Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2004 Jul;203(3):740-3.
doi: 10.1002/path.1597.

Exploring the pathogenesis of severe acute respiratory syndrome (SARS): the tissue distribution of the coronavirus (SARS-CoV) and its putative receptor, angiotensin-converting enzyme 2 (ACE2)

K F To  1 , Anthony W I Lo
Affiliations

Exploring the pathogenesis of severe acute respiratory syndrome (SARS): the tissue distribution of the coronavirus (SARS-CoV) and its putative receptor, angiotensin-converting enzyme 2 (ACE2)

K F To et al. J Pathol. 2004 Jul.

Abstract

Severe acute respiratory syndrome (SARS) is an emerging infectious disease associated with a new coronavirus, SARS-CoV. Pulmonary involvement is the dominant clinical feature but extra-pulmonary manifestations are also common. Factors that account for the wide spectrum of organ system involvement and disease severity are poorly understood and the pathogenesis of SARS-CoV infection remains unclear. Angiotensin converting enzyme 2 (ACE2) has recently been identified as the functional cellular receptor for SARS-CoV. Studies of the tissue and cellular distribution of SARS-CoV, and ACE2 protein expression, reveal new insights into the pathogenesis of this deadly disease. ACE2 is expressed at high level in the primary target cells of SARS-CoV, namely pneumocytes and surface enterocytes of the small intestine. Despite the fact that SARS-CoV can infect the lung and intestine, the tissue responses in these two organs are different. All other tissues and cell types expressing ACE2 may be potential targets of SARS-CoV infection. Remarkably, endothelial cells, which express ACE2 to a high level, have not been shown to be infected by SARS-CoV. There is also evidence that cell types without detectable ACE2 expression may also be infected by the virus. Furthermore, studies in a new human cell culture model have indicated that the presence of ACE2 alone is not sufficient for maintaining viral infection. Therefore, other virus receptors or co-receptors may be required in different tissues. Moreover, the interaction between SARS-CoV and the immunological or lymphoid system remains to be defined. It is clear that we are only at the dawn of our understanding of the pathogenesis of SARS. As our knowledge of the pathogenic mechanisms improves, a more rational approach to therapeutic and vaccine development can be designed in order to combat this new and fatal human disease.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Detection of SARS‐CoV membrane (M) protein in tissues from SARS patients by immunohistochemistry (1 : 100) using an anti‐peptide antibody with a previously described routine protocol 22. Note the cytoplasmic expression of this protein in SARS‐CoV‐infected cells (arrows). (A) Pneumocytes of the lung (original magnification ×400) and (B) surface enterocytes of the small intestine (original magnification ×200). Similar results were obtained using anti‐peptide antibodies against N (nucleocapsid) and S (spike) proteins. These antibodies were generated from rabbits immunized with a KLH‐conjugated synthetic peptide selected from the N‐ or C‐termini of the respective SARS‐CoV proteins. These figures are from autopsy samples, which were used as part of our ongoing project on SARS, approved by the local ethical committee
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. WHO . Summary of probable SARS cases with onset of illness from 1 November 2002 to 31 July 2003. http://www.who.int/csr/sars/country/table 2004_04_21/en/ [Accessed 28 April 2004].
    1. WHO . Severe acute respiratory syndrome (SARS). http://www.who.int/csr/don/archive/disease/severe_acute_respiratory_synd... [Accessed 28 April 2004].
    1. Stadler K, Masignani V, Eickmann M, et al. SARS—beginning to understand a new virus. Nature Rev Microbiol 2003; 1: 209–218. - PMC - PubMed
    1. Chinese SMEC. Molecular evolution of the SARS coronavirus during the course of the SARS epidemic in China. Science 2004; 303: 1666–1669. - PubMed
    1. Chim SS, Tsui SK, Chan KC, et al. Genomic characterisation of the severe acute respiratory syndrome coronavirus of Amoy Gardens outbreak in Hong Kong. Lancet 2003; 362: 1807–1808. - PMC - PubMed

Publication types

MeSH terms

LinkOut - more resources