Researchers at the Johns Hopkins Bloomberg School of Public Health have determined the mechanism that allows hantaviruses to persist in rodents. Hantaviruses are deadly to humans, but do not cause illness in rats that carry the virus. According to the researchers, hantaviruses modulate the rat’s immune system T cells, which then regulate proteins that enable the virus to persist within the rat. The study is published in the September 25 issue of PNAS. “Hantaviruses can exploit regulatory systems in their rodent hosts to maintain persistent infection” said the study’s lead author, Judith Easterbrook, a graduate student in the Bloomberg School’s Department of Molecular Microbiology and Immunology. For the study, the research team examined Norway rats infected with Seoul virus, which is a form of hantavirus. They observed significantly higher numbers of regulator T cells in rats with persistent Seoul virus. To determine the role that regulatory T cells play in virus persistence, the researchers inactivated these T cells, which reduced the presence of hantavirus in the rats. “These data are of public health significance as they illustrate that regulatory T cell responses allow hemorrhagic fever viruses to persist in their reservoirs which increases the likelihood of transmission to humans,” said Sabra Klein, PhD, senior author of the study and assistant professor in the Department of Molecular Microbiology and Immunology. “Regulatory T cells enhance persistence of the zoonotic pathogen Seoul virus in its reservoir host” was written by Judith D. Easterbrook, M. Christine Zink and Sabra L. Klein. The research was supported by a grant from the National Institutes of Health. Public Affairs media contacts for the Johns Hopkins Bloomberg School of Public Health: Tim Parsons or Kenna L. Lowe at 410-955-6878 or paffairs@jhsph.edu. | 
