Lauren B. Rodda1,6, Jason Netland1,6, Laila Shehata1,7, Kurt B. Pruner1,7, Peter A. Morawski2,7, 4
Chris Thouvenel3, Kennidy K. Takehara1, Julie Eggenberger4, Emily Hemann4, Hayley R. 5
Waterman2, Mitchell L. Fahning2, Yu Chen3, Jennifer Rathe4, Caleb Stokes4, Samuel Wrenn5, 6
Brooke Fiala5, Lauren Carter5, Jessica A. Hamerman1,2, Neil P. King5, Michael Gale Jr4, Daniel 7
J. Campbell1,2, David Rawlings1,3, Marion Pepper1,8
The recently emerged SARS-CoV-2 virus is currently causing a global pandemic and
continue to rise. The majority of infected individuals experience mildly
coronavirus disease 2019 (COVID-19), but it is unknown whether this can induce
immune memory that might contribute to herd immunity. Thus, we performed
longitudinal assessment of individuals recovered from mildly symptomatic COVID-19
determine if they develop and sustain immunological memory against the virus. We
that recovered individuals developed SARS-CoV-2-specific IgG antibody and
plasma, as well as virus-specific memory B and T cells that not only persisted, but in
cases increased numerically over three months following symptom onset. Furthermore,
SARS-CoV-2-specific memory lymphocytes exhibited characteristics associated with
antiviral immunity: memory T cells secreted IFN-γ and expanded upon antigen re-
encounter, while memory B cells expressed receptors capable of neutralizing virus when
expressed as antibodies. These findings demonstrate that mild COVID-19 elicits memory
lymphocytes that persist and display functional hallmarks associated with antiviral
protective immunity.
continue to rise. The majority of infected individuals experience mildly
coronavirus disease 2019 (COVID-19), but it is unknown whether this can induce
immune memory that might contribute to herd immunity. Thus, we performed
longitudinal assessment of individuals recovered from mildly symptomatic COVID-19
determine if they develop and sustain immunological memory against the virus. We
that recovered individuals developed SARS-CoV-2-specific IgG antibody and
plasma, as well as virus-specific memory B and T cells that not only persisted, but in
cases increased numerically over three months following symptom onset. Furthermore,
SARS-CoV-2-specific memory lymphocytes exhibited characteristics associated with
antiviral immunity: memory T cells secreted IFN-γ and expanded upon antigen re-
encounter, while memory B cells expressed receptors capable of neutralizing virus when
expressed as antibodies. These findings demonstrate that mild COVID-19 elicits memory
lymphocytes that persist and display functional hallmarks associated with antiviral
protective immunity.
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