Research could lead to more effective Q fever therapeutics

Closeup of Manish Chauhan at work in a laboratory.
Manish Chauhan works in the laboratory.

A study exploring how the human immune system mounts a defense against the highly infectious bacteria that causes Q fever could pave the way to new and more effective therapeutics and vaccines to combat the disease and others like it.

The bacteria, Coxiella burnetii, poses significant health risks to both animals and humans and has been designated as a potential bioterrorism agent by the Centers for Disease Control and Prevention.

While previous studies primarily focused on innate immune responses during the early phases of C. burnetii infection, researchers in Washington State University’s College of Veterinary Medicine aimed to understand the immune system’s defense during later stages. They found the presence and activation of a protein known as STING (Stimulator of Interferon Genes) is crucial in determining how well a host can fend off the bacteria.

 The findings were published in the journal Cell Death and Disease.

“When this study was started nothing was known about innate immune responses during late stages of infection by this highly infectious organism,” said lead researcher Manish Chauhan, a postdoctoral research associate in Alan Goodman’s lab in the School of Molecular Biosciences. “We now know how the host responds when it is infected by the bacteria and how the innate immune system responds, which can help us as we pursue new therapeutics and even vaccines.”

C. burnetii naturally infects animals like goats, sheep and cattle, causing abortions, stillbirth, infertility and pneumonia. Farms with infected animals can have significant economic losses.

Humans can contract bacteria by inhaling contaminated dust from the birth products, urine, feces, and milk of infected animals. The bacteria can aerosolize and survive for months in the environment. Ticks also play a role in transmitting the bacteria to livestock.

Fewer than 1,000 cases are reported annually in the United States, however, incidents have been steadily rising during the past two decades. While many individuals infected with Q fever don’t exhibit symptoms, others may develop fever, pneumonia or hepatitis. Pregnant women face heightened risks of miscarriage, stillbirth or preterm birth, and people with pre-existing heart conditions are at an increased risk of developing chronic diseases such as endocarditis. People who develop a more serious infection called chronic Q fever often require 12-48 months of antibiotic treatments.

To survive during the early stages of infection, C. burnetii conceals itself to not alert the immune system. In most people, the STING protein triggers inflammatory responses that leads to apoptosis – or programmed cell death – as a defense mechanism against invading pathogens. Apoptosis, Chauhan said, is like a jailed state for infectious pathogens that prevents the cells from bursting and spreading pathogenic material.

“What we found is at later stages of infection, STING is activated and tries to counter the bacteria and the bacterial load,” Chauhan said. “When STING is present the bacterial load is lower, and when it is absent bacterial load shoots up, almost two to three times higher.”

Chauhan noted there are several variants of the STING protein in the human population. Most possess a version that effectively combats C. burnetii, while people with the less effective variant may be at risk of developing a more serious infection that leads to chronic Q fever.

Understanding STING’s involvement in the immune response will open avenues for improvements to vaccines and the development of new antibiotics and drugs to fight the disease.

C. burnetii could be just one mutation away from developing resistance to the current therapeutic intervention, and it has the potential to become a superbug that would be really difficult to fight,” he said.

The insights gained from the study, Chauhan said, could have broader implications for combating other pathogens with similar evasion mechanisms, such as Mycobacterium tuberculosis, which is becoming increasingly resistant to antibiotics.

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