What is immunological memory

Immunity to SARS-CoV-2: The Complexity of Immunological Memory

SARS-CoV-2 and protective immunological memory

The formation of a protective antibody memory presupposes a high level of contamination of the population, the repeated infection of individual individuals or the persistence of the infectious agent in the individual individual until primary and secondary immune reactions take place in direct succession. In a two-phase immune reaction, memory B lymphocytes are created first and then memory plasma cells from reactivated memory B lymphocytes. Neither obviously applies to SARS-CoV-2. Secondary infections are rare because the prevalence of the population is low; In most infected people, the virus disappears after a few days and the induced antibodies are no longer measurable in many within months after infection. In the event of a renewed infection, however, the reactive immunological memory would significantly reduce the course of the disease. SARS-CoV-2 behaves like many other viruses, at least in the infected, in which there is no severe clinical course. In order to achieve a stable protective immunological memory through neutralizing antibodies against SARS-CoV-2, it would be possible to let the pandemic run its course and thus induce protective antibodies through secondary immune reactions. In view of the COVID-19-associated morbidity and mortality as well as the fact that neither dose, route nor target persons of the infection can be controlled, this approach should be viewed rather critically. Vaccines, on the other hand, can be given repeatedly without drastic side effects in order to specifically induce primary and secondary immune reactions and thus a stable protective immunological memory and thereby avoid the formation of disease-aggravating antibodies. What is more, vaccines can be dosed in such a way that the antibodies can effectively neutralize even high doses of the infectious agent. It is justified to hope that a vaccine will also make a decisive contribution to ending the pandemic with SARS-CoV-2.



1. Nabel, G.J. Designing tomorrow's vaccines. N Engl J Med 2013. 368: 551-560.
2. Chang, H.D., Tokoyoda, K. and Radbruch, A. Immunological memories of the bone marrow. Immunol Rev 2018. 283: 86-98.
3. Riedel, R. et al. Discrete populations of isotype-switched memory B lymphocytes are maintained in murine spleen and bone marrow. Nat Commun 2020. 11:2570.
4. McGregor, D.D. and Gowans, J.L. The Antibody Response of Rats Depleted of Lymphocytes by Chronic Drainage from the Thoracic Duct. J Exp Med 1963. 117: 303-320.
5. Grifoni, A. et al. Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals. Cell 2020. 181: 1489-1501 e1415.
6. Braun, J. et al. SARS-CoV-2-reactive T cells in healthy donors and patients with COVID-19. Nature 2020.
7. Altmann, D.M. and Boyton, R.J. SARS-CoV-2 T cell immunity: Specificity, function, durability, and role in protection. Sci Immunol 2020. 5.
8. Kellam, P. and Barclay, W. The dynamics of humoral immune responses following SARS-CoV-2 infection and the potential for reinfection. J Gen Virol 2020.
9. Guo, X. et al. Long-Term Persistence of IgG Antibodies in SARS-CoV Infected Healthcare Workers. medRxiv 2020: 2020.2002.2012.20021386.
10. Long, Q. X. et al. Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections. Nat Med 2020.
11. Gao, G. et al. Absent immune response to SARS-CoV-2 in a 3-month recurrence of coronavirus disease 2019 (COVID-19) case. Infection 2020.
12. Cornelis, R. et al. Stromal Cell-Contact Dependent PI3K and APRIL Induced NF - & # x3ba; B Signaling Prevent Mitochondrial- and ER Stress Induced Death of Memory Plasma Cells. Cell Reports 2020. 32.
13. Liu, L. et al. Anti-spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection. JCI Insight 2019. 4.

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