Researchers in Austria say that an enzyme that regulates blood pressure is also involved in the SARS virus, and the discovery could lead to new ways of treating diseases that cause lung failure.
According to Dr. Josef Penninger of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences, learning how SARS (severe acute respiratory syndrome) became a deadly threat could possibly teach how to actively fight such diverse and dreadful diseases as SARS, avian flu or even the effects of such biotech weapons as anthrax.
Penninger says his research may have wider implications for a type of lung failure known as acute respiratory distress syndrome, which can occur in cases such as sepsis, aspiration of gastric contents, pneumonia and both avian and human influenza.
Penninger and colleagues found in a study with mice, that angiotensin-converting enzyme 2 (ACE2) is a crucial receptor for the SARS virus.
This results in a disruption of the body's protective renin-angiotensin system, which leads to respiratory distress syndrome, as fluids seep into the air sacks.
The renin-angiotensin system uses enzymes to regulate sodium balance, fluid volume and blood pressure.
SARS which originated in China, was first identified in 2003, and spread rapidly to Asia, Canada and elsewhere.
Almost 800 people died and travel, economics and even some scientific meetings were disrupted.
The researchers when they discovered that disabling ACE2 allowed lung damage to occur, then considered whether providing more of the enzyme would help reverse this effect. When they did create more ACE2 in the mice, the mice appeared to be protected from the lung failure effects of SARS.
Penninger says this happened in two ways.
The ACE2 first combined with the virus and prevented it from binding to normal cells, and then the enzyme protected the mice from acute lung failure.
Penninger says the SARS virus has indicated a protein that may help millions affected by a previously untreatable disease.
John Nicholls and Malik Peiris of the University of Hong Kong agree that the findings indicate a productive field for investigation, but do note that there are differences in the way SARS binds with human ACE2 and ACE2 in mice.
The research was funded by the Austrian Academy of Sciences, Austrian National Bank, Marie Curie Fellowship of the European Union, Beijing Committee of Science and Technology, National Natural Science Foundation of China, Joincare Corporation, Canadian Institutes of Health Research, Canada Foundation for Innovation and the German Research Council.
The report is published in Nature Medicine.