell ratio decreases with microbial cell density, questioning the idea that viral abundance is always 10-fold higher.
Mutation of a mismatch repair gene accelerated the genomic mutation rate of Salmonella Enteritidis infecting an immunocompromized individual, leading to levels of evolution that parallel those found in successful host-restricted bacterial pathogens.
Whole genomes of 185 atypical enteropathogenic Escherichia coli (aEPEC) isolates reveal 30 LEE (locus of enterocyte effacement) subtypes in 3 major lineages, varying in insertion site preference and their complement of non-LEE encoded effector genes.
Comparative genomics of 70 lethal, non-lethal symptomatic and asymptomatic enteropathogenic Escherichia coli (EPEC) isolates identifies the virulence-associated genes that are significantly more prevalent in symptomatic and lethal infections.
Streptococcus pyogenes (also known as group A Streptococcus or GAS) streptolysin S (SLS)-mediated red blood cell lysis occurs through disruption of the function of major erythrocyte anion exchange protein, band 3, leading to Cl- ion influx.
Tetrahydropyrazo[1,5-a]pyrimidine-3-carboxamide (THPP) targets the essential non-catalytic enoyl-CoA hydratase homologue EchA6 of Mycobacterium tuberculosis, and not MmpL3 as previously thought.
Combining a map of human and animal melioidosis cases and the presence of environmental Burkholderia pseudomallei in a formal modelling framework to estimate the global burden of the disease reveals that it is severely under-reported.