<?xml version="1.0"?>
<oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:title>Advances in Rickettsia pathogenicity</dc:title>
  <dc:creator>Balraj, P.</dc:creator>
  <dc:creator>Renesto, P.</dc:creator>
  <dc:creator>/Raoult, Didier</dc:creator>
  <dc:subject>actin-based motility</dc:subject>
  <dc:subject>adhesins</dc:subject>
  <dc:subject>phagosomal escape</dc:subject>
  <dc:subject>PLD</dc:subject>
  <dc:subject>rickettsia</dc:subject>
  <dc:subject>T4SS</dc:subject>
  <dc:description>One century after the first description of rickettsiae as human pathogens, the rickettsiosis remained poorly understood diseases. These microorganisms are indeed characterized by a strictly intracellular location which has, for long, prohibited their detailed study. Within the last ten years, the completion of the genome sequences of several strains allowed gaining a better knowledge about the molecular mechanisms involved in rickettsia pathogenicity. Here, we summarized available data concerning the critical steps of rickettsia-host cell interactions that should contribute to tissue injury and diseases, that is, adhesion, phagosomal escape, motility, and intracellular survival of the bacteria.</dc:description>
  <dc:date>2009</dc:date>
  <dc:type>text</dc:type>
  <dc:identifier>https://www.documentation.ird.fr/hor/fdi:010046181</dc:identifier>
  <dc:identifier>fdi:010046181</dc:identifier>
  <dc:identifier>Balraj P., Renesto P., Raoult Didier. Advances in Rickettsia pathogenicity. 2009, 1166,  94-105</dc:identifier>
  <dc:language>EN</dc:language>
</oai_dc:dc>
