Chlamydia trachomatis is a frighteningly accomplished human pathogen. It's the most frequently reported bacterial STD in the United States, the number one cause of acquired blindness in developing countries, and the leading cause of infertility in the Western world. And yet, many of the molecular mechanisms by which chlamydia spreads remain poorly understood.

Now, a team of microbiologists led by UCSF's Joanne Engel has discovered that one of the world's most pernicious sexually transmitted diseases infiltrates its host's cells by employing one of history's most famous military stratagems.


In the latest issue of PLoS Pathogens, Engel and her team reveal that chlamydia gains access to its host's cells by coating itself in a protein called Fibroblast Growth Factor 2 (FGF2) โ€” a protein produced naturally by the cells of the bacteria's host.

Chlamydia's FGF2-disguise allows it to bind the outside of one of its host's cells. The cell, fooled by chlamydia's seemingly innocuous camouflage, provides the bacteria access to its interior. The cell is subsequently undone from the inside out, helping produce more and more chlamydia bacteria in the process.


But before it dies, the chlamydia that have invaded the cell order it to increase its production of FGF2, such that when the cell finally does perish and its cell wall splits, the surplus FGF2 is released. This provides other chlamydia the means to disguise themselves and repeat the infiltration process, resulting in a positive feedback loop between chlamydia and FGF2 that the researchers believe enhances the efficiency and spread of subsequent rounds of infection.

I always appreciate studies like this one for their ability to put things into perspective. I mean, chlamydia infections are curable, and yet there's so much about this bacteria that we simply don't understand. And if you think about it, pretty much all scientific progress hinges on that very dynamic โ€” that sense of knowing and not knowing at the same time. It's exciting to think about. Even โ€” incredibly enough โ€” when it means thinking about STDs.

Via PLoS Pathogens โ€” doi:10.1371/journal.ppat.1002285 (No Subscription Required)
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