Table 1.

Accessory proteins and their roles in SARS‐CoV and SARS‐CoV‐2.

Name	Protein identity with SARS‐CoV (Frankfurt 1)	Function in SARS‐CoV‐2
ORF3a	73 % identity (divergence in N‐terminus)	ion channel activity; inflammasome activation; replication and pathogeneses; possible links to cell death. [91] Viruses lacking ORF3a (but not ORF8a) and E are not viable. [92]
ORF3b	Minimal (ORF3b is located in different regions of Orf3a in SARS‐CoV1 and 2)	Not necessarily a genuine ORF. [93] Potential interferon antagonist. [94] Lost in population. [88]
ORF3c	Not present in SARS‐CoV	Predicted to be a transmembrane protein. [74]
ORF3d	Not present in SARS‐CoV	A potential novel gene product that is poorly characterized (overlaps partly with ORF3c). [95]
ORF6	69 % (variation in body and C terminus)	Antagonizes interferon signaling. [75]
ORF7a	85 %	Deletions in the viral population have been identified. [96] This is a transmembrane protein regulating host/virus interplay. [97] May also regulate cell death.
ORF7b	81 % (only 43 amino acids long)	May be incorporated into the virus; may suppress interferon signaling. [80]
ORF8	weak versus both ORF8a and ORF8b	SARS‐CoV‐2 ortholog can form high order oligomers that cannot occur in SARS‐CoV. [98] Antagonizes interferon signaling, [99] and downregulates MHC‐1. [100]
ORF8b	Not present in SARS‐Cov‐2	SARS‐CoV protein is prone to aggregation. Can trigger cell death and activate inflammasome. Triggers ER stress and activates autophagy/lysosomes. [90]
ORF9b	72 % (divergence mainly in N‐terminus)	This is also a suppressor of interferon responses. [101] Antibodies have been detected in SARS‐CoV‐2 patients. [102]
ORF9c	Not present in SARS‐CoV	Linked to avoiding the immune response. This is a transmembrane protein. [87]
ORF10	Not present in SARS‐CoV	Unknown/potentially not translated