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In two independent cohorts, NNRTI-based cART regimens are associated with significantly lower cell-associated HIV RNA levels than PI-based regimens, suggesting more potent suppression of residual virus replication by NNRTI-based regimens.

The diguanylate cyclase activity of SiaD is activated by its binding partner SiaC thourgh a dynamic mechanism of promoting the formation of active SiaD dimers.

Electron cryo-tomography reveals that bacteria can form structurally-diverse outer membrane extensions with various protein complexes associated with them.

Intranasal immunization of inactivated whole cell of some Gram-negative bacteria induces very rapid and efficient protection against bacterial pulmonary by training alveolar macrophage response, which can be harnessed to design rapid-effecting vaccine against multidrug-resistant bacteria infection.

Parasite life cycles may be more flexible than traditionally thought, potentially allowing single-cell infections of insect vectors and transmission between hosts even at very low parasite densities.

The parasite that causes African sleeping sickness can be transmitted from mammals to tsetse flies in two stages of its lifecycle, rather than one as was previously thought.

Specific amino acids in the N-terminus of the replication initiator protein DnaA inhibit translation elongation upon carbon starvation, illustrating that the identity of the N-terminal amino acids of a protein can modulate protein synthesis yield under changing conditions.

The activity, localization, and essentiality of TbFUT1, together with its ability to complement Leishmania parasites lacking the homologous gene, suggest the presence of an uncommon and conserved mitochondrial fucosylation pathway required for kinetoplastid parasites viability.

Type I interferon and interferon-γ signaling redundantly protects mice from the tick-borne pathogen Rickettsia parkeri in the skin, and interferon receptor-deficient mice are a tractable model for investigating rickettsiosis.

Analysis of viral DNA from human remains suggests that the transatlantic slave trade may have introduced new pathogens that contributed to the devastating disease outbreaks in colonial Mexico.