Anti-viral properties of interferon beta treatment in patients with multiple sclerosis

被引:40
作者
Hong, J
Tejada-Simon, MV
Rivera, VM
Zang, YCQ
Zhang, JZ
机构
[1] Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA
[2] Dept Neurol, Multiple Sclerosis Res Unit, Houston, TX USA
[3] Baylor Methodist Multiple Sclerosis Ctr, Houston, TX USA
关键词
human herpesvirus-6; interferon beta; multiple sclerosis;
D O I
10.1191/1352458502ms794oa
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Viral infections are potentially associated with the etiology and pathogenesis of multiple sclerosis (MS). It has been speculated that the treatment efficacy of interferon beta (IFN beta) in MS may relate to its anti-viral properties. The study was undertaken to evaluate the in vivo anti-viral effects of IFN beta-1a in patients with MS. Human herpesvirus-6 (HHV-6) was studied as an example for being a latent neurotropic virus. IFN beta used at concentrations of approximately 0.5 mug/ml was shown to significantly reduce in vitro HHV-6 replication in a susceptible T-cell line. Sera derived from 23 MS patients treated with IFN beta-la were examined for serum cell-free DNA of HHV-6 as an indicator for viral replication and the reactivity of IgM antibodies to a recombinant HHV-6 virion protein containing a known immunoreactive region. The results were compared with those of control sera obtained from untreated MS (n = 29) and healthy individuals (n = 21). The findings indicated that IFN beta treatment significantly reduced HHV-6 replication as evident by decreased cell-free DNA in treated MS specimens. The results correlated with decreased IgM reactivity to the HHV-6 antigen in treated MS patients compared to untreated controls, suggesting reduced exposure to HHV-6. The findings were confirmed in paired sera obtained from seven MS patients before and after the treatment. The study provides new evidence indicating that IFN beta has potent in vivo anti-viral effects that may contribute to the treatment efficacy in MS.
引用
收藏
页码:237 / 242
页数:6
相关论文
共 28 条
[1]   The function of type I interferons in antimicrobial immunity [J].
Bogdan, C .
CURRENT OPINION IN IMMUNOLOGY, 2000, 12 (04) :419-424
[2]   Subacute leukoencephalitis caused by CNS infection with human herpesvirus-6 manifesting as acute multiple sclerosis [J].
Carrigan, DR ;
Harrington, D ;
Knox, KK .
NEUROLOGY, 1996, 47 (01) :145-148
[3]   PLAQUE-ASSOCIATED EXPRESSION OF HUMAN HERPESVIRUS-6 IN MULTIPLE-SCLEROSIS [J].
CHALLONER, PB ;
SMITH, KT ;
PARKER, JD ;
MACLEOD, DL ;
COULTER, SN ;
ROSE, TM ;
SCHULTZ, ER ;
BENNETT, JL ;
GARBER, RL ;
CHANG, M ;
SCHAD, PA ;
SEWART, PM ;
NOWINSKI, RC ;
BROWN, JP ;
BURMER, GC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) :7440-7444
[4]   Viruses and multiple sclerosis [J].
Dalgleish, AG .
ACTA NEUROLOGICA SCANDINAVICA, 1997, 95 :8-15
[5]   INTERFERON BETA-1B IS EFFECTIVE IN RELAPSING-REMITTING MULTIPLE-SCLEROSIS - CLINICAL-RESULTS OF A MULTICENTER, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL [J].
DUQUETTE, P ;
GIRARD, M ;
DESPAULT, L ;
DUBOIS, R ;
KNOBLER, RL ;
LUBLIN, FD ;
KELLEY, L ;
FRANCIS, GS ;
LAPIERRE, Y ;
ANTEL, J ;
FREEDMAN, M ;
HUM, S ;
GREENSTEIN, JI ;
MISHRA, B ;
MULDOON, J ;
WHITAKER, JN ;
EVANS, BK ;
LAYTON, B ;
SIBLEY, WA ;
LAGUNA, J ;
KRIKAWA, J ;
PATY, DW ;
OGER, JJ ;
KASTRUKOFF, LF ;
MOORE, GRW ;
HASHIMOTO, SA ;
MORRISON, W ;
NELSON, J ;
GOODIN, DS ;
MASSA, SM ;
GUTTERIDGE, E ;
ARNASON, BGW ;
NORONHA, A ;
REDER, AT ;
MARTIA, R ;
EBERS, GC ;
RICE, GPA ;
LESAUX, J ;
JOHNSON, KP ;
PANITCH, HS ;
BEVER, CT ;
CONWAY, K ;
WALLENBERG, JC ;
BEDELL, L ;
VANDENNOORT, S ;
WEINSHENKER, B ;
WEISS, W ;
REINGOLD, S ;
PACHNER, A ;
TAYLOR, W .
NEUROLOGY, 1993, 43 (04) :655-661
[6]   The distinction blurs between an autoimmune versus microbial hypothesis in multiple sclerosis [J].
Hafler, DA .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (05) :527-529
[7]   Ubiquitous pathogens - Links between infection and autoimmunity in MS? [J].
Hunter, SF ;
Hafler, DA .
NEUROLOGY, 2000, 55 (02) :164-165
[8]   Intramuscular interferon beta-1 alpha for disease progression in relapsing multiple sclerosis [J].
Jacobs, LD ;
Cookfair, DL ;
Rudick, RA ;
Herndon, RM ;
Richert, JR ;
Salazar, AM ;
Fischer, JS ;
Goodkin, DE ;
Granger, CV ;
Simon, JH ;
Alam, JJ ;
Bartoszak, DM ;
Bourdette, DN ;
Braiman, J ;
Brownscheidle, CM ;
Coats, ME ;
Cohan, SL ;
Dougherty, DS ;
Kinkel, RP ;
Mass, MK ;
Munschauer, FE ;
Priore, RL ;
Pullicino, PM ;
Scherokman, BJ ;
WeinstockGuttman, B ;
Whitman, RH ;
Baird, WC ;
Fillmore, M ;
Bona, LM ;
ColonRuiz, ME ;
Nadine, BS ;
Donovan, A ;
Bennett, S ;
Kieffer, YM ;
Umhauer, MA ;
Miller, CE ;
Kilic, AK ;
Sargent, EL ;
Schachter, M ;
Shucard, DW ;
Weider, V ;
Catalano, BA ;
Cervi, JM ;
Czekay, C ;
Farrell, JL ;
Filippini, JS ;
Matyas, RC ;
Michienzi, KE ;
Ito, M ;
OMalley, JA .
ANNALS OF NEUROLOGY, 1996, 39 (03) :285-294
[9]   THE VIROLOGY OF DEMYELINATING DISEASES [J].
JOHNSON, RT .
ANNALS OF NEUROLOGY, 1994, 36 :S54-S60
[10]  
KENNEDY PGE, 1994, Q J MED, V87, P523