Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Intracellular parasites and bacteria deploy an array of molecular tactics to invade host cells. Once inside, these pathogens subvert and co-opt host resources for survival and reproduction. Stealthy disguises help pathogens evade the immune response, and effector molecules enable a safe refuge for them to thrive. Equally, host cells defend, eliciting an arms race and intriguing battle involving a complex interplay of pathogen-host factors that shape the outcome of an infection. Unravelling such molecular determinants of intracellular infection promises a roadmap for developing novel therapeutics while illuminating the remarkable adaptability of life and the struggle for dominance at the tiniest scales.
For this Collection, we welcome any submissions focusing on pathogen-host biology and involving intracellular bacteria and parasites. Original research Articles characterising and validating molecular factors essential for pathogen growth in vitro and in vivo are welcome. In addition, we will also consider Reviews, Perspectives and Comments covering these topics. All submissions will be processed as regular Communications Biology Articles.
The immunodominant surface antigen GP60 undergoes dynamic changes in expression profile and localization during parasite invasion and development and is a key molecule mediating host infectivity and pathogenicity.
Mycobacterium tuberculosis regulates membrane proteins associated with copper stress to evade host-induced copper toxicity, highlighting the importance of understanding its adaptive mechanisms in copper-rich environments.
This study shows that MfpC is a GEF of MfpB. MfpC regulates MfpB through a G protein-like model, which affects MfpA at the translational level and alters the fluoroquinolones efficacy in Mycobacterium smegmatis.
Autophagy and apoptosis play a role in the defense against C. parvum. This study shows that miR-199a-3p targets MTOR transcripts, thus downregulating MTOR function, and subsequently reduces the C. parvum burden by promoting autophagy and apoptosis.
IDO downregulation in dMDSCs induced by Toxoplasma gondii infection regulates expression of TGF-β and IL-10 through the Kyn/AhR/SP1 signal pathway, eventually contributing to the dysfunction of dNK cells.
A study suggests that TBC9, one of the Rab GTPase Activating Proteins, is crucial for early vesicular transport and inner membrane complex formation by regulating Rab2, Rab11A and Rab11B in Toxoplasma gondii.
A modelling framework characterising the dynamics of Plasmodium vivax lactate dehydrogenase provides estimates of key biological parameters to facilitate the development of improved diagnostic tools for the detection of P. vivax.
The bacterial T3SS effector YfiD interacts with the catalytic domain of host PARP1 during infection. Inhibition of PARP1 activity impairs the pro-inflammatory response against bacterial infection.
The Fic2 enzyme of the pathogen Coxiella burnetii can act as a bifunctional histone modification enzyme, capable of AMPylation (as monomer) and deAMPylation (as dimer) upon DNA binding by a C-terminal helix-turn-helix domain.