Molecular aspects of poliovirus biology with a special focus on the interactions with nerve cells

被引:34
作者
Blondel, B [1 ]
Duncan, G
Couderc, T
Delpeyroux, F
Pavio, N
Colbère-Garapin, F
机构
[1] Inst Pasteur, Unite Neurovirol & Regenerat Syst Nerveaux, F-75724 Paris 15, France
[2] Inst Pasteur, Lab Epidemiol Mol Enterovirus, F-75724 Paris 15, France
关键词
poliovirus; neurovirulence; persistence; host range;
D O I
10.3109/13550289809113478
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Poliovirus (PV), the pathogenic agent of paralytic poliomyelitis, is the prototype of the picornavirus family. Although paralytic poliomyelitis has been nearly totally eradicated in most industrialized countries, PV continues to be an important public health problem in many developing countries. Moreover, in industrialized countries, two current concerns are the occurence, albeit at a very low frequency, of vaccine-associated paralytic poliomyelitis, due to the genetic instability of the attenuated oral PV strains in vaccinees, and the emergence of a neuro-muscular pathology in many survivors of the acute disease, called the post-polio syndrome. PV has been targeted by the World Health Organization for world-wide eradication in the coming decade and continues to be the subject of intensive research. The advances made in the molecular biology of PV, taken together with the development of new animal and cell models, have permitted a new look at a key step in the pathogenesis of poliomyelitis, i.e. the interactions between PV and nerve cells. These aspects of PV biology are developed in this review according to three themes: (i) the PV host range; (ii) the molecular determinants of PV neurovirulence and attenuation; and (iii) the persistence of PV in nerve cells, which has proven to be an interesting new domain in the field of PV research.
引用
收藏
页码:1 / 26
页数:26
相关论文
共 299 条
[91]  
GHENDON Y, 1972, VIROLOGY, V10, P260
[92]   Activation of the translational suppressor 4E-BP1 following infection with encephalomyocarditis virus and poliovirus [J].
Gingras, AC ;
Svitkin, Y ;
Belsham, GJ ;
Pause, A ;
Sonenberg, N .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (11) :5578-5583
[93]   Internal ribosomal entry site substitution eliminates neurovirulence in intergeneric poliovirus recombinants [J].
Gromeier, M ;
Alexander, L ;
Wimmer, E .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (06) :2370-2375
[94]  
Gromeier M, 1997, J NEUROVIROL, V3, pS35
[95]   KINETICS OF POLIOVIRUS UNCOATING IN HELA-CELLS IN A NONACIDIC ENVIRONMENT [J].
GROMEIER, M ;
WETZ, K .
JOURNAL OF VIROLOGY, 1990, 64 (08) :3590-3597
[96]   MOUSE NEUROPATHOGENIC POLIOVIRUS STRAINS CAUSE DAMAGE IN THE CENTRAL-NERVOUS-SYSTEM DISTINCT FROM POLIOMYELITIS [J].
GROMEIER, M ;
LU, HH ;
WIMMER, E .
MICROBIAL PATHOGENESIS, 1995, 18 (04) :253-267
[97]  
Gutierrez AL, 1997, J VIROL, V71, P3826
[98]   Attenuation stem-loop lesions in the 5' noncoding region of poliovirus RNA: Neuronal cell-specific translation defects [J].
Haller, AA ;
Stewart, SR ;
Semler, BL .
JOURNAL OF VIROLOGY, 1996, 70 (03) :1467-1474
[99]  
Haller Aurelia A., 1995, P113
[100]   TRANSLATIONAL ENHANCEMENT OF THE POLIOVIRUS 5' NONCODING REGION MEDIATED BY VIRUS-ENCODED POLYPEPTIDE-2A [J].
HAMBIDGE, SJ ;
SARNOW, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (21) :10272-10276