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In a recent study published in The Journal of Infectious Diseases, researchers identified that among healthy young adults, the development of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) triggered memory B cell and antibody reactions were equivalent following mildly symptomatic or asymptomatic infections.
SARS-CoV-2, the etiologic agent of coronavirus disease of 2019 (COVID-19), can cause clinical outcomes ranging from asymptomatic to severe respiratory failure. Among unvaccinated populations, 40 to 50% of SARS-CoV-2 infections are asymptomatic, with younger people more prone to asymptomatic COVID-19.
Relative to symptomatic infection, the protective immunity and immune memory of people with asymptomatic COVID-19 are not well characterized. From the public health standpoint, assessing immune memory following asymptomatic SARS-CoV-2 infection is critical.
People with an asymptomatic SARS-CoV-2 infection may have a greater or lesser amount of SARS-CoV-2 immune memory than those who experienced a symptomatic COVID-19. While asymptomatic COVID-19 patients generate neutralizing and binding antibodies against the virus, they are often of lesser quantity and may have distinct decay kinetics than those in symptomatic instances. In addition, data on adaptive immune memory among young adults and memory B cells across asymptomatic SARS-CoV-2 infections are scarce.
The present work assessed antibody and memory B cell responses in COVID-19 Health Action Response for Marines (CHARM) participants, aiming to close knowledge gaps surrounding memory B cells in asymptomatic SARS-CoV-2 infections. The researchers sought to learn more about immune memory among young adults with COVID-19 who were asymptomatic as opposed to those who were symptomatic. The study was performed before the emergence of SARS-CoV-2 variants of concern (VOCs) or the availability of COVID-19 vaccines.
The authors examined the SARS-CoV-2 memory B cell reactions,(PSV) titers, and spike (S) antibody titers in Marine recruits who were COVID-19 polymerase chain reaction (PCR) positive and experienced symptomatic or asymptomatic infection.
From May to November 2020, all subjects attended recruit training for the United States Marine Corps (USMC). Only study volunteers who were SARS-CoV-2 receptor-binding domain (RBD)-seronegative at trial enrollment time were included in the evaluations, independent of S immunoglobulin G (IgG) status.
Besides, the La Jolla Institute of Immunology's Normal Blood Donor Program provided unexposed donors. All subjects submitted written informed consent before enrolling. In 24 hours, peripheral blood mononuclear cells (PBMCs) were extracted and kept in liquid nitrogen until they were used to measure-specific memory B cells.
The study results illustrated that the subjects were mainly young men, i.e., 93.9% male, with a median age of 18. While four of the 30 symptomatic participants reported one to two symptoms at a single timestamp, the remainder reported at least three symptoms or symptoms at two or more separate timestamps following infection, with the range of symptoms documented at each encounter varying from one to 11. None of the symptomatic patients received any medicine besides symptomatic therapy, like acetaminophen or non-steroidal anti-inflammatory medications, and all were treated as outpatients.
The authors discovered that in young adults with asymptomatic SARS-CoV-2 infection, memory B cell reactions were similar to those in patients with mild symptoms. Furthermore, antigen-selective memory B cell reactions were linked with antibody responses.
The S IgG, IgA, and PSV neutralization titers of 36 asymptomatic COVID-19 patients were comparable to those of 30 symptomatic participants. As a result, the team stated that SARS-CoV-2 infections that were mildly symptomatic or asymptomatic generated similar rapid IgA and IgG reactions that were effective at neutralizing the virus.
Significantly favorable associations were observed between PSV neutralization and S IgG titers and the proportion of memory B cells. SARS-CoV-2-infected young adults with asymptomatic infection demonstrated similar S- and RBD-attaching memory B cell percentages to those who were mildly symptomatic among the current cohort.
The connection with increased memory B cell or antibody responses typically indicated a longer or higher viral burden. However, no link was found in the current investigation, suggesting antigen load might not be a significant factor differentiating most asymptomatic patients from mildly symptomatic cases in young adults. Indeed, the team discovered no variations in the days of SARS-CoV-2 PCR positivity duration or the assessed SARS-CoV-2 PCR swab cycle threshold (Ct) values between mildly symptomatic and asymptomatic subjects. Hence, there were no virological disparities between the two patient cohorts.
According to the study findings, memory B cell and antibody responses brought on by asymptomatic SARS-CoV-2 infection in young adults were equivalent to mild symptomatic illness. Therefore, in the case of asymptomatic or mildly symptomatic COVID-19, healthy young adults exhibit comparable antibody and memory B cell responses. Additionally, the current data shows that reported COVID-19 symptomology cannot be used to predict the diversity of both antibody and memory B cell responses among young adults.