Dödligt virus från Kina orsakar panik (SARS-CoV-2, COVID-19)

Abstract

To date, the pathogenesis of severe acute respiratory syndrome (SARS) in humans
is still not well understood. SARS coronavirus (SARS-CoV)-specific CTL
responses, in particular their magnitude and duration of postinfection
immunity, have not been extensively studied. In this study, we found that
heat-inactivated SARS-CoV elicited recall CTL responses to newly identified
spike protein-derived epitopes (SSp-1, S978, and S1202) in peripheral blood of
all HLA-A*0201(+) recovered SARS patients over 1 year postinfection.
Intriguingly, heat-inactivated SARS-CoV elicited recall-like CTL responses to
SSp-1 but not to S978, S1202, or dominant epitopes from several other human
viruses in 5 of 36 (13. 8%) HLA-A*0201(+) healthy donors without any contact
history with SARS-CoV. SSp-1-specific CTLs expanded from memory T cells of both
recovered SARS patients, and the five exceptional healthy donors shared a
differentiated effector CTL phenotype, CD45RA(+)CCR7(-)CD62L(-), and expressed
CCR5 and CD44. However, compared with the high avidity of SSp-1-specific CTLs
derived from memory T cells of recovered SARS patients, SSp-1-specific CTLs
from the five exceptional healthy donors were of low avidity, as determined by
their rapid tetramer dissociation kinetics and reduced cytotoxic reactivity,
IFN-gamma secretion, and intracellular production of IFN-gamma, TNF-alpha,
perforin, and granzyme A. These results indicate that SARS-CoV infection
induces strong and long-lasting CTL-mediated immunity in surviving SARS
patients, and that cross-reactive memory T cells to SARS-CoV may exist in the T
cell repertoire of a small subset of healthy individuals and can be reactivated
by SARS-CoV infection.