SARS was the ?rst new plague of the twenty-?rst century. Within months, it spread worldwide from its “birthplace” in Guangdong Province, China, affecting over 8,000 people in 25 countries and territories across ?ve continents. SARS exposed the vulnerability of our modern globalised world to the spread of a new emerging infection. SARS (or a similar new emerging disease) could neither have spread so rapidly nor had such a great global impact even 50 years ago, and arguably, it was itself a product of our global inter-connectedness. Increasing af?uence and a demand for wild-game as exotic food led to the development of large trade of live animal and game animal markets where many species of wild and domestic animals were co-housed, providing the ideal opportunities for inter-species tra- mission of viruses and other microbes. Once such a virus jumped species and attacked humans, the increased human mobility allowed the virus the opportunity for rapid spread. An infected patient from Guangdong who stayed for one day at a hotel in Hong Kong led to the transmission of the disease to 16 other guests who travelled on to seed outbreaks of the disease in Toronto, Singapore, and Vietnam, as well as within Hong Kong itself. The virus exploited the practices used in modern intensive care of patients with severe respiratory disease and the weakness in infection control practices within our health care systems to cause outbreaks within hospitals, further amplifying the spread of the disease. Health-care itself has become a two-edged sword.
Viral Entry.- Cellular Entry of the SARS Coronavirus: Implications for Transmission, Pathogenicity and Antiviral Strategies.- The Cell Biology of the SARS Coronavirus Receptor, Angiotensin-Converting Enzyme 2.- Structural Molecular Insights into SARS Coronavirus Cellular Attachment, Entry and Morphogenesis.- Structures Involved in Viral Replication and Gene Expression.- RNA Higher-Order Structures Within the Coronavirus 5? and 3? Untranslated Regions and Their Roles in Viral Replication.- Programmed –1 Ribosomal Frameshifting in SARS Coronavirus.- Viral Proteins.- Expression and Functions of SARS Coronavirus Replicative Proteins.- SARS Coronavirus Replicative Enzymes: Structures and Mechanisms.- Quaternary Structure of the SARS Coronavirus Main Protease.- The Nucleocapsid Protein of the SARS Coronavirus: Structure, Function and Therapeutic Potential.- SARS Coronavirus Accessory Gene Expression and Function.- SARS Accessory Proteins ORF3a and 9b and Their Functional Analysis.- Molecular and Biochemical Characterization of the SARS-CoV Accessory Proteins ORF8a, ORF8b and ORF8ab.- Viral pathogenesis and host immune response.- SARS Coronavirus Pathogenesis and Therapeutic Treatment Design.- Modulation of Host Cell Death by SARS Coronavirus Proteins.- SARS Coronavirus and Lung Fibrosis.- Host Immune Responses to SARS Coronavirus in Humans.- The Use of Retroviral Pseudotypes for the Measurement of Antibody Responses to SARS Coronavirus.- SARS Coronavirus Spike Protein Expression in HL-CZ Human Promonocytic Cells: Monoclonal Antibody and Cellular Transcriptomic Analyses.- Signaling Pathways of SARS-CoV In Vitro and In Vivo.