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Quasispecies dynamics and molecular evolution of human norovirus capsid P region during chronic infection
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
University of Kalmar.
Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi.
Swedish Institute for Infectious Disease Control.
Vise andre og tillknytning
2009 (engelsk)Inngår i: Journal of General Virology, ISSN 0022-1317, E-ISSN 1465-2099, Vol. 90, s. 432-441Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

In this novel study, we have for the first time identified evolutionarily conserved capsid residues in an individual chronically infected with norovirus (GGII.3). From 2000 to 2003, a total of 147 P1-1 and P2 capsid sequences were sequenced and investigated for evolutionarily conserved and functionally important residues by the evolutionary trace (ET) algorithm. The ET algorithm revealed more absolutely conserved residues (ACR) in the P1-1 domain (47/53, 88 %) as compared with the P2 domain (86/133, 64 %). The capsid P1-1 and P2 domains evolved in time-dependent manner, with a distinct break point observed between autumn/winter of year 2000 (isolates P1, P3 and P5) and spring to autumn of year 2001 (isolates P11, P13 and P15), which presumably coincided with a change of clinical symptoms. Furthermore, the ET analysis revealed a similar receptor-binding pattern as reported for Norwalk and VA387 strains, with the CS-4 and CS-5 patch (Norwalk strain) including residues 329 and 377 and residues 306 and 310, respectively, all being ACR in all partitions. Most interesting was that residues 343, 344, 345, 374, 390 and 391 of the proposed receptor A and B trisaccharide binding site (VA387 strain) within the P2 domain remained ACR in all partitions, presumably because there was no selective advantage to alter the histo blood group antigens (HBGA) receptor binding specificity. In conclusion, this study provides novel insights to the evolutionary process of norovirus during chronic infection.

sted, utgiver, år, opplag, sider
2009. Vol. 90, s. 432-441
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-16852DOI: 10.1099/vir.0.005082-0OAI: oai:DiVA.org:liu-16852DiVA, id: diva2:174396
Tilgjengelig fra: 2009-02-21 Laget: 2009-02-20 Sist oppdatert: 2017-12-13
Inngår i avhandling
1. Human Caliciviruses: a study of viral evolution, host genetics and disease susceptibility
Åpne denne publikasjonen i ny fane eller vindu >>Human Caliciviruses: a study of viral evolution, host genetics and disease susceptibility
2012 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

The viruses described in this thesis are the norovirus and sapoviruses, which belong to the family of human caliciviruses and are known to cause gastroenteritis in humans. Gastroenteritis has emerged as a global health problem and is based on the large number of infected considered as one of the most common diseases today. According to estimates of the World Health Organization (WHO), gastroenteritis causes over five times more pediatric deaths compared to pediatric deaths caused by HIV/AIDS worldwide. Norovirus, the cause of the famous “winter vomiting disease”, is alone responsible for more than 200 000 deaths each year in children less than 5 years of age.

The mechanism for emergence and evolution of new human calicivirus strains, as well as protective immunity in the human population is poorly understood. The main focus for this thesis was to elucidate the possible correlation between human calicivirus evolution, host genetics and disease susceptibility. One of the main findings presented in this thesis is the documentation of in vivo capsid gene evolution and quasispecies dynamics during chronic NoV GI.3 infection (Paper 1). In paper II, we reported that the G428A nonsense mutation in the FUT2 gene provides strong but not absolute protection against symptomatic GII.4 NoV infection. In my last two papers (Paper III and IV), we were the first to investigate host genetic susceptibility factors during authentic SaV infection.

To summarize, the results presented in this thesis show that the success of human calicivirus infection probably is determined by a delicate interplay between virus evolution and susceptibility of the host, both genetically and immunologically.

sted, utgiver, år, opplag, sider
Linköping: Linköping University Electronic Press, 2012. s. 77
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1303
HSV kategori
Identifikatorer
urn:nbn:se:liu:diva-76036 (URN)978-91-7519-922-1 (ISBN)
Disputas
2012-04-12, Eken, Hälsouniversitetet, Campus US, Linköpings univeristet, Linköping, 09:00 (svensk)
Opponent
Veileder
Tilgjengelig fra: 2012-03-23 Laget: 2012-03-23 Sist oppdatert: 2012-05-07bibliografisk kontrollert

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