Mouse Anti-SARS-CoV-2 IgG2a ELISA Kit

SARS-CoV-2 caused a major outbreak of COVID-19 in late 2019, which can lead to potentially fatal acute respiratory distress syndrome (ARDS). SARS-CoV-2 belongs to the genus Sarbecovirus and shares 79% sequence similarity with SARS-CoV, with a genome that encodes several structural, non-structural and accessory proteins. Structural proteins include membrane proteins, nucleocapsid proteins, envelope proteins, and spike glycoproteins, which together with host lipid bilayers form the enveloped viral particles that deliver viral genomic RNA into the cell. The accessory proteins are involved in viral replication and usually have immune-evading activity. Spike proteins form trimers on the viral surface that can determine viral tropism. S proteins contain two subunits, S1 and S2, where S1 is responsible for host entry by binding to the angiotensin-converting enzyme 2 (ACE2) receptor and S2 is responsible for mediating membrane fusion. When humans are naturally infected with the virus, SARS-CoV-2 first infects cellular multiciliated cells in the nasopharynx or trachea, or sustentacular cells in the nasal olfactory mucosa, and upon entry begins to produce viral proteins, a process that produces double-membrane vesicles that protect transcriptional intermediates from detection by cytoplasmic pattern recognition receptors (PRRs). In the absence of innate or adaptive clearance, SARS-CoV-2 can gradually spread along the upper respiratory tract to the lower respiratory tract, eventually causing alveolar infections that cause inflammation and restrict gas exchange.

Figure 1. Molecular of SARS-CoV-2
(Source: Lamers MM, et al. 2022)

Coronavirus transcriptional discontinuity, combined with the fact that SARS-CoV-2 has a large RNA genome, results in high rates of recombination, insertions, deletions and point mutations. The successful generation of new gene variants depends largely on natural selection. In particular, positive selection is associated with mutations that are beneficial to the virus. T cells are an important part of the body's adaptive immune response to SARS-CoV-2 infection and are involved in protection against severe COVID-19 infection. It was found that early vaccine-induced immunoprotection may be largely dependent on T cells. Functional T cell responses target a wide range of viral proteins, with the degree of response correlating with the level of expression of the viral proteins, with a predominance of responses to S, N, and M proteins, as well as significant responses to ORF3a and the non-structural proteins NSP3 and NSP12. Because the T cell response targets epitopes throughout the SARS-CoV-2 genome, the footprint of T cell escape is more widespread than antibody-driven changes. Prolonged infection of immunocompromised hosts with SARS-CoV-2 may provide additional opportunities for T-cell escape. There are two mechanisms by which T cells can lose their ability to respond to specific epitopes, including disruption of antigen processing by amino acid changes in epitopes or flanking regions, and disruption of major histocompatibility complex (MHC) binding to epitopes by changes in anchoring residues.

Figure 2. Potential impact of SARS-CoV-2 variants on T cell responses and innate immunity
(Source: Carabelli AM, et al. 2023)

severe acute respiratory syndrome coronavirus 2 IgG2a ELISA Kit