The Role of Severe Acute Respiratory Syndrome (SARS)-Coronavirus Accessory Proteins in Virus Pathogenesis

A respiratory disease caused by a novel coronavirus, termed the severe acute respiratory syndrome coronavirus (SARS-CoV), was first reported in China in late 2002. The subsequent efficient human-to-human transmission of this virus eventually affected more than 30 countries worldwide, resulting in a mortality rate of ~10% of infected individuals. The spread of the virus was ultimately controlled by isolation of infected individuals and there has been no infections reported since April 2004. However, the natural reservoir of the virus was never identified and it is not known if this virus will re-emerge and, therefore, research on this virus continues. The SARS-CoV genome is about 30 kb in length and is predicted to contain 14 functional open reading frames (ORFs). The genome encodes for proteins that are homologous to known coronavirus proteins, such as the replicase proteins (ORFs 1a and 1b) and the four major structural proteins: nucleocapsid (N), spike (S), membrane (M) and envelope (E). SARS-CoV also encodes for eight unique proteins, called accessory proteins, with no known homologues. This review will summarize the current knowledge on SARS-CoV accessory proteins and will include: (i) expression and processing; (ii) the effects on cellular processes; and (iii) functional studies.     

Unconventional use of LC3 by coronaviruses through the alleged subversion of the ERAD tuning pathway

Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens to infect host cells is crucial to generate targets for therapeutic intervention. Here we review recent data indicating that coronaviruses probably co-opt membranous carriers derived from the endoplasmic reticulum, which contain proteins that regulate disposal of misfolded polypeptides, for their replication. In addition, we also present models describing potential mechanisms that coronaviruses could employ for this hijacking.     

Elevated Plasma Tissue-type Plasminogen Activator （t-PA） and Soluble Thrombomodulin in Patients Suffering From Severe Acute Respiratory Syndrome （SARS） as a Possible Index for Prognosis and Treatment Strategy

INTRODUCTION Severe acute respiratory syndrome(SARS)is a life-threatening infectious disease associated with endothelial injury,coagulation activation,and intravascular fibrin deposition.A recent study of138patients in Hong Kong has shown that44.8%of the patients have thrombocytopenia,45.0%have elevated level of D-dimers,and42.8%have a prolonged activated partial-thromboplastin time[1],suggesting that SARS infection is associated with disseminated intravascular coagulation(DIC)[2-4].…