Fig. 1

Proposed models of virus-specific humoral immunity induced by SARS-CoV-2 infection or an mRNA vaccine. (1) SARS-CoV-2 infection: SARS-CoV-2 invades host cells by both endocytosis and membrane fusion for viral entry through binding of the viral spike (S) glycoprotein to the viral receptor ACE2. Next, SARS-CoV-2 is processed by APCs, exposing its hidden epitopes. Subsequently, APCs present viral antigens to Th cells, followed by activation and lymphokine secretion and B cell activation; viral antigens may also directly stimulate B cells. Under stimulation with viral antigens, the majority of B cells proliferate and differentiate into plasma cells to produce specific antibodies against SARS-CoV-2. Simultaneously, a small proportion of B cells develop into SARS-CoV-2-specific memory B cells. Upon SARS-CoV-2 reinfection, the virus-specific memory B cells can be rapidly transformed into plasma cells to produce specific antibodies. The specific antibodies (primarily neutralizing antibodies) produced by plasma cells can neutralize SARS-CoV-2 and block the interaction between the spike protein and ACE2. (2) SARS-CoV-2 vaccine: after inoculation, an mRNA vaccine encoding the relevant S protein encapsulated by lipid nanoparticles enters a cell, and the S protein is synthesized by ribosomes. Subsequently, B cells are stimulated by the S protein to proliferate and differentiate into specific plasma and memory B cells. Finally, the plasma cells produce large amounts of specific antibodies against SARS-CoV-2, which may play a protective role in viral reinfection. ACE2 angiotensin-converting enzyme 2, APC antigen-presenting cell, BCR B cell receptor, SARS-CoV-2 severe acute respiratory syndrome coronavirus 2, Th cells T helper cells