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A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis
Linköping University, Department of Clinical and Experimental Medicine, Molecular Virology . Linköping University, Faculty of Health Sciences.
Department of Medicine Karolinska University Hospital Huddinge.
Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Clinical Microbiology . Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Microbiology.
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2008 (English)In: Journal of Infectious Diseases, ISSN 0022-1899, Vol. 197, no 2, 266-269 p.Article in journal (Refereed) Published
Abstract [en]

Tickborne encephalitis (TBE) virus infections can be asymptomatic or cause moderate to severe injuries of the central nervous system. Why some individuals develop severe disease is unknown, but a role for host genetic factors has been suggested. To investigate whether chemokine receptor CCR5 is associated with TBE, CCR5Δ32 genotyping was performed among Lithuanian patients with TBE (n = 129) or with aseptic meningoencephalitis (n = 76) as well as among control subjects (n = 134). We found individuals homozygous for CCR5Δ32 (P = .026) only among patients with TBE and a higher allele prevalence among patients with TBE compared with the other groups studied. CCR5Δ32 allele prevalence also increased with the clinical severity of disease. © 2007 by the Infectious Diseases Society of America. All rights reserved.

Place, publisher, year, edition, pages
2008. Vol. 197, no 2, 266-269 p.
Keyword [en]
Alleles Encephalitis, Tick-Borne/epidemiology/*genetics/physiopathology *Gene Deletion Gene Frequency *Genetic Predisposition to Disease Homozygote Humans Lithuania/epidemiology Meningoencephalitis/genetics Receptors, CCR5/*genetics Severity of Illness In
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-43369DOI: 10.1086/524709Local ID: 73655OAI: diva2:264228
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2010-04-27Bibliographically approved
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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