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Host genetic resistance to symptomatic norovirus (GGII.4) infections in Denmark
Linköping University, Department of Molecular and Clinical Medicine, Molecular Virology. Linköping University, Faculty of Health Sciences.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Clinical Microbiology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Microbiology.
Department of Virology, Statens Serum Institut, Copenhagen, Denmark4;.
Department of Microbiology, Hvidovre Hospital, Hvidovre, Denmark.
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2007 (English)In: Journal of Clinical Microbiology, ISSN 0095-1137, E-ISSN 1098-660X, Vol. 45, no 8, 2720-2722 p.Article in journal (Refereed) Published
Abstract [en]

A total of 61 individuals involved in five norovirus outbreaks in Denmark were genotyped at nucleotides 428 and 571 of the FUT2 gene, determining secretor status, i.e., the presence of ABH antigens in secretions and on mucosa. A strong correlation (P = 0.003) was found between the secretor phenotype and symptomatic disease, extending previous knowledge and confirming that nonsense mutations in the FUT2 gene provide protection against symptomatic norovirus (GGII.4) infections. Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Place, publisher, year, edition, pages
2007. Vol. 45, no 8, 2720-2722 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-40699DOI: 10.1128/JCM.00162-07Local ID: 53918OAI: diva2:261548
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2010-04-27
In thesis
1. Host genetic risk factors to viral diseases - a double-edged sword: Studies of norovirus and tick-borne encephalitis virus
Open this publication in new window or tab >>Host genetic risk factors to viral diseases - a double-edged sword: Studies of norovirus and tick-borne encephalitis virus
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

It is today well known that the outcome of a certain infection depends on factors of both the host and the pathogen. Studies of host genetic susceptibility to infectious diseases aim to increase the understanding of why some individuals are more susceptible than others, to a certain infection. Knowledge of genetic susceptibility to a viral disease may be used in development of new therapeutic means, and also to recognize individuals who are at increased risk of severe symptoms if infected with a pathogen. It seems however that a risk factor for one disease may play a protective role in another situation; like a double-edged sword.

In this thesis I have studied genetic factors affecting susceptibility to norovirus (NoV) and factors affecting the risk of developing tick-borne encephalitis (TBE) after infection with TBE virus (TBEV). NoV is the cause of the “winter vomiting disease”, affecting millions of people every year, and causing up to 200,000 fatalities among children in developing countries, each year. It is today recognized that the secretor status of an individual, i.e. the ability to express ABO blood groups and related antigens, in secretions and on mucosa, affect the risk of being infected by NoV. By studying authentic NoV outbreaks in Denmark, Spain and Sweden and by comparing the secretor status of affected and unaffected individuals we were able to confirm that secretor status have indeed great impact on susceptibility to some NoV strains, but also that there are strains circulating, which infect individuals regardless of secretor status.

TBEV is endemic in many parts of Europe and Asia but studies have shown that 70-95% of all infections are asymptomatic or sub-clinical. Some individuals do however develop TBE, a severe disease including meningitis or encephalitis with or without myelitis. Also, many patients suffer from long-time sequelae and TBEV infections may in worst case be fatal. The reason for difference in disease outcome is not known and we have chosen to study if genetic factors affecting the immune response may play a role in disease outcome. To do this we used a prospectively collected Lithuanian material with samples from patients with TBE, AME (aseptic meningoencephalitis) and matched healthy controls. So far we have found that a deletion in chemokine receptor 5 (CCR5), a gene encoding a receptor involved in cell migration, is a risk factor for developing disease. We have also data showing that toll-like receptor 3 (TLR3), a receptor recognizing double stranded RNA (dsRNA), which is a product of TBEV replication, may instead of being protective increase the risk of TBE.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2010. 77 p.
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1183
National Category
Microbiology in the medical area
urn:nbn:se:liu:diva-54923 (URN)978-91-7393-393-3 (ISBN)
Public defence
2010-05-28, Berzeliussalen, Campus US, Linköpings universitet, Linköping, 09:00 (English)
Available from: 2010-04-27 Created: 2010-04-22 Last updated: 2010-04-27Bibliographically approved

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Kindberg, ElinÅkerlind, BrittSvensson, Lennart
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