The multiple sclerosis-associated retrovirus and its HERV-W endogenous family: a biological interface between virology, genetics, and immunology in human physiology and disease

被引:70
作者
Dolei, Antonina [1 ,2 ]
Perron, Herve [3 ]
机构
[1] Univ Sassari, Microbiol Sect, Dept Biomed Sci, I-07100 Sassari, Italy
[2] Univ Sassari, Ctr Excellence Biotechnol Dev & Biodivers Res, I-07100 Sassari, Italy
[3] GeNeuro, Geneva, Switzerland
关键词
endogenous retroviruses; HERV-W; MSRV; multiple sclerosis; schizophrenia; syncytin; REVERSE-TRANSCRIPTASE ACTIVITY; LEPTOMENINGEAL CELL-LINE; TWIN PAIRS DISCORDANT; SIMPLEX-VIRUS TYPE-1; MOLECULAR CHARACTERIZATION; IMMUNE-RESPONSES; ENVELOPE PROTEIN; IN-VITRO; BIPOLAR DISORDER; OPTIC NEURITIS;
D O I
10.1080/13550280802448451
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
This mini-review summarizes current knowledge of MSRV (multiple sclerosis-associated retrovirus), founder member of the type W family of human endogenous retroviruses (HERVs), its pathogenic potential and association with diseases. As retrotransposable elements, HERVs behave differently from stable genes, and cannot be studied with Mendelian genetics concepts only. They also display complex interactions with other HERV families, and with classical viruses. These concepts may contribute to unravelling the etiopathogenesis of complex diseases such as multiple sclerosis, schizophrenia, and other chronic multifactorial diseases.
引用
收藏
页码:4 / 13
页数:10
相关论文
共 82 条
  • [1] Envelope gene of the human endogenous retrovirus HERV-W encodes a functional retrovirus envelope
    An, DS
    Xie, YM
    Chen, ISY
    [J]. JOURNAL OF VIROLOGY, 2001, 75 (07) : 3488 - 3489
  • [2] Human endogenous retrovirus glycoprotein-mediated induction of redox reactants causes oligodendrocyte death and demyelination
    Antony, JM
    van Marle, G
    Opii, W
    Butterfield, DA
    Mallet, F
    Yong, VW
    Wallace, JL
    Deacon, RM
    Warren, K
    Power, C
    [J]. NATURE NEUROSCIENCE, 2004, 7 (10) : 1088 - 1095
  • [3] Comparative expression of human endogenous retrovirus-W genes in multiple sclerosis
    Antony, Joseph M.
    Zhu, Yu
    Izad, Maryam
    Warren, Kenneth G.
    Vodjgani, Mohammed
    Mallet, Francois
    Power, Christopher
    [J]. AIDS RESEARCH AND HUMAN RETROVIRUSES, 2007, 23 (10) : 1251 - 1256
  • [4] Quantitative analysis of human endogenous retrovirus-W env in neuroinflammatory diseases
    Antony, Joseph M.
    Izad, Maryam
    Bar-Or, Amit
    Warren, Kenneth G.
    Vodjgani, Mohammed
    Mallet, Francois
    Power, C.
    [J]. AIDS RESEARCH AND HUMAN RETROVIRUSES, 2006, 22 (12) : 1253 - 1259
  • [5] The human endogenous retrovirus envelope glycoprotein, syncytin-1, regulates neuroinflammation and its receptor expression in multiple sclerosis: A role for endoplasmic reticulum chaperones in astrocytes
    Antony, Joseph M.
    Ellestad, Kristofor K.
    Hammond, Robert
    Imaizumi, Kazunori
    Mallet, Francois
    Warren, Kenneth G.
    Power, Christopher
    [J]. JOURNAL OF IMMUNOLOGY, 2007, 179 (02) : 1210 - 1224
  • [6] Arru Giannina, 2007, Int J Biomed Sci, V3, P292
  • [7] High copy number in human endogenous retrovirus families is associated with copying mechanisms in addition to reinfection
    Belshaw, R
    Katzourakis, A
    Paces, J
    Burt, A
    Tristem, M
    [J]. MOLECULAR BIOLOGY AND EVOLUTION, 2005, 22 (04) : 814 - 817
  • [8] Rate of recombinational deletion among human endogenous retroviruses
    Belshaw, Robert
    Watson, Jason
    Katzourakis, Aris
    Howe, Alexis
    Woolven-Allen, John
    Burt, Austin
    Tristem, Michael
    [J]. JOURNAL OF VIROLOGY, 2007, 81 (17) : 9437 - 9442
  • [9] Prognostic factors in multiple sclerosis
    Bergamaschi, Roberto
    [J]. NEUROBIOLOGY OF MULTIPLE SCLEROSIS, 2007, 79 : 423 - 447
  • [10] Genomewide screening for fusogenic human endogenous retrovirus envelopes identifies syncytin 2, a gene conserved on primate evolution
    Blaise, S
    de Parseval, N
    Bénit, L
    Heidmann, T
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (22) : 13013 - 13018