Pathogenesis of severe acute respiratory syndrome.
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.
Lau
Yu Lung
YL
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
Peiris
J S Malik
JS
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*