Division of Molecular Virology

The research at division of molecular virology focus on several different aspects including pathphysiology mechanisms of viral diseases, viral immunity, vaccines and human genetic factors of viral infections.

Lennart Svensson. Head

Principial investigator

PhD students

Elin Kindberg, elin.kindberg@liu.se
Beatrice Karlsson, beatrice.karlsson@liu.se
Malin Vildevall, malin.vildevall@liu.se
Johan Nordgren, johno@imk.liu.se
Filemon Bucardo, fili_bucardo@hotmail.com

Technician

Carolin Jönsson, carolin.jonsson@liu.se
Marie Hagbom, marie.hagbom@liu.se

Post Doc. Claudia Istrate

Research projects

The research group study pathophysiology mechanism of viral inte pathogens and explore host genetic mechanisms of infectious diseases

Pathophysiology mechanisms of rotavirus

Rotavirus is the leading cause of infantile gastroenteritis worlswide and is responsible for 600.000 deaths every year predominantly in developing countries. Despite the significant clinical importance and the research conducted over several decades are the phathophysiological mechanisms by which rotavirus cause diarrhoea, vomiting and nausea unresolved. We have previously reported that rotavirus evoke inestinal fluid and electrolyte secretion by activation of the enteric nervous system, VIP and serotonin (Lundgren et al Science.2000, Kortdasti et al in adult mice Gut 2004) and that Rotavirus infection is not associated with small intestinal fluid secretion (Kordasti et al JV.2006). Our research is currently aimed to determine the role of human enterochromaffin "sensor celles" cells in triggering clinical symptoms such as vomitin, nausea and diarrhea of rotavirus and norovirus.

Identification of human genetic factors associated with suseptibility of Viral infections.
The observation that certain individuals appear to have an inherited factor making them more susceptible or resistant to common infections is not new. Indeed, most of us know individuals who are more frequently ill tha others or is seldim ill. However not long time ago it was assumed that the clinical outcome of an infectious diseade was mainly due to virulence factors associated with the microorganism and little attention was given to the host genetic set up. Today we start to reveal that a complex interplay between environmental (microbial and nonmicrobial) and human (genetic and nongenetic) factors determine immunity to infection and the resultin outcome of an infection. Our reeaseach is aimed to identify human genetic factors associated with increased susceptibility or resistance to cliniccaly importan viral infections.

Identification of human genetic factors associated with suseptibility of viral infections

The observation that certain individuals appear to have an inherited factor making then more susceptible or resistant to common infections is not new. Indeed, most of us know individuals who are more frequently ill than others or is seldom ill. However not long time ago it was assumed that the clinical outcome of an infectious disease was mainly due to virulence factors associated with the microorganism and little attention was given to the host genetic set up. Today we start to reveal that a complex interplay between environmental (microbial and nonmicriobial) and human (genetic and nongenetic) factors determine immunity to infection and the resulting outcome of an infection. Our reeaseach is aimed to identify human genetic factors associated with increased susceptibility or resistance to cliniccaly important viral infections.

Norovirus

Noroviruses have emerged as a major cause of acute gastroenteritis in human of all ages. We have previously shown that a nonsense mutation in the FUT2 gene determine resistance to authentic symptomatic norovirus infections (Thorven et al J Virol.2005, Kindberg et al Sem in immunol 2007, Kindberg et al 2006). Our research focus is to explore this observation further by human intestinal receptor studies with synthetic produced norovirus and to elucidate if the nonsence 428G>A mutation in FUT2 is operating outside Europe. Furthermore development of mice model for human norovirus is requested.

TBE

Tickborne encephalitis (TBE) is caused by the TBE virus (TBEV), TBE infection can be asymptomatic or cause moderate to severe injuries of the central nervous system. A most intriguing question is why certain individuals respond with severe clinical symptoms after infection while the majority either remains asymptomatic or develops only mild disease. We have recently reported that Lithuanian individuals homozygous for CCR5^32 have an increased risk to develop encephalitis (Kindberg et al 2008). Current research is aimed to determine the molecular mechanism for this and to determine if the increased susceptibility is valid also in Scandinavia.

The research group consist of 5PhD students, 1 post-dok and 2 technicians. The research is funded by the Swedish Research Council (VR) and the Swedish International Development Cooperation agency (SIDA)