Full Answer Section

The adaptive response, more specific and long-lasting, involved T and B lymphocytes. Dendritic cells presented viral antigens to naïve T helper (Th) cells, which, upon activation, differentiated into Th1 cells, secreting cytokines like interferon-gamma (IFN-γ) to enhance macrophage activity and cytotoxic T lymphocyte (CTL) function. CTLs, recognizing viral antigens presented on infected cells via MHC-I, directly killed these cells. Simultaneously, B cells, encountering viral antigens, were activated with Th cell help. They proliferated and differentiated into plasma cells, producing virus-specific antibodies (IgM initially, then IgG). These antibodies neutralized the virus, preventing it from infecting new cells, and facilitated its clearance by phagocytes. Memory T and B cells were also generated, providing long-term immunity.  

Three months later, the student’s second infection triggered a faster and more robust response. Memory T cells and B cells, already primed to recognize the virus, were rapidly activated. Memory Th cells quickly released cytokines, and memory CTLs efficiently eliminated infected cells. Memory B cells swiftly differentiated into plasma cells, producing high levels of IgG antibodies, leading to faster viral neutralization and clearance. Therefore, the response during the second infection is normally quicker, and less severe due to the presence of immunological memory. However, regarding Covid-19, reinfections can very in severity, and it is possible for people to have similar, or even more severe symptoms during a reinfection.