title: Pathogenesis of severe acute respiratory syndrome.
abstract: Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441-700 of the spike protein (S protein) as the major epitope.
authors.affiliation: Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road, Hong Kong. lauylung@hkucc.hku.hk
authors.forename: Yu Lung
authors.initials: YL
authors.lastname: Lau
authors.forename: J S Malik
authors.initials: JS
authors.lastname: Peiris
mesh_terms: D000818:Animals; D020022:Genetic Predisposition to Disease; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000821:virology; D045473:Severe acute respiratory syndrome-related coronavirus / Q000276:immunology* / Q000472:pathogenicity* / Q000502:physiology; D045169:Severe Acute Respiratory Syndrome / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000821:virology*