Transition metals are essential nutrients that are required for all forms of life. For example, metals such as manganese, iron, cobalt, nickel, copper and zinc all play key roles in biological systems. Recently, transition metals have been implicated in host responses to bacterial infection. In particular, the phenomenon of nutritional immunity involves either the limitation or oversaturation of the intracellular levels of transition metals as part of the innate immune response.

Streptococcus pneumoniae is a gram positive, facultative anaerobic bacterium and the leading bacterial cause of pneumonia, meningitis and sepsis¹ . S. pneumoniae infection is highly prevalent in developing countries where it is estimated that infection by this organism is responsible for 11% of all non-HIV positive deaths in children up until the age of 6 years² .

The oversaturation of the pathogen with the transition metal zinc is an established host response to infection by S. pneumoniae. Under zinc stress conditions, a number of S. pneumoniae proteins    undergo either changes in expression levels or activities (or both) in order to effectively combat these potentially toxic conditions. Functions of proteins implicated in this system include regulation of transcription, response to oxidative stress and maintenance of the metal buffering glutathione pool. This project aims to structurally characterize proteins implicated in the response of S. pneumoniae to zinc stress. Progress towards this aim will be presented.