Adaptive Immune Responses and Immunity to SARS-CoV-2

Abstract

Since the onset of the COVID-19 pandemic, the medical field has been forced to apply the basic knowledge of immunology with the most up-to-date SARS-CoV-2 findings and translate it to the population of the whole world in record time. Following the infection with the viral antigen, adaptive immune responses are activated mainly by viral particle encounters with the antigen-presenting cells or B cell receptors, which induce further biological interactions to defend the host against the virus. After the infection has been warded off, the immunological memory is developed. The SARS-CoV cellular immunity has been shown to persist even 17 years after the infection, despite the undetectable humoral component. Similar has been demonstrated for the SARS-CoV-2 T cell memory in a shorter period by assessing interferon-gamma levels when heparinized blood is stimulated with the virus-specific peptides. T cells also play an irreplaceable part in a humoral immune reaction as the backbone of a cellular immune response. They both provide the signals for B cell activation and the maturation, competence, and memory of the humoral response. B cell production of IgA was shown to be of significant influence in mediating mucosal immunity as the first part of the defense mechanism and in the development of nasal vaccines. Here, we interpret the recent SARS-CoV-2 available research, which encompasses the significance and the current understanding of adaptive immune activity, and compare it among naive, exposed, and vaccinated blood donors. Our recent data showed that those who recovered from COVID-19 and those who are vaccinated with EMA-approved vaccines had a long-lasting cellular immunity. Additionally, we analyze the humoral responses in immunocompromised patients and memory mediated by cellular immunity and the impact of clonality in the SARS-CoV-2 pandemic regarding breakthrough infections and variants of concern, both B.1.617.2 (Delta) and B.1.1.529 (Omicron) variants.

Potential links between COVID-19 and periodontitis: a bioinformatic analysis based on GEO datasets

“…Antibodies produced by B cells inhibit pathogens from attaching to target cells, stopping further infection. Moreover, after the antibody binds to the pathogen's surface, the complement is activated, and an antigen–antibody-complement complex is formed, bringing the pathogen to the phagocyte and making it easier to devour [ 43 ]. Various immune cell infiltrations were present in the periodontitis lesions, with B cells accounting for approximately 18% of all infiltrating leukocytes [ 16 ].…”

“…Furthermore, a single B cell cloning technique can be used to select monoclonal antibodies against SARS-CoV-2, which has implications for the diagnosis and treatment of COVID-19 disease. [ 43 ] T cells are important in the immune response to periodontitis and COVID-19. In response to the activation of a periodontal pathogen, periodontal tissue expresses chemokines, and chemotactic polymorphonuclear granulocytes and monocytes migrate to the site of inflammation [ 46 ].…”

Global “flu-ization” of COVID-19: A perspective from Vietnam

“…The adaptive immune response to SARS-CoV-2 infection is not sterilizing. People can become reinfected, even after vaccination ( 29 ), usually with an isolate that is a discrete variant of the one to which they were previously exposed ( 30 ). The level and rate of attainment of herd immunity to COVID-19 achieved through natural infection are now greatly enhanced by multiple vaccination of a high proportion of a country's residents.…”

Differentially induced immunity in buccal and nasal mucosae after vaccination for SARS–CoV–2: Prospects for mass scale immunity-screening in large populations

“…A plethora of scientific reports has since then provided a significant insight into the efficacy and safety profile of these vaccines ( 7 ). However, although the post-vaccination immunological response has been extensively investigated in blood, far less is known about the mounted immunity at the mucosal surfaces of the upper respiratory system, which also constitute the main route of entry of the virus ( 8 , 9 ). Secretory IgA antibodies (Abs) are the main but not exclusive component of mucosal humoral immunity, as IgG Abs either plasma-derived or locally produced are also prevalent on mucosal surfaces ( 10 ).…”