| Literature DB >> 25013204 |
Jussi Hepojoki1, Tomas Strandin1, Udo Hetzel2, Tarja Sironen1, Jonas Klingström3, Jussi Sane1, Satu Mäkelä4,5, Jukka Mustonen4,5, Seppo Meri6, Åke Lundkvist7, Olli Vapalahti8,2,1, Hilkka Lankinen1, Antti Vaheri8,1.
Abstract
Hantaviruses are zoonotic viruses that cause life-threatening diseases when transmitted to humans. Severe hantavirus infection is manifested by impairment of renal function, pulmonary oedema and capillary leakage. Both innate and adaptive immune responses contribute to the pathogenesis, but the underlying mechanisms are not fully understood. Here, we showed that galectin-3-binding protein (Gal-3BP) was upregulated as a result of hantavirus infection both in vitro and in vivo. Gal-3BP is a secreted glycoprotein found in human serum, and increased Gal-3BP levels have been reported in chronic viral infections and in several types of cancer. Our in vitro experiments showed that, whilst Vero E6 cells (an African green monkey kidney cell line) constitutively expressed and secreted Gal-3BP, this protein was detected in primary human cells only as a result of hantavirus infection. Analysis of Gal-3BP levels in serum samples of cynomolgus macaques infected experimentally with hantavirus indicated that hantavirus infection induced Gal-3BP also in vivo. Finally, analysis of plasma samples collected from patients hospitalized because of acute hantavirus infection showed higher Gal-3BP levels during the acute than the convalescent phase. Furthermore, the Gal-3BP levels in patients with haemorrhagic fever with renal syndrome correlated with increased complement activation and with clinical variables reflecting the severity of acute hantavirus infection.Entities:
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Year: 2014 PMID: 25013204 DOI: 10.1099/vir.0.066837-0
Source DB: PubMed Journal: J Gen Virol ISSN: 0022-1317 Impact factor: 3.891