Press Release from Umeå University

New findings challenge view of key part of immune defense

[2011-02-28] The natural killer cells of our immune defense are activated for an extended period after the acute infection, which challenges the prevailing view that the elevation and activation of cells quickly pass. This is shown in a study regarding vole fever that was recently published by researchers at Umeå University, Sweden in Journal of Experimental Medicine.

These are findings of a years-long project where patients with vole fever, a northern Swedish hemorrhagic fever that has been studied with regard to natural killer (NK) cells. Vole fever is a common infection in northern Sweden that is caused by a hantavirus, Puumala virus, which is prevalent in bank voles and infects humans primarily via inhalation of virus-contaminated dust.



The symptoms are primarily high fever, head and muscle pain, abdominal pain, and generally impacted condition. Involvement of the kidneys and lungs are common. There is no dedicated and effective treatment today. As vole fever is a hemorrhagic fever, there is often a pronounced reduction in blood platelets, and bleeding complications occur. Some 30 % of the diagnosed cases are hospitalized. Mortality is 0.5 % owing to bleeding, shock, and multiple organ failure. 



The Umeå researchers, led by assistant professor Clas Ahlm, have used a unique patient cohort to study the expansion of NK cells and their activity in the course of the infection in collaboration with scientists at the Karolinska institute. The material was gathered during and following the major outbreak of vole fever in 2007. There have been few previous studies of NK cells in acute viral infections in humans, even though they are regarded as part of our so-called innate immunity. The Puumala virus itself is not cytopatogenic, i.e. doesn’t kill the infected cells. The Umeå scientists’ hypothesis is therefore that part of the pathological mechanism in vole fever involves the immune defense against the virus infection, which is further supported by these findings.



The study revealed an expansion of NK cells. This expansion persisted for an extended period after the acute infection, which surprised the researchers. This finding challenges to some extent the previous view that the elevation and activation of NK cells quickly subsides in acute viral infections. The results of the study indicate that some NK cells may have memory-like functions. 



The article “Rapid expansion and long-term persistence of elevated NK cell numbers in humans infected with hantavirus”. (J Exp Med 2011 Jan 17) can be found at 

http://jem.rupress.org/content/208/1/13

Immediately after publication the article was selected by the “Faculty of 1000”, which places it among the upper two percent of articles published in biology and medicine; see 
http://f1000.com/7906956



Hemorrhagic fevers are best known as exotic diseases with high mortality rates that primarily ravage Africa. They are caused by hantaviruses that often infect humans from animals, so-called zoonos.

The Ebola virus is probably the best-known variant. See http://en.wikipedia.org/wiki/Ebola
The Marburg virus is another. See http://en.wikipedia.org/wiki/Marburg_virus
Viruses that cause hemorrhagic fevers are most often categorized as class 3-4 infectious agents, the class that requires the highest level of security when handled, see 
http://en.wikipedia.org/wiki/Biosafety_level#Biosafety_level_4 for more information about this.

More information about Clas Ahlms research project is found at:

http://www.medfak.umu.se/english/research/show_project/?code=533&currentView=base

For more information, please contact Clas Ahlm, assistant professor at the Department of Clinical Microbiology, infectious diseases, at:

telephone +46 (0)90-785 23 09;

e-mail clas.ahlm@climi.umu.se

A high-resolution portrait picture of Clas Ahlm is found at

http://www.umu.se/digitalAssets/65/65144_ahlm_clas_0813_110301_mpn.jpg

Editor: Vetenskapsrådet
Tel: 090-786 60 58

Link to news:
http://www.umu.se/english/news/.cid154144


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Page Editor: Communication and International Relations Office
2011-03-04