Researchers at the University of Northern Colorado and the University of New Mexico School of Medicine have discovered a mechanism by which deer mice might escape disease despite being infected with the virus.

Sin Nombre virus (SNV) is the cause of hantavirus cardiopulmonary syndrome (HCPS), an often-fatal infection acquired by exposure to deer mice. More than 100 patients have contracted HCPS in rural areas of Colorado and New Mexico alone. While this disease is very severe in humans and lacks a specific treatment, deer mice, the native carriers of SNV, are completely resistant to the disease and do not suffer ill effects from their infections.

Now, researchers at the University of Northern Colorado and the University of New Mexico School of Medicine have discovered a mechanism by which deer mice might escape disease despite being infected with the virus. Their studies also suggest why the virus may persist in deer mice and offer a new potential treatment option for human hantavirus infections. The new findings were published today in the online edition of The Proceedings of the National Academy of Sciences.

 HCPS is characterized by blood plasma leaking from blood vessels into the lungs of infected patients, affecting lung functions and causing a severe drop in cardiac output. In HCPS, the virus does not cause damage to infected cells, but instead induces a harmful inflammatory immune response that causes the disease. HCPS has an overall fatality rate of about 35% in the U. S. and has killed four of six people infected in Colorado this year.

The work, led by Tony Schountz, PhD, in the School of Biological Sciences at UNC and Brian Hjelle, MD, in the Department of Pathology at UNM, found that the immune response to hantaviruses in deer mice appears to be controlled by a specific type of immune cell, termed a regulatory T cell (Treg cell). These Treg cells turn off inflammatory immune responses, thus prevent diseases caused by inflammation.

Since these cells have been shown to prevent clearance of other viruses, their prominence in deer mice that are infected with SNV suggests they may be responsible for SNV’s persistent, but innocuous, infection of rodents.

The Treg cells from the deer mice expressed a protein, transforming growth factor beta (TGF beta) during persistent infection. This protein is a potent anti-inflammatory molecule that can inhibit inflammatory immune responses. It is possible that TGF beta may be used some day to treat patients infected with hantaviruses, which may suppress the inflammatory response that is responsible for causing human HCPS.

In a companion article in the journal, researchers led by Sabra Klein, PhD, at the Johns Hopkins Bloomberg School of Public Health, found nearly identical results using another hantavirus. Together, these studies provide a general understanding of how hantaviruses can persistently infect their rodent hosts without causing disease. Drs. Schountz and Hjelle each received grant support from the National Institutes of Health to carry out their work.
Contact: Cindy Foster, 272-3322