TY - JOUR
T1 - The Etiology of Multiple Sclerosis: Genetic Evidence for the Involvement of the Human Endogenous Retrovirus HERV-Fc1
AU - Nexø, Bjørn Andersen
AU - Christensen, Tove
AU - Frederiksen, Jette
AU - Møller-Larsen, Anné
AU - Oturai, Annette Bang
AU - Villesen, Palle
AU - Hansen, Bettina
AU - Nissen, Kari K
AU - Laska, Magdalena J
AU - Petersen, Trine Skov
AU - Bonnesen, Sandra
AU - Hedemand, Anne
AU - Wu, Tingting
AU - Wang, Xinjie
AU - Zhang, Xiuqing
AU - Brudek, Tomasz
AU - Maric, Romana
AU - Søndergaard, Helle
AU - Sellebjerg, Finn Thorup
AU - Brusgaard, Klaus
AU - Kjeldbjerg, Anders L
AU - Rasmussen, Henrik B
AU - Nielsen, Anders L
AU - Nyegaard, Mette
AU - Petersen, Thor
AU - Børglum, Anders D
AU - Pedersen, Finn S
PY - 2011/1/1
Y1 - 2011/1/1
N2 - We have investigated the role of human endogenous retroviruses in multiple sclerosis by analyzing the DNA of patients and controls in 4 cohorts for associations between multiple sclerosis and polymorphisms near viral restriction genes or near endogenous retroviral loci with one or more intact or almost-intact genes. We found that SNPs in the gene TRIM5 were inversely correlated with disease. Conversely, SNPs around one retroviral locus, HERV-Fc1, showed a highly significant association with disease. The latter association was limited to a narrow region that contains no other known genes. We conclude that HERV-Fc1 and TRIM5 play a role in the etiology of multiple sclerosis. If these results are confirmed, they point to new modes of treatment for multiple sclerosis.
AB - We have investigated the role of human endogenous retroviruses in multiple sclerosis by analyzing the DNA of patients and controls in 4 cohorts for associations between multiple sclerosis and polymorphisms near viral restriction genes or near endogenous retroviral loci with one or more intact or almost-intact genes. We found that SNPs in the gene TRIM5 were inversely correlated with disease. Conversely, SNPs around one retroviral locus, HERV-Fc1, showed a highly significant association with disease. The latter association was limited to a narrow region that contains no other known genes. We conclude that HERV-Fc1 and TRIM5 play a role in the etiology of multiple sclerosis. If these results are confirmed, they point to new modes of treatment for multiple sclerosis.
U2 - 10.1371/journal.pone.0016652
DO - 10.1371/journal.pone.0016652
M3 - Journal article
C2 - 21311761
SN - 1932-6203
VL - 6
SP - e16652
JO - P L o S One
JF - P L o S One
IS - 2
ER -