{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T04:42:33Z","timestamp":1793335353952,"version":"4.5.0"},"reference-count":743,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2001,7,1]],"date-time":"2001-07-01T00:00:00Z","timestamp":993945600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Microbiol Rev"],"published-print":{"date-parts":[[2001,7]]},"abstract":"<jats:sec>\n                    <jats:title>SUMMARY<\/jats:title>\n                    <jats:p>The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/cmr.14.3.584-640.2001","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T05:56:57Z","timestamp":1027749417000},"page":"584-640","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1812,"title":["<i>Listeria<\/i>\n                    Pathogenesis and Molecular Virulence Determinants"],"prefix":"10.1128","volume":"14","author":[{"given":"Jose\u0301 A.","family":"Va\u0301zquez-Boland","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Grupo de Patoge\u0301nesis Molecular Bacteriana, Facultad de Veterinaria, Universidad Complutense de Madrid, Madrid,1 and"},{"name":"<!--label omitted: 2-->Universidad de Leo\u0301n, Leo\u0301n,2 Spain;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Kuhn","sequence":"additional","affiliation":[{"name":"<!--label omitted: 3-->Lehrstuhl fu\u0308r Mikrobiologie, Theodor-Boveri-Institut fu\u0308r Biowissenschaften der Universita\u0308t Wu\u0308rzburg, 97074 Wu\u0308rzburg,3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick","family":"Berche","sequence":"additional","affiliation":[{"name":"<!--label omitted: 4-->Unite\u0301INSERM U411, Faculte\u0301 de Me\u0301decine Necker, 75730 Paris, France4; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trinad","family":"Chakraborty","sequence":"additional","affiliation":[{"name":"<!--label omitted: 5-->Institut fu\u0308r Medizinische Mikrobiologie, Justus-Liebig-Universita\u0308t, 35392 Giessen,5 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gustavo","family":"Dom\u0131\u0301nguez-Bernal","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Grupo de Patoge\u0301nesis Molecular Bacteriana, Facultad de Veterinaria, Universidad Complutense de Madrid, Madrid,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Werner","family":"Goebel","sequence":"additional","affiliation":[{"name":"<!--label omitted: 3-->Lehrstuhl fu\u0308r Mikrobiologie, Theodor-Boveri-Institut fu\u0308r Biowissenschaften der Universita\u0308t Wu\u0308rzburg, 97074 Wu\u0308rzburg,3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruno","family":"Gonza\u0301lez-Zorn","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Grupo de Patoge\u0301nesis Molecular Bacteriana, Facultad de Veterinaria, Universidad Complutense de Madrid, Madrid,1 and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ju\u0308rgen","family":"Wehland","sequence":"additional","affiliation":[{"name":"<!--label omitted: 6-->Department of Cell Biology and Immunology, Gesellschaft fu\u0308r Biotechnologische Forschung (GBF), 38124 Braunschweig,6 Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ju\u0308rgen","family":"Kreft","sequence":"additional","affiliation":[{"name":"<!--label omitted: 3-->Lehrstuhl fu\u0308r Mikrobiologie, Theodor-Boveri-Institut fu\u0308r Biowissenschaften der Universita\u0308t Wu\u0308rzburg, 97074 Wu\u0308rzburg,3"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02898648"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.58.8.2715-2718.1990"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1998.00790.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.62.6.795"},{"key":"e_1_3_2_6_2","doi-asserted-by":"crossref","first-page":"711","DOI":"10.2460\/javma.1992.200.05.711","article-title":"Bovine abortions attributable to Listeria ivanovii: four cases (1988\u20131990).","volume":"200","author":"Alexander A. 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