How the SARS coronavirus causes disease: host or organism?

J Pathol. 2006 Jan;208(2):142-51. doi: 10.1002/path.1897.

Abstract

The previous epidemic of severe acute respiratory syndrome (SARS) has ended. However, many questions concerning how the aetiological agent, the novel SARS coronavirus (CoV), causes illness in humans remain unanswered. The pathology of fatal cases of SARS is dominated by diffuse alveolar damage. Specific histological changes are not detected in other organs. These contrast remarkably with the clinical picture, in which there are apparent manifestations in multiple organs. Both pathogen and host factors are important in the pathogenesis of SARS. The choice of specific receptors and the unique genome of the SARS-CoV are important elements in understanding the biology of the pathogen. For the host cells, the outcome of SARS-CoV infection, whether there are cytopathic effects or not, depends on the cell types that are infected. At the whole-body level, immune-mediated damage, due to activation of cytokines and/or chemokines and, perhaps, autoimmunity, may play key roles in the clinical and pathological features of SARS. Continued research is still required to determine the pathogenetic mechanisms involved and to combat this new emerging human infectious disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin-Converting Enzyme 2
  • Animals
  • Carboxypeptidases / metabolism
  • Chemokines / immunology
  • Disease Models, Animal
  • Humans
  • Immunity, Innate / immunology
  • Immunogenetics
  • Lectins / metabolism
  • Lung / pathology
  • Peptidyl-Dipeptidase A
  • Receptors, Virus / metabolism
  • Severe Acute Respiratory Syndrome / immunology
  • Severe Acute Respiratory Syndrome / pathology
  • Severe Acute Respiratory Syndrome / virology*
  • Severe acute respiratory syndrome-related coronavirus / immunology
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity*

Substances

  • Chemokines
  • Lectins
  • Receptors, Virus
  • Carboxypeptidases
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2