The study of antibody duration closely follows the time course of the first known infected patients

The study of antibody duration closely follows the time course of the first known infected patients. in Wuhan, Hubei, China at the end of 2019, and then it spread rapidly, forming a large-scale global outbreak. SARS-CoV-2 is an enveloped single-stranded, positive-sense RNA virus, belonging to the Betacoronavirus genus (1). There are 14 open reading frames (ORFs) in the SARS-CoV-2 genome, encoding four structural proteins: the spike glycoprotein (S), envelope (E), membrane (M), and nucleocapsid (N); 16 nonstructural proteins (NSP 116), and nine accessory proteins (ORF3a, Polygalacic acid ORF3b, ORF6, ORF7a, ORF7b, ORF8, ORF9a, ORF9b, ORF10) (2,3). The viral capsid formed by the N protein wraps the viral genome, while the E and M proteins participate in the assembly and release of the virion. Polygalacic acid The S protein is the key protein for viral invasion of cells (4). The S protein consists of S1 and S2 subunits. S1 folds into the N-terminal domain (NTD), receptor-binding domain (RBD), and two C-terminal domains (CTDs) (5,6). The RBD of S1 interacts with human angiotensin-converting enzyme (hACE2) to promote fusion between the cell membrane and the virus envelope, and the virion can reproduce in the cells (3,510).Figure 1shows a schematic diagram of the viral infection and replication. == Figure 1. == The life cycle of SARS-CoV-2 and the specific immune response to the virus. The virus particles of SARS-CoV-2 are composed of four major proteins, envelope (E), spike glycoprotein (S), membrane (M), and the nucleocapsid (N). SARS-CoV-2 promotes virus invasion through the interaction between the S protein, hACE2, and TMPRSS2. After successful invasion, the viral genome RNA is released in the cytoplasm, and then initiates the translation of the genome. The translated polymeric proteins are cleaved by Mpro and PLpro to generate non-structural proteins (nsps). These nsps are involved in viral replication and transcription. With the nucleocapsid (N) protein-encapsidated genomic RNA, the structural proteins are translocated to the endoplasmic reticulum (ER) membrane and assembled into a new virus in the ER-to-Golgi intermediate compartment (ERGIC). Finally, virus particles are secreted from infected cellsviaexocytosis. APC, B cells, CD4+ T cells, and CD8+ T cells are the main cells that participate in adaptive immunity. The virus is recognized by professional antigen-presenting cells (such as dendritic cells and macrophages), and the viral peptides are presented to CD4+ T cells through the major histocompatibility complex (MHCII) class II. Then, the CD4+ T cells differentiate into a series of helper cells, which in turn help activate CD8+ T cells and B cells. CD8+ T cells can kill infected cells with the assistance of CD4+ T cells and MHCI. Simultaneously, B cells transform into plasma cells to produce neutralizing antibodies to prevent the virus from invading again. The immune system can be broadly divided into the innate immune system and the adaptive immune system. Innate immunity is the first line of defense of the immune system (11). The innate immunity system restricts virus replication in infected cells and produces an antiviral state in the local tissue environment, which slows down the replication and spread of the virus. In addition, the innate immune response is critical to trigger the adaptive immune response (12). Rabbit Polyclonal to RPS12 Adaptive immunity takes time to generate enough virus-specific cells to control the infection. Adaptive immunity involves three main cell types: CD8+ T cells, CD4+ T cells, and Polygalacic acid B cells (12). After the virus enters the tissue cells, viral peptides are presented to CD8+ cytotoxic T cells through the class I major histocompatibility complex (MHC) protein, and CD8+ cytotoxic T cells can produce cytotoxic effects on virus-infected tissue cells and induce apoptosis through perforin, granzyme, and other mechanisms (13). Professional antigen-presenting cells (e.g., macrophages and dendritic cells) recognize viruses and viral particles, and the class II major histocompatibility complex (MHCII) presents viral peptides to CD4+ T cells. In patients with SARS-CoV-2 infection, CD4+ T cells.