Common STI fueled by bug world’s version of Harry Potter’s invisibility cloak

By Mark Waghorn via SWNS

A common sexually transmitted infection is fueled by the bug world's version of Harry Potter's invisibility cloak.

It helps chlamydia dodge the body's immune system - and hide undetected inside host cells.

The stealth device contains a veil of microbes. Now scientists have grasped its hem - and plan to pull it apart.

"We knew there was the potential to kill chlamydia," said lead author Professor Jorn Coers, of Duke University.

"But when we did experiments with the human-adapted form, Chlamydia trachomatis, it was very good at growing in human cell cultures."

The US team used an immune stimulant to alert the cell's defense systems of its presence. But nothing happened.

"We said, there's the pathogen. Our defense system should see it. Why does it not see it?," Coers said.

They found a gene called GarD (gamma resistance determinant) blocks cells from marking a chlamydia infection for attack

Mutating the protein left the bacteria vulnerable to destruction. Coers said: "GarD is the stealth factor."

It interferes with the ability of an enzyme called mysterin (RNF213) to sense small bits of bacterial molecules poking out of the shell of the storage vessel - or inclusion.

"RNF213 is basically the eyes of the immune system," Coers said

Having blinded mysterin in this fashion, the killing signal is never started.

The inside of a cell is swarming with 'bags' called vacuoles - tiny bubbles covered by membranes. Most are friends, but some, like the chlamydia inclusion, are foes.

"There's so many different types of membranes and vacuoles that live inside a cell," Coers said.

"How is the immune system able to find the rare vacuole that contains a pathogen? In the case of chlamydia, we really don't have the answer to that question. But whatever it is, we believe mysterin is seeing it."

The experiments were repeated using a mouse-adapted version of the bacteria in human cells to see how the immune system responded to an alien pathogen.

"Humans don't get mouse chlamydia because it evolved with mice and human chlamydia evolved with humans," Coers said.

"So there's this really fine-tuned adaptation the pathogen has undergone.”

The rodent model of the bacterial inclusion was readily identified and labelled for destruction in human cells.

"Chlamydia trachomatis is so good at evading our human responses. It still causes an inflammatory disease, but it's a very slow disease," Coers said.

The evolutionary arms race between the immune system and the pathogen has been going on for millions of years.

"Mouse and human adapted Chlamydia have a common ancestor. However, this common ancestor may go back as far as when humans and rodents basically split from each other," Coers said.

"This is a long time for the bacteria to really fine-tune their interactions with their host species."

The key to a therapy now lies in figuring out how GarD blinds mysterin, Coers said.

"If you could find a mechanism to deactivate GarD, then you can turn human chlamydia into mouse chlamydia," he said.

"That would allow us to harness the powers of our own immune system to clear infection."

It is particularly common in teenagers and young adults - and passed on through unprotected sex.

The NHS recommends sexually active under 25s are tested once a year - especially if not using condoms with new or casual partners.

Most people with chlamydia do not know they have it. But symptoms can include pain when peeing or unusual discharge or bleeding from the vagina, penis or bottom. The study was published in Cell Host & Microbe.