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Curr Opin Immunol. 2005 Aug;17(4):404-10.

Pathogenesis of severe acute respiratory syndrome.

Author information

1
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

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.

PMID:
15950449
DOI:
10.1016/j.coi.2005.05.009
[Indexed for MEDLINE]

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