Using HIV Drugs for Staphylococcus aureus Infections?

Staphylococcus aureus (cdc.gov)

Here is an interesting article by Alonzo et al just published in Nature looking at the pore-forming toxin "leukotoxin ED" (LukED) secreted by many Staphylococcus aureus bacteria. Pore-forming toxins create channels in human cells that disrupt cell function and ultimately lead to cell death.

These authors found that a receptor on human T cells, CCR5, which also happens to be a co-receptor for HIV entrance into T cells, is required for LukED activity.

This is interesting in that we already have a drug (maraviroc) used to treat HIV that blocks the CCR5 receptor, thereby disrupting HIV's ability to gain entrance into human T cells. Alonzo et al found that maroviroc disrupted LukED killing of T cells in vitro. These authors used an in vivo model looking at LukED's effect on mice with and without the CCR5 receptor and found mice with the receptor were more likely to die (the implication being LukED cytotoxicity is dependent to a large extent on the CCR5 receptor). 

Not all Staphlococcus aureus isolates harbor the LukeED toxin, and it is not clear if these study findings will translate into real benefits in humans. However, Staphlococcus aureus is a major cause of morbidity and mortality globally, and the above study opens up intriguing new treatment possibilities that may aid in treating these serious infections. More research is warranted.