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Journal of Virology, August 2006, p. 8279-8282, Vol. 80, No. 16
0022-538X/06/$08.00+0 doi:10.1128/JVI.00742-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Center for Microbiological Preparedness, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden,1 Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, S-171 77 Stockholm, Sweden,2 Mabtech AB, Box 1233, S-131 52 Nacka Strand, Sweden,3 Cancer Center Karolinska, Department of Oncology-Pathology, Karolinska Institute and Hospital, S-171 76 Stockholm, Sweden,4 Division of Infectious Diseases, Department of Clinical Microbiology, Umeå University, S-901 85 Umeå, Sweden5
Received 12 April 2006/ Accepted 16 May 2006
Hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome are two diseases caused by hantaviruses. Capillary leakage is a hallmark of hantavirus infection. Pathogenic hantaviruses are not cytotoxic, but elevated levels of serum lactate dehydrogenase (LDH), indicative of cellular damage, are observed in patients. We report increased levels of serum perforin, granzyme B, and the epithelial cell apoptosis marker caspase-cleaved cytokeratin-18 during Puumala hantavirus infection. Significant correlation was observed between the levels of LDH and perforin and the levels of LDH and caspase-cleaved cytokeratin-18, suggesting that tissue damage is due to an immune reaction and that epithelial apoptosis contributed significantly to the damage.
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