During Staphylococcus aureus infections, bacterial cells bifurcate into distinct, specialized cell types that localize physically in different colonization tissues to simultaneously generate different infection types.

Description of the transcriptional and clonal landscape of virus-specific CD4⁺ T cells in acute and chronic viral infections, and a new reference map to interpret CD4 T cell diversity across tissues and biological models.

Under conditions where the force of HIV infection per cell is high, partial attenuation of infection with inhibitors can increase the number of live infected cells and may paradoxically be beneficial for viral spread.

Development of a robust Th1 response to infection against an intracellular parasite requires T-cell intrinsic MyD88 signaling, mostly through the upstream IL-18 receptor, for the induction of genes involved in proliferation, cytokine production and migration.

The co-stimulatory molecule CD28 is required after T cell priming for helper T cell polarization in response to an infection.

The human immunodeficiency virus HIV-1 primarily spreads between cells using a method called cell-to-cell infection, suggesting that this process may be a target for anti-viral drugs.

In the context of SARS-CoV-2 infection, Nsp14 alters gene expression of the host cell through the interaction with the cellular enzyme IMPDH2.

A novel virus-inclusive single cell RNA-Seq approach enables identification of novel pro- and antiviral host factors in human cells in response to dengue and Zika virus infection.

T cell receptor signal strength correlates positively with Th1 generation during acute infection but negatively during chronic infection.

Longitudinal tracking of individual T-cell clones reveals the expansion of pre-existing T-cell memory in response to SARS-CoV-2 infection.