The role of severe acute respiratory syndrome (SARS)-coronavirus accessory proteins in virus pathogenesis

Abstract

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.

Figure 1

Organization of severe acute respiratory syndrome coronavirus (SARS-CoV) genome showing the position of the accessory genes. The eight accessory open reading frames (ORFs) (grey shaded boxes) encode for ORFs 3a, 3b, 6, 7a, 7b, 8a, 8b and 9b. The ORFs encoding for the replicase genes (ORF 1a and ORF 1b) and structural genes, spike (S), membrane (M), envelope (E) and nucleocapsid (N) are also shown (not drawn to scale).