The spread of prions through the body in naturally acquired transmissible spongiform encephalopathies

被引:93
作者
Beekes, Michael
McBride, Patricia A.
机构
[1] Robert Koch Inst, D-13353 Berlin, Germany
[2] Inst Anim Hlth, Neuropathogenesis Unit, Edinburgh, Midlothian, Scotland
关键词
naturally acquired TSEs; prion; prion diseases; prion protein; prion routing; prion spread; transmissible spongiform encephalopathies;
D O I
10.1111/j.1742-4658.2007.05631.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Transmissible spongiform encephalopathies are fatal neurodegenerative diseases that are caused by unconventional pathogens and affect the central nervous system of animals and humans. Several different forms of these diseases result from natural infection (i.e. exposure to transmissible spongiform encephalopathy agents or prions, present in the natural environment of the respective host). This holds true also for scrapie in sheep, bovine spongiform encephalopathy in cattle, chronic wasting disease in elk and deer, or variant Creutzfeldt-Jakob disease in humans, all of which are assumed to originate predominantly from peroral prion infection. This article intends to provide an overview of the current state of knowledge on the spread of scrapie, chronic wasting disease, bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease agents through the body in naturally affected hosts, and in model animals experimentally challenged via the alimentary tract. Special attention is given to the tissue components and spreading pathways involved in the key stages of prion routing through the body, such as intestinal uptake, neuroinvasion of nerves and the central nervous system, and centrifugal spread from the brain and spinal cord to peripheral sites (e.g. sensory ganglia or muscles). The elucidation of the pathways and mechanisms by which prions invade a host and spread through the organism can contribute to efficient infection control strategies and the improvement of transmissible spongiform encephalopathy diagnostics. It may also help to identify prophylactic or therapeutic approaches that would impede naturally acquired transmissible spongiform encephalopathy infections.
引用
收藏
页码:588 / 605
页数:18
相关论文
共 165 条
[11]   Early accumulation of pathological PrP in the enteric nervous system and gut-associated lymphoid tissue of hamsters orally infected with scrapie [J].
Beekes, M ;
McBride, PA .
NEUROSCIENCE LETTERS, 2000, 278 (03) :181-184
[12]   Cerebral targeting indicates vagal spread of infection in hamsters fed with scrapie [J].
Beekes, M ;
McBride, PA ;
Baldauf, E .
JOURNAL OF GENERAL VIROLOGY, 1998, 79 :601-607
[13]   PrP-expressing tissue required for transfer of scrapie infectivity from spleen to brain [J].
Blattler, T ;
Brandner, S ;
Raeber, AJ ;
Klein, MA ;
Voigtlander, T ;
Weissmann, C ;
Aguzzi, A .
NATURE, 1997, 389 (6646) :69-73
[14]   COPURIFICATION OF SP33-37 AND SCRAPIE AGENT FROM HAMSTER BRAIN PRIOR TO DETECTABLE HISTOPATHOLOGY AND CLINICAL-DISEASE [J].
BOLTON, DC ;
RUDELLI, RD ;
CURRIE, JR ;
BENDHEIM, PE .
JOURNAL OF GENERAL VIROLOGY, 1991, 72 :2905-2913
[15]   Natural and experimental oral infection of nonhuman primates by bovine spongiform encephalopathy agents [J].
Bons, N ;
Mestre-Frances, N ;
Belli, P ;
Cathala, F ;
Gajdusek, DC ;
Brown, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (07) :4046-4051
[16]   Prions in skeletal muscle [J].
Bosque, PJ ;
Ryou, C ;
Telling, G ;
Peretz, D ;
Legname, G ;
DeArmond, SJ ;
Prusiner, SB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (06) :3812-3817
[17]  
Bradley R, 2001, CONTRIB MICROBIOL, V7, P105
[18]  
Bradley R., 2004, V11, P146
[19]   A prion lexicon (out of control) [J].
Brown, P ;
Cervenakova, L .
LANCET, 2005, 365 (9454) :122-122
[20]   SURVIVAL OF SCRAPIE VIRUS AFTER 3 YEARS INTERNMENT [J].
BROWN, P ;
GAJDUSEK, DC .
LANCET, 1991, 337 (8736) :269-270