SARS-CoV-1 Antigens

SARS Coronavirus Membrane Protein

SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs, 1a and 1b, both of which are polyproteins. ORFs 1a and 1b encode the replicase and there are four major structural proteins: nucleocapsid, spike, membrane and envelope. It also encodes for eight unique proteins, known as the accessory proteins, all with no known homologues. The matrix protein M (221 aa), which is an integral membrane protein involved in budding and which interacts with the nucleocapsid and S proteins (Opstelten et al., 1995Narayanan et al., 2000). As a component of the viral envelope it plays a central role in virus morphogenesis and assembly via its interactions with other viral proteins.

Immunization with one or more SARS-CoV subunit antigens, either administered as purified protein or expressed from viral or DNA vaccine vectors, has been proposed for designing a vaccine against SARS (Buchholz et al., 2004). The M protein has dominant cellular immunogenicity and elicits a strong humoral response which suggests it would serve as a potential target in SARS-CoV vaccine design (Liu et al., 2010).

SARS Coronavirus Envelope Protein

The coronaviral genome encodes four major structural proteins: the spike (S) protein, nucleocapsid (N) protein, membrane (M) protein, and the envelope (E) protein, all of which are required to produce a structurally complete viral particle. The E protein is the smallest of the major structural proteins. During the replication cycle, E is abundantly expressed inside the infected cell, but only a small portion is incorporated into the virion envelope. E participates in viral assembly, release of virions and pathogenesis of the virus. The majority of the protein is localised at the site of intracellular trafficking, the ER, Golgi, and ERGIC, where it participates in CoV assembly and budding. Recombinant CoVs lacking E exhibit significantly reduced viral titres, crippled viral maturation, or yield propagation incompetent progeny, demonstrating the importance of E in virus production and maturation (reviewed in Schoeman and Fielding, 2019).