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Scale-up of piped water coverage in the local community strongly protects against S. haematobium re-infection intensity among primary school-going children following treatment with praziquantel.

A cytorhabdovirus phosphoprotein hijacks host CCR4 to trigger turnover of viral nucleoprotein (N)-bound cellular RNAs, thereby releasing nascent RNA-free N protein molecules to bind viral genomic RNAs for optimal replication.

Cells must acquire multiple viral spacer sequences to neutralize mutant escaper phages and form colonies during the CRISPR-Cas immune response.

The response of bacteria to the threat posed by phages depends on their local environment.

Genomic data for the parasites that cause visceral leishmaniasis provides the first global picture of the diversity and evolution of the pathogen and the epidemiology of this fatal tropical disease.

For initiation of cell-wall insertion, the cross-linking enzyme PBP2 stably binds to a component of the cell envelope that is different from MreB filaments.

Lytic transglycosylase enhances the activity of its protein partner, and its catalytic domain can be targeted to disrupt cell-wall integrity, protein partner function, and bacterial survival (Neisseria meningitidis) in hosts.

A key enzyme of central energy metabolism, citrate synthase, regulates bacterial cell cycle progression at a very specific stage (S-phase) and independently of its enzymatic activity.

A herpesvirus harnesses the unfolded protein response to regulate its own life cycle, revealing an unexpected role of XBP1u as a potent repressor of the most important viral promoter.

Mycobacterium tuberculosis penetrates the airway mucosa through M cells via the mycobacterial virulence factor EsxA and the host M cell surface receptor scavenger receptor B1.