Analysis of Virulence factors in understudied Salmonella serovars

In this project we will study Salmonella in both cellular and animal infection models and we will use a mix of molecular biology, microscopy and biochemistry techniques to understand how Salmonella serovars infection can result in different manifestations.
The genus Salmonella contains several important pathogens for humans and animals and is one of the largest contributors of food borne illness worldwide. The genus comprises only 2 species: S. bongori and S. enterica. However, S. enterica contains 6 subspecies and more than ~2000 serovars characterised according to different surface antigens. Importantly, different serovars are responsible for causing very different diseases with some, such as Salmonella enterica Typhi (S. Typhi) and Salmonella enterica Paratyphi (S. Paratyphi), also called "typhoidal Salmonellae", causing systemic, life-threatening diseases in human, while others (non-typhoidal Salmonellae) infect a range of hosts and cause mild, self-limiting, gastroenteritis that could become severe in immunocompromised hosts
For decades, the research focussed on two major serovars: S. Typhi, for its paramount importance in human health, and on S. Typhimurium because is one of the most common in both human and animals. However, the information available thanks to the steep increase in genomic sequencing of clinical and environmental samples, have challenged a number of "dogmas" based on the Typhi/Typhimurium comparison. For example, the discovery that what was initially described as S. Typhi specific toxin, is also expressed by other 47 non-typhoidal serovars. This discovery pushed for a revision of the previous accepted model and spurred a plethora of new studies about the toxin role and its biology. In addition, the abundance of genomic data allowed us to study with good grade of confidence the relations between some virulence factors in the different serovars. Indeed, we have preliminary data showing that the acquisition of a virulence factor does not necessary result in increased virulence and some of them are functionally non compatible and we suggest that disease type (systemic or self-limiting) and severity are determined by the set of virulence factors "picked" during the evolution of a certain serovar.