Book chapter
Severe Acute Respiratory Syndrome: Epidemiology, Pathogenesis, and Animal Models
Nidoviruses, pp.299-311
ASM Press
12/07/2007
DOI: 10.1128/9781555815790.ch19
Abstract
Quantitative studies on viral load in the upper respiratory tract and the feces of patients infected with severe acute respiratory syndrome‐coronavirus (SARS‐CoV) revealed a progressive increase in viral load, peaking around day 10 after onset of disease symptoms. This explains the epidemiological observation that transmission mainly occurs after the fifth day of illness. Clinical and pathological studies of SARS cases indicate that cells in the lower respiratory tract, particularly type 1 pneumocytes, are the prime targets of SARS, with macrophages subsequently being infected. Although angiotensin‐converting enzyme 2 (ACE2) is the primary receptor for SARS, other receptors such as L‐SIGN and DC‐SIGN may facilitate virus infection, even under circumstances when the virus has not fully adapted to a new host. Epithelial lung damage together with macrophage activation results in increased levels of proinflammatory cytokines. The initial phase of lung disease exists for 10 to 14 days, after which many of the changes present can be attributed to the sequelae of diffuse lung damage, including the effects of mechanical ventilation. As with many other newly emerging infections, SARS had zoonotic origins, highlighting the need for a better understanding of the virus ecology of both wild and domestic animals. As many of these zoonoses do not cause disease in their natural host, surveillance needs to encompass viruses causing unobvious infections as well as those causing overt disease and will require the cooperation of multiple agencies, including those dealing with public health, veterinary medicine, and wildlife or the environment.
Details
- Title: Subtitle
- Severe Acute Respiratory Syndrome: Epidemiology, Pathogenesis, and Animal Models
- Creators
- John NichollsJ. S Malik PeirisStanley Perlman
- Contributors
- Stanley Perlman (Editor)Thomas Gallagher (Editor)Eric J Snijder (Editor)
- Resource Type
- Book chapter
- Publication Details
- Nidoviruses, pp.299-311
- DOI
- 10.1128/9781555815790.ch19
- Publisher
- ASM Press; Washington, DC, USA
- Number of pages
- 13
- Language
- English
- Date published
- 12/07/2007
- Academic Unit
- Microbiology and Immunology; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Infectious Disease (Pediatrics)
- Record Identifier
- 9984072065202771
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