 If the lysine at residue 132 in TSST-O is changed to a glutamate, the mutant regains little superantigenicity, but becomes lethal, meaning that the ability to cause TSS results from the glutamate at residue 132.The loss of activity from these mutations is not due to changes in the protein's conformation, but instead these residues appear to be critical in the interactions with T-cell receptors.Samples of TSST-1 can be purified from bacterial cultures to use in "in vitro" testing environments, however this is not ideal due to the large number of factors that contribute to pathenogenesis in an "in vivo" environment.