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\begin{document}

\title{T-cell Immunity Against COVID-19 and UK Variant in Infected and
Vaccinated Individuals}



\author[1]{Stanley Jordan}%
\author[1]{Bong-Ha Shin}%
\author[1]{Terry-Ann Milfordgadsden}%
\author[1]{Maggie Chu}%
\author[1]{Anna Petrosyan}%
\author[1]{Catherine Le}%
\author[1]{Rachel Zabner}%
\author[1]{Jillian Oft}%
\author[1]{Isabel Pedraza}%
\author[1]{Norkio Ammerman}%
\author[1]{Susan Cheng}%
\author[1]{Ashley Vo}%
\author[1]{Jasmine Plummer}%
\author[1]{Anders Berg}%
\author[1]{Shili Ge}%
\author[1]{Mieko Toyoda}%
\author[1]{Ruan Zhang}%
\affil[1]{Cedars Sinai Med Ctr}%


\vspace{-1em}



  
  \date{May 23, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Understanding the composition of human immune responses to SARS-CoV-2
and vaccines is essential for predicting protection from infection and
determining vaccine efficacy. Here, we explored T-cell immune responses
to SARS-CoV-2 and the UK (B.1.1.7) variant of concern (VOC) in infected
and vaccinated individuals. In infected patients, CD4+ T-cells
demonstrated consistent, robust responses against Spike peptides, while
CD8+ T-cells had heterogeneous responses to 5 SARS-CoV-2 proteins. We
found 80\% of infected and vaccinated individuals showed positive CD4+
T-cell immunity against SARS-CoV-2. Moreover, CD4+/CD8+ T-cell responses
to SARS-CoV-2 and the United Kingdom (B.1.1.7) variant are robust and
nearly identical in infected and vaccinated individuals. Thus, the UK
variant did not interfere with T-cell recognition and elicited
responses. These observations will be of critical importance in
assessing human immune responses to emerging VOCs.%
\end{abstract}%



\sloppy


T-cell Immunity Against COVID-19 and UK Variant in Infected and
Vaccinated Individuals

Stanley C Jordan, MD\selectlanguage{romanian}\textsuperscript{1, ƒ} Bong-Ha
Shin,PhD\textsuperscript{1,ƒ} Terry-Ann M
Gadsden,BS\textsuperscript{1}Maggie Chu,BS\textsuperscript{1} Anna
Petrosyan,BS\textsuperscript{1}Catherine N Le,MD\textsuperscript{2}
Rachel Zabner,MD\textsuperscript{2}Jillian Oft,MD\textsuperscript{2}
Isabel Pedraza,MD\textsuperscript{2}Susan Cheng,MD\textsuperscript{3}
Ashley Vo,PharmD\textsuperscript{1}Noriko
Ammerman,PharmD\textsuperscript{1} Jasmine
Plummer,PhD\textsuperscript{4}, Shili Ge\textsuperscript{1}, PhD, Anders
Berg\textsuperscript{5}, PhD, Mieko Toyoda,PhD\textsuperscript{1} and
Ruan Zhang,PhD\textsuperscript{1}. \textsuperscript{1}Comprehensive
Transplant Center, Transplant Immunology
Laboratory,\textsuperscript{2}Division of Infectious
Diseases,\textsuperscript{3}Cardiology,
\textsuperscript{4}Bioinformatics \& Functional Genomics, and Department
of Pathology \& Laboratory Medicine\textsuperscript{5} Cedars-Sinai
Medical Center, Los Angeles, CA 90048.\textsuperscript{ƒ}Authors share
first authorship.

Word Count Summary: 130

Word Count Text: 2015

Address Correspondence:

Stanley C. Jordan, MD, FASN, FAST

Director, Nephrology \& Transplant Immunology

Cedars-Sinai Medical Center

8700 Beverly Blvd

Los Angeles, CA 90048

Phone: 3130-423-2641

Email: stan.jordan@cshs.org

\textbf{Data Availability Statement:}

Request for data relevant to the manuscript will be considered after
assessment and review.

\textbf{Competing Interest:}

None of the authors report competing interest that are relevant to data
presented in this manuscript.

\textbf{Funding:}

Funding of this study was entirely from internal resources at
Cedars-Sinai Medical Center including funding from the Borstenin Family
Foundation, Los Angeles.

\textbf{Author Contributions:}

Stanley C. Jordan,MD: Was involved in the design and execution of the
research and was primarily responsible for writing and editing of the
manuscript.

Bong-Ha Shin, PhD: Primarily involved in designing the T-cell assay and
generating data for manuscript

Terry-Ann M Gadsden,BS: Involved in performance of the T-cell and
antibody assays

Maggie Chu, BS: Involved in performance of the T-cell and antibody
assays

Anna Petrosyan,BS: Involved in performance of the antibody assays

Catherine N Le,MD: Involved in gathering, analyzing data and writing the
manuscript

Rachel Zabner,MD: Involved in gathering and analyzing data for the
manuscript

Jillian Oft, MD: Involved in gathering and analyzing data for the
manuscript

Isabel Pedraza, MD: Involved in gathering and analyzing data for the
manuscript

Susan Cheng, MD: Provided technical and editing support for the project

Ashley Vo,PharmD: Provided support for developing protocol and
regulatory documents

Noriko Ammerman,PharmD: Provided regulatory support for development of
the project

Jasmine Plummer, PhD: Provided laboratory support and editing for
project

Shili Ge, PhD: Helped in assay development and implementation

Anders Berg, PhD: Aided in development and implementation of antibody
assays and interpretation.

Mieko Toyoda,PhD: Helped develop and implement the T-cell assay

Ruan Zhang, PhD: Primarily involved in the development of the assays and
project. Contributed to writing and editing of the manuscript.

\textbf{Summary}

Understanding the composition of human immune responses to SARS-CoV-2
and vaccines is essential for predicting protection from infection and
determining vaccine efficacy. Here, we explored T-cell immune responses
to SARS-CoV-2 and the UK (B.1.1.7) variant of concern (VOC) in infected
and vaccinated individuals. In infected patients, CD4+ T-cells
demonstrated consistent, robust response against Spike peptides, while
CD8+ T-cells had heterogeneous responses to 5 SARS-CoV-2 proteins. We
found 80\% of infected and vaccinated individuals showed positive CD4+
T-cell immunity against SARS-CoV-2. Moreover, CD4+/CD8+ T-cell responses
to SARS-CoV-2 and the United Kingdom (B.1.1.7) variant are robust and
nearly identical in infected and vaccinated individuals. Thus, the UK
variant did not interfere with T-cell recognition and elicited
responses. These observations will be of critical importance in
assessing human immune responses to emerging VOCs.

\textbf{Introduction:}

To date, there have been more than 200,757,931 COVID-19 cases and
4,266,367 deaths documented world-wide\textsuperscript{1}. This has led
to massive human suffering and disruption of global economies. The
limited efficacy of most treatments and high death rates have focused on
vaccines as the last best hope for stemming the pandemic. In general,
this has been true\textsuperscript{2}. However, the persistence of the
SARS-CoV-2 epidemic, driven primarily by variants of concern (VOC), have
raised concerns that this will pose potential challenges to our ability
to provide effective sterilizing and durable immunity through
vaccination\textsuperscript{3}. This brings into question whether the
composition of SARS-CoV-2 immunity garnered by previous infection or
vaccination could respond effectively to emerging VOC or would require
constant re-vaccination with an ever-changing composition of viral mRNAs
or peptides to meet the potential pathogenic threat.

Since the advent of the epidemic, attempts to define the composition and
duration of immune responses in infected and, more recently, vaccinated
individuals have been ardently pursued\textsuperscript{4,5}. Important
early advances were achieved in describing antibody responses after
infection, but concerns arose regarding the rapid and unpredictable
dissipation of IgG responses to SARS-CoV-2 peptides and the potential
effect on long-term immunity\textsuperscript{5-7}. In addition, reports
have shown that IgG spike protein immune responses to the BNT162b2
(Pfizer) vaccine may have reduced activity against the United Kingdom
(UK, B.1.1.7) variant\textsuperscript{8}.

A better understanding of this important issue would benefit from
analysis of CD4+/CD8+ T-cell responses to SARS-CoV-2 spike peptides and
variants\textsuperscript{9-11}. SARS-CoV-2-specific T-cell immunity was
detected in COVID-19 patients as well as uninfected healthy
controls\textsuperscript{9,10}. Early and/or robust T-cell immunity has
been associated with rapid viral clearance and mild symptoms in COVID-19
patients\textsuperscript{11,12}. Thus, an analysis of T-cell reactivity
to SARS-CoV-2 and VOC would aid in our understanding of the breadth and
depth of human immune responses after infection and vaccination.

Here we report on the development of a sensitive whole blood assay to
detect CD4+/CD8+ T-cell cytokine responses to SARS-CoV-2 and variant
peptides. This information could be helpful in understanding the
composition and durability of human immunity to SARS-CoV-2 and a VOC.

\textbf{Patients \& Methods}

\emph{Participants and Sample Collection}

Informed consent was obtained prior to study initiation. This study was
approved by the institutional review board at Cedars-Sinai Medical
Center (protocol IRB numbers: 000 42267 and 000 00621). The study was
conducted in accordance with the ethical guideline based on federal
regulations and the common rule. The study was composed and written
entirely by the authors who vouch for the results presented here.

Nineteen healthy controls, 134 patients with confirmed COVID-19
infection (of which, 14 received vaccination), and 38 vaccinated healthy
individuals without history of SARS-CoV-2 infection were enrolled in the
study with similar age and gender composition. The demographics of 134
patients are shown in Table 1. The time of blood draw from previously
infected patients ranged from day 16 to day 388 (Median = 102) after
reported SARS-CoV-2 infection by viral PCR and/or antibody test. The
blood from vaccinated individuals was drawn 1-month post
2\textsuperscript{nd} dose of Pfizer BNT162b2 mRNA vaccine. Fresh whole
blood was collected in sodium heparinized tubes and stimulated with
SARS-CoV-2 peptides overnight. Plasma obtained was stored at -80\selectlanguage{ngerman}°C for
SARS-CoV-2 Spike IgG analysis.

\emph{T-cell Stimulation with SARS-CoV-2 and VOC Peptides}

Whole blood was incubated with 1 \selectlanguage{greek}μ\selectlanguage{english}g/mL SARS CoV-2 Spike glycoprotein
(S), or variant B.1.1.7 Spike (B.1.1.7). For patients with previous
infection, additional peptides were tested. These included virus
membrane protein (VME), nucleoprotein (NCAP), protein 3A (AP3A), and
non-structural protein 7A (NS7A) (JPT Peptide Technologies GmbH, Berlin,
Germany). For all conditions, Brefeldin A and anti-CD28/CD49d (BD
Biosciences, San Jose, CA) were added and incubated for 9 hours at
37\textsuperscript{O}C. Negative and positive controls included cells
not incubated with peptides and those stimulated with phytohemagglutinin
(PHA).

\emph{Cytokine Flow Cytometry Analysis}

Fresh whole blood was incubated with SARS-CoV-2-specific peptides for 9
hours and immune cells were stained for surface markers. Cells were
stained with fluorochrome conjugated antibodies to CD3+ (FITC), CD4+
(PerCP Cy5.5), CD8+ (V450), CD45+ (V500) and CD56+ (PE-CF594) (BD
Bioscience, CA). After erythrocytes were lysed by permeabilization,
intracellular cytokines were stained with fluorochrome conjugated
antibodies to IL-2 (APC), IFN-\selectlanguage{greek}γ \selectlanguage{english}(PE), and TNF-\selectlanguage{greek}α \selectlanguage{english}(PE-Cy7) (BD Bioscience,
CA). The CD4+ (IL-2/TNF-\selectlanguage{greek}α\selectlanguage{english})\textsuperscript{+} cells and CD8+
(TNF-\selectlanguage{greek}α/\selectlanguage{english}IFN-\selectlanguage{greek}γ\selectlanguage{english})\textsuperscript{+} stimulated with S, B.1.1.7 S, VME,
NCAP, AP3A, NS7A were enumerated and defined as CoV-2-specific T-cells
after deducting the background levels in blood only conditions. Dual
cytokines \% in CD4+ or CD8+ cells [?] 0.05\% were considered positive.

\emph{Measurement of Nucleocapsid-Specific IgG Levels}

Nucleocapsid-specific IgG titer in serum of patients was analyzed using
SARS-CoV-2 IgG assay (Abbott Core Laboratory) on the Architect
instrument according to the manufacturer instructions.

\emph{Measurement of SARS-CoV-2-Spike-specific IgG in Plasma}

We next determined the levels of SARS-CoV-2 Spike IgG using CoVS1-RBD
ELISA kit (Ray Biotech, GA) per the manufacture's manual. Briefly, the
96 well plates coated with the SARS-CoV-2 S1 RBD protein were incubated
with plasma followed by biotinylated anti-human IgG. After washing,
HRP-conjugated streptavidin was added, and spike-specific IgG was
quantitated by OD450 nm reading.

\emph{Statistical analysis}

Data were congregated in Excel and Graphpad Prism for statistical
analysis. Student t-test was used for analyzing the statistical
difference between two groups. Correlation between T-cell immune
response and IgG titer was analyzed by Pearson's correlation coefficient
test. P-value less than 0.05 was considered significant.

\textbf{Results}

\emph{SARS-CoV-2-specific T-cell Detection in Whole Blood}

IL-2 is a key growth factor for activated T-cells, while TNF-\selectlanguage{greek}α \selectlanguage{english}and IFN-\selectlanguage{greek}γ
\selectlanguage{english}are considered canonical inflammatory cytokines mediating
effector/memory T-cell functions. Analysis of cytokine production in
stimulated T-cells confirmed that IL-2 and TNF-\selectlanguage{greek}α \selectlanguage{english}were consistent markers
for activated CD4+ T-cells, while activated CD8+ T-cells mainly produced
TNF-\selectlanguage{greek}α \selectlanguage{english}and IFN-\selectlanguage{greek}γ. \selectlanguage{english}After incubating whole blood with SARS-CoV-2 Spike
peptide pool, we were able to discern Spike-reactive T-cells by dual
cytokine gating (Figure 1). Here, healthy individuals without history of
SARS-CoV-2 infection demonstrated no significant T-cell responses to
SARS-CoV-2 spike peptide. However, T-cells from SARS-CoV-2-infected or
vaccinated individuals showed substantial spike-specific CD4+ and CD8+
T-cells.

\emph{T-cell Immunity in Infected Individuals}

To explore the breadth and depth of memory T-cell immunity against
SARS-CoV-2, we examined responses in 34 selected patients with
documented SARS-CoV-2 infection (Figure 2A). T-cell immune responses to
peptide pools of 5 major SARS-CoV-2 proteins (Spike, VME, NCAP, AP3A,
and NS7A) were analyzed. In healthy control individuals, no significant
CD4+ T-cell responses to the 5 SARS-CoV2 proteins were seen (Figure 2B,
IL-2+TNF-\selectlanguage{greek}α\selectlanguage{english}+(\%) in CD4+ \textless{}0.05\%, mean = 0.01\%). However, 20\%
of healthy individuals showed heterogenous TNF-\selectlanguage{greek}α\selectlanguage{english}+/IFN-\selectlanguage{greek}γ\selectlanguage{english}+ CD8+ T-cell
(\textgreater{}0.05\%) responses to the 5 SARS-CoV-2 proteins, which
could represent cross-reaction of CD8+ T-cells generated from previous
endemic coronavirus infection (Figure 2B)\textsuperscript{9,10}. Based
on the background level of CD4+ T-cell response in healthy controls, we
set 0.05\% of dual-positive CD4+ and CD8+ T-cells as the cutoff level
determining positive T-cell immunity against SARS-CoV-2. Overall, we
observed 88\% (30 of 34) infected patients had either positive CD4+ or
CD8+ T-cell immunity to one or more of 5 CoV-2 peptides. Most patients
showed positive CD4+ T-cell immunity (85\%, 29 of 34), and CD4+ T-cells
demonstrated immunodominant responses to Spike peptides as previously
described\textsuperscript{11,12} (Figure 2A). CD8+ T-cells showed
similar responses to the 5 proteins; 68\% (23 of 34) had positive CoV-2
specific CD8+ T-cells to one or more of 5 CoV-2 proteins.

\emph{T-cell Immunity in Vaccinated Individuals}

Next, we analyzed Spike-specific CD4+/CD8+ immune responses to the
Pfizer BNT162b2 vaccine. We compared Spike-specific T-cell immunity to
19 healthy controls, 38 infected patients, and 38 vaccinated individuals
1 month after the 2\textsuperscript{nd} vaccine dose (Figure 2B). No
healthy unvaccinated individuals showed positive CD4+ T-cells against
SARS-CoV-2, but infected patients and vaccinated individuals
demonstrated substantial spike-specific CD4+ T-cell immunity: 87\% (33
of 38) and 89\% (34 of 38) respectively. CD8+ T-cells from healthy
controls, infected patients, and vaccinated individuals showed 21\% (4
of 19), 34\% (13 of 38), and 58\% (22 of 38) positive immune responses
against SARS-CoV-2 spike peptides, respectively. Therefore, the Pfizer
BNT162b2 vaccine induced T-cell reactivity to Spike-specific peptides
that was equivalent to that seen in infected patients after recovery.

\emph{Association of T-cell Immunity with IgG Serology}

T-cell immunity to SARS-CoV-2 was generally associated with
Spike-specific IgG responses\textsuperscript{11,12}. Serum from
SARS-CoV-2 patients were submitted for clinical nucleoprotein IgG titer.
In 25 patients with nucleocapsid IgG positivity, we analyzed the
association with CD4+ T-cell immunity to the 5 SARS-CoV-2 peptides (the
highest response was compared). Although the T-cell immunity was not
nucleocapsid-specific, there was a significant association between CD4+
T-cell immunity and nucleocapsid IgG titers (p=0.022; R= 0.457; Figure
2C).

We then examined Spike-specific IgG levels in 80 SARS-CoV2 infected
patients and compared them to Spike-specific T-cell immunity. Here,
72.58\% of patients with positive Spike-specific CD4+ T-cells had
positive Spike-specific IgG levels. For patients with negative
Spike-specific T-cell immunity, 61.11\% also showed negative
Spike-specific IgG levels. In 13 patients with high Spike-specific CD4+
T-cell immunity (IL-2+TNF-\selectlanguage{greek}α\selectlanguage{english}+(\%) in CD4+ \emph{\textgreater{}} 0.3\%),
we also observed a correlation between T-cell immunity and level of
Spike-specific IgG (p=0.0316; R=0.5288; Figure 2D). Therefore, T-cell
immunity in SARS-CoV-2 patients, in general, was associated with
positive IgG levels. However, 39\% of previously infected patients with
positive Spike-IgG antibodies did not demonstrate T-cell immunity. This
may represent variability in the composition of immune responses from
one individual to another as has been reported\textsuperscript{4-6}.

\emph{UK Variant and Immune Evasion}

The B.1.1.7 variant contains the E484K mutation which renders resistance
to serologic responses in infected individuals\textsuperscript{8}.To
determine if this VOC evaded T-cell immunity, we analyzed 19
infected/recovered patients and 18 vaccinated individuals for CD4+/CD8+
T-cell responses against B.1.1.7 variant Spike protein. As shown in
Figure 3, there is no significant reduction in CD4+/CD8+ T-cell
responses to the variant B.1.1.7 Spike peptides as compared to the
original Wuhan Spike peptides (mean of infected patients: 0.23\%
original to 0.18\% variant; mean of vaccinated individuals: 0.16\%
original to 0.14\% variant). Five of 20 infected patients and 6 of 18
vaccinated individuals had no detectable CD8+ T-cells against the
original or variant Spike peptides (data not shown). The other 15
infected and 12 vaccinated individuals demonstrated nearly identical
CD8+ responses to the original Wuhan Spike and variant Spike (Figure
3B). When the individual T-cell responses to the original and variant
spikes were compared, those with higher CD4+ T-cell immunity tend to
lose some reactivity to the variant peptide, but not at a significant
level (Figure 3C and 3D). In summary, T-cell memory induced by
SARS-CoV-2 infection or vaccination establishes effective immune
response against the B.1.1.7 variant. This would suggest protective
immunity against B.1.1.7 infection and possibly other
VOC\textsuperscript{13}.

\textbf{Discussion}

Assessing the composition, scope, and durability of protective immunity
generated after SARS-CoV-2 infection or vaccination are critical for
control of the pandemic and future vaccination strategies. It is likely
that analyzing immune responses to SARS-CoV-2 has garnered more
attention and information than any other human infection in history.
Traditional assessments have included antibody responses which are often
transient or rapidly declining in patients with moderate infections.
However, we now know that T-cell immunity against SARS-CoV-2 is more
diverse and cross-reactive with peptides expressed on other
Coronaviruses\textsuperscript{9,11-12}. These observations suggest that
robust T-cell responses are an important and essential element of
long-term immunity to SARS-CoV-2. However, assessments of T-cell
immunity to SARS-CoV-2 are not readily available. In this regard, we
present data from a flow cytometry-based assay detecting dual
cytokine-producing, SARS-CoV-2-antigen-specific memory T-cells which
demonstrates specificity and accuracy for detection of CD4+/CD8+ T-cell
responses to SARS-CoV-2 peptides and differentiates infected and
vaccinated individuals from those not exposed to SARS-CoV-2.

Finally, analysis of T-cell responses to an important VOC (B.1.1.7)
showed that exposure to SARS-CoV-2 infection or BNT162b2 vaccine
elicited nearly equivalent T-cell responses. Recent observations suggest
that IgG responses to SARS-CoV-2 infection did not reduce viremia in
patients infected with the B.1.1.7 variant\textsuperscript{8} however,
SARS-CoV-2 T-cell responses were not explored in that study. Long term
analysis of immune responses will be important since memory responses
differ greatly from acute responses, especially at the antibody
level\textsuperscript{7,14-15}. Here, dormancy of memory T-cells,
B-cells, and plasma cells that can rapidly be activated upon re-exposure
to SARS-CoV-2 exposure are likely to have an important role in
preventing SARS-CoV-2 infection and possibly infection from current and
emerging VOC\textsuperscript{13}.

\textbf{Acknowledgements} :

We wish to thank the members of the Transplant Immunology Laboratory and
Division of Infectious Diseases at Cedars-Sinai Medical Center for their
hard work and dedication to this project. We also want to express our
gratitude to the patients with COVID-19 and vaccine participants for
donating their time and blood for this study.

\textbf{Figure Legends} :

Figure 1. Detection of SARS-CoV-2-specific T-cells in whole blood. Fresh
whole blood from participants was stimulated by SARS-CoV-2 Spike
peptides. Activated CD4+ T-cells were identified as
CD45+CD3+CD4+IL-2+/TNF-\selectlanguage{greek}α\selectlanguage{english}+ cells while activated CD8+ T-cell were
CD45+CD3+CD8+TNF-\selectlanguage{greek}α\selectlanguage{english}+/IFN-\selectlanguage{greek}γ\selectlanguage{english}+ cells. Also shown is Blood + PHA which is
positive control and Blood only which is negative control.

Figure 2. T cell immune response in SARS-CoV-2 infected patients and
vaccinated individuals. A.CD4+ and CD8+ T-cell immune responses to
SARS-CoV-2 peptides from 134 patients with confirmed SARS-CoV-2
infection. T-cells were stimulated separately using 5 major CoV-2
peptides: Spike, VME, NCAP, AP3A, NS7A. Activated CD4+ and CD8+ T cells
were enumerated in Figure 1. Each dot represents one individual reading.
B. CD4+ and CD8+ T-cell immune responses to SARS-CoV-2 Spike peptides in
healthy, infected and vaccinated individuals. C. The correlation of
Nucleocapsid-specific IgG levels with CD4+ T-cell immune responses to
one or more of 5 major SARS-CoV-2 peptides in 25 patients. D. The
correlation between Spike-specific CD4+ T-cell immune responses and
Spike-specific IgG levels in 13 patients with elevated CD4+
Spike-specific T-cell immune responses (IL-2+/TNF-\selectlanguage{greek}α\selectlanguage{english}+ cell\% in CD4+
\textgreater{} 0.3\%).

Figure 3. Immunogenicity of variant B.1.1.7 spike peptides. A\&B. CD4+
\& CD8+ T-cell immune responses to Spike-specific peptides are shown in
infected/recovered and vaccinated patients. T cells were stimulated by
the original SARS-CoV-2 Spike (Wuhan) or variant B.1.1.7 Spike peptides.
Activated CD4+ (A) and CD8+ T- cell (B) in 19 infected patients and 18
vaccinated individuals are shown. C\&D.The paired data for immune
responses to SARS-CoV-2 Spike peptides and UK (B.1.1.7)Spike peptides
for each individual.

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\end{enumerate}

\textbf{Hosted file}

\verb`Table 1 COVID-Tc.docx`  available at \url{https://authorea.com/users/380273/articles/711317-t-cell-immunity-against-covid-19-and-uk-variant-in-infected-and-vaccinated-individuals}

\textbf{Hosted file}

\verb`COVID Tc Figures 07-28-2021  -  Read-Only.pptx`  available at \url{https://authorea.com/users/380273/articles/711317-t-cell-immunity-against-covid-19-and-uk-variant-in-infected-and-vaccinated-individuals}

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