Clinical Microbiology and Infection 29 (2023) 1188e1195

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Clinical Microbiology and Infection

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Original article

Association between reactogenicity and immunogenicity after

BNT162b2 booster vaccination: a secondary analysis of a prospective
cohort study
Anselm Jorda 1, Felix Bergmann 1, 2, Robin Ristl 3, Helga Radner 4, Daniela Sieghart 4,
Daniel Aletaha 4, Markus Zeitlinger 1, *
1)
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
2)
Department of Plastic, Reconstructive and Aesthetic Surgery, Medical University of Vienna, Vienna, Austria
3)
Section for Medical Statistics, Center for Medical Data Science, Medical University of Vienna, Vienna, Austria
4)
Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna, Vienna, Austria

a r t i c l e i n f o a b s t r a c t

Article history: Objectives: A weak correlation between symptom severity and antibody levels after primary immuni-
Received 11 January 2023 zation against COVID-19 has already been shown. This study aimed to describe the association between
Received in revised form reactogenicity and immunogenicity after booster vaccination.
17 May 2023
Methods: This secondary analysis of a prospective cohort study included 484 healthcare workers who
Accepted 22 May 2023
Available online 25 May 2023
received a booster vaccination with BNT162b2. Anti-receptor binding domain (RBD) antibodies were
assessed at baseline and 28 days after booster vaccination. Side effects were graded (none, mild, mod-
Handling Editor: L. Scudeller erate, or severe) and reported daily for 7 days after booster vaccination. Spearman correlation coefficient
(rho) was used to determine the correlations between the severity of each symptom and anti-RBD levels
Keywords: before vaccination and 28 days after. The Bonferroni method was used to adjust p values for multiple
Adverse events comparisons.
Antibody titers Results: Most of the 484 participants reported at least one local (451 [93.2%]) or systemic (437 [90.3%])
COVID-19 post-booster symptom. No correlations between the severity of local symptoms and antibody levels were
SARS-CoV-2
found. Except for nausea, systemic symptoms showed weak but statistically significant correlations with
Side effects
28-day anti-RBD levels (fatigue [rho ¼ 0.23, p < 0.01], fever [rho ¼ 22, p < 0.01], headache [rho ¼ 0.15, p
Symptoms
Vaccine 0.03], arthralgia [rho ¼ 0.2, p < 0.01], myalgia [rho ¼ 0.17, p < 0.01]). There was no association between
post-booster symptoms and pre-booster antibody levels.
Discussion: This study showed only a weak correlation between the severity of systemic post-booster
symptoms and anti-SARS-CoV-2 antibody levels at 28 days. Therefore, self-reported symptom severity
cannot be used to predict immunogenicity after booster vaccination. Anselm Jorda, Clin Microbiol
Infect 2023;29:1188
© 2023 The Authors. Published by Elsevier Ltd on behalf of European Society of Clinical Microbiology and
Infectious Diseases. This is an open access article under the CC BY-NC-ND license (http://
creativecommons.org/licenses/by-nc-nd/4.0/).

Introduction have investigated the association between reactogenicity and

The ongoing, unprecedented vaccination campaign against
COVID-19 has raised questions about the correlation between the
extent of symptoms after vaccination and the level of protection
conferred by the vaccine. To address these concerns, several studies
* Corresponding author. Markus Zeitlinger, Department of Clinical Pharmacology,
Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
E-mail address: markus.zeitlinger@meduniwien.ac.at (M. Zeitlinger).
immunogenicity after primary immunization with the different
COVID-19 vaccines [1e5]. These studies have suggested a weak but
consistent association between the occurrence and severity of post-
vaccination symptoms and antibody levels, most of which were
measured 4 weeks after vaccination. However, in many parts of the
world, primary immunizations are largely complete, and recent
developments suggest that COVID-19 vaccines, similar to influenza
vaccines, will require seasonal or periodic boosters. To date, only
two studies have examined the interplay between reactogenicity

https://doi.org/10.1016/j.cmi.2023.05.028
1198-743X/© 2023 The Authors. Published by Elsevier Ltd on behalf of European Society of Clinical Microbiology and Infectious Diseases. This is an open access article under
the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
 A. Jorda et al. / Clinical Microbiology and Infection 29 (2023) 1188e1195
and immunogenicity after COVID-19 booster vaccination [6,7].
These studies had small sample sizes (47 and 62, respectively),
which limited the strengths of their findings. Surprisingly, one of
these studies claimed that the association between post-booster
symptoms and antibody levels disappeared after booster vaccina-
tion [6]. The second study focused only on fever and also failed to
detect a statistically significant association between the presence of
fever and antibody levels at 4 weeks [7]. These conflicting results
highlight the need for further investigation into the relationship
between reactogenicity and immunogenicity after booster vacci-
nation. In this regard, we performed a secondary analysis of a
prospective cohort study of healthcare workers to elucidate the
relationship between reactogenicity and immunogenicity after
BNT162b2 booster vaccination. Our study aimed to provide a more
comprehensive understanding of the immune response to COVID-
19 booster vaccination and to clarify the potential impact of post-
vaccination symptoms on antibody production. Overall, these
findings may help inform patient counselling and management in
clinical practice, particularly when it comes to managing patient
expectations and concerns about the effectiveness of COVID-19
vaccines.
Methods
Study design and participants
The main study was a single-centre, prospective, open-label
cohort study that was originally designed to examine the immu-
nogenicity and tolerability after a concomitant administration of
BNT162b2 (Pfizer-BioNTech) and seasonal influenza vaccine
compared with the administration of BNT162b2 alone [8]. Here, we
performed a post-hoc analysis to investigate the association be-
tween post-booster symptoms and immunogenicity after booster
vaccination with BNT162b2 (Pfizer-BioNTech). To obtain a homog-
enous study population, we included only the study arm that
received a booster with BNT162b2 alone. The study included
healthcare workers aged 18 years or older and affiliated with the
Medical University of Vienna and the Vienna General Hospital, who
received their primary immunization with BNT162b2 (Pfizer-Bio-
NTech) or ChAdOx1 (AstraZeneca) at least 4 months before
screening. The study protocol and all relevant documents were
approved by competent authorities (Eudra-CT: 2021-005094-28)
and the local ethics committee (MUV-EK: 1954/2021). All partici-
pants gave their oral and written consent before enrolment into the
study.
Assessment of immunogenicity
Blood was collected immediately before and 4 weeks
(28 ± 4 days) after booster vaccination with BNT162b2. IgG anti-
bodies against the receptor binding domain of the viral spike pro-
tein (anti-RBD antibodies) and antibodies against the SARS-CoV-2
nucleocapsid protein were measured. Anti-RBD antibodies were
quantified using the Elecsys® Anti-SARS-CoV-2-S immunoassay
(upper limit of quantification of 75 000.0 BAU/mL) [9]. We deter-
mined anti-nucleocapsid antibodies using the qualitative Elecsys®
Anti-SARS-CoV-2 assay to assess whether participants had previ-
ously been infected with SARS-CoV-2 [10]. Both assays were per-
formed on a cobas® e801 analyzer (Roche Diagnostics, Rotkreuz,
Switzerland). Patients with incomplete immunogenicity data were
removed from the analysis.
1189
Assessment of reactogenicity
During the first 7 days after the booster vaccination, all partic-
ipants were required to submit a daily report of their post-booster
symptoms using an electronic diary. Solicited adverse events
included local symptoms (pain, erythema, and pruritus) and sys-
temic symptoms (fatigue, fever, headache, nausea, arthralgia, and
myalgia). All adverse events were graded according to the toxicity
grading criteria of the Food and Drug Administration [11]. Symp-
toms were classified on a severity scale as none, mild, moderate, or
severe. Injection site erythema was graded according to its diam-
eter: mild, 2e5 cm; moderate, 5.1e10 cm; and severe, >10 cm. Body
temperatures of 38.0e38.4 C, 38.5e38.9 C, and >38.9 C were
graded as mild, moderate, and severe fever, respectively. Partici-
pants also indicated whether they had seen a doctor, taken anal-
getic or antipyretic medication, and/or called in sick during the first
week after vaccination. Patients who did not report their symptoms
at least once were excluded from the analysis.
Outcome measures
The outcome measures of this study were the baseline and 28-
day antibody levels. The exposure variable was the post-
vaccination symptom severity (none, mild, moderate, or severe).
The primary outcome of this study was the correlation between the
severity of local and systemic post-booster symptoms and 28-day
antibody levels. The secondary analysis was the correlation be-
tween post-booster symptoms and pre-booster antibody levels. As
an exploratory analysis, we created a multivariate linear regression
model with the 28-day antibody level as the dependent variable.
Moreover, we assessed the correlation between the systemic
symptom severity and the relative increase in antibodies (i.e. the
ratio between 28-day to pre-booster antibody levels).
Statistical analysis
Characteristics of participants are described by mean and
standard deviation, median and interquartile range, or absolute
numbers and percentages (%).
We reported the pooled and separate frequency of local and
systemic post-booster symptoms. For each symptom, the highest
level of severity (none, mild, moderate, or severe) within 7 days
after vaccination was used for the analysis. Because antibody con-
centrations showed normal distribution after log10-transformation,
we reported geometric means and medians of antibody levels at
baseline and after 28 days. The correlation between symptom
severity and antibody levels was calculated using the non-
parametric Spearman correlation test. Correlation coefficients
(rho) of 0.1 to <0.2, 0.2 to <0.4, 0.4 to <0.7, and 0.7 were inter-
preted as very weak, weak, moderate, and strong correlations,
respectively [12]. The Bonferroni method was used to adjust p
values for multiple comparisons. Adjusted p values below 0.05
were considered statistically significant.
We performed a multivariate linear regression analysis with
log10-transformed 28-day antibody levels as the dependent vari-
able. We included covariates that were considered to have a po-
tential impact on immunogenicity after vaccination: baseline
demographics (age, sex, body mass index) [13]; previous SARS-
CoV-2 infection; analgetic or antipyretic medication after vaccina-
tion [14]; primary immunization compound (BNT162b2 or ChA-
dOx1) [15]; and chronic comorbidities (hypertension, pulmonary
diseases, heart diseases, and thyroid disorders) [16]. We also
1190 A. Jorda et al. / Clinical Microbiology and Infection 29 (2023) 1188e1195

included all post-booster symptoms, which showed a statistically
significant correlation with 28-day antibody levels in univariate
analyses. Diagnostic plots (Fig. S1) were visually assessed, and
linear regression assumptions were considered to be adequately
met. No influential data points were detected. Residual distribution
was close to normal. Coefficients of the linear regression model
were exponentiated and interpreted as the percentage increase in
anti-RBD levels per-unit increase of the independent variable. To
assess the risk of multicollinearity in the model, we calculated the
univariate correlation coefficients between the independent vari-
ables and the variance inflation factor (VIF). The VIF indicates how
much the variance of an estimated regression coefficient is
increased because of collinearity. In this study, we considered VIF
values of >2.5 as meaningful collinearity and values > 10 as sig-
nificant collinearity.
To assess the potential impact of selection bias on our findings,
we performed two sensitivity analyses, which assumed that pa-
tients, who were excluded because they did not report symptoms,
experienced either no systemic symptoms (Model 1) or severe
systemic symptoms (Model 2).
All analyses were carried out using RStudio (R version 4.1.2 [1
November 2021]).
thyroid disorders (51 [10.5%] of 484). As determined by the pres-
ence of anti-nucleocapsid antibodies at baseline, few had previous
infections with SARS-CoV-2 (24 [5.0%] of 484). Of the 484 partici-
pants, primary immunization was performed with BNT162b2
(Pfizer-BioNTech) in 148 (30.6%) participants and with ChAdOx1
(AstraZeneca) in 336 (69.4%) participants.
Symptoms and treatment after vaccination
Most participants (473 [97.8%] of 484) experienced at least one
adverse reaction within 7 days of vaccination (Fig. 1). Any severe
post-booster symptom occurred in 170 (35.1%) of 484 participants.
Any local symptom occurred in 451 (93.2%) of 484 participants. Any
systemic symptom occurred in 437 (90.3%) of 484 participants. The
most common local symptom was pain at the injection site (445
[91.9%]). The most common systemic symptoms were fatigue (388
[80.2%]) and headache (321 [66.3%]). Analgetic or antipyretic
medication for post-booster symptoms was taken by 133 (27.5%)
participants. Only 7 (1.4%) of 484 participants consulted a medical
doctor.
Association between local symptoms and antibody levels

Results
Study participants
In the primary study, 558 patients received the BNT162b2 vac-
cine. Nineteen patients were excluded because they did not receive
their primary immunization with AstraZeneca or BNT162b2.
Thirty-four patients had missing baseline (n ¼ 2) or follow-up
(n ¼ 32) antibody levels. Twenty-one patients did not report
symptoms and were removed from the analysis. A total of 484
participants were included in the final analysis. The characteristics
of the study participants are provided in Table 1. Most participants
were healthy and had no chronic diseases (340 [70.2%] of 484). The
most common conditions were hypertension (48 [9.9%] of 484) and
Table 1
Baseline characteristics of study population
Fig. 2 depicts the associations between the severity of local post-
booster symptoms and antibody levels before and 28 days after
booster vaccination. No correlations between the severity of local
symptoms and antibody levels were found (Fig. 2).
Association between systemic symptoms and antibody levels
Fig. 3 depicts the associations between the severity of systemic
post-booster symptoms and the antibody levels before and 28 days
after booster vaccination. The severity of fatigue, fever, headache,
arthralgia, and myalgia showed a very weak or weak but statisti-
cally significant correlation with 28-day antibody levels. The
strongest correlation with 28-day antibody levels was observed for
fatigue (rho ¼ 0.23) and fever (rho ¼ 0.22).
No statistically significant correlation between systemic post-
booster symptoms and pre-booster antibody levels was found
(Fig. 3).

Overall Linear regression model

Number of participants 484
Age (y), median (IQR) 45 (32e54) Table 2 lists the multivariate linear regression model. Figure S2
BMI (kg/m2), median (IQR) 24.2 (21.7e27.1) shows the Spearman correlation coefficients between the inde-
Smoking, n (%) pendent variables of the regression models. Moderate correlations
Current smoker 79 (17.8)
Former 255 (57.3)
(rho ranging from 0.27 to 0.66) were found between the individual
Never 111 (24.9) systemic post-vaccination symptoms, with the highest correlation
Chronic conditions, n (%) between myalgia and arthralgia (rho ¼ 0.66). The VIF of all included
Hypertension 48 (9.9) variables was below 2.5, indicating a low risk of multicollinearity
Chronic obstructive pulmonary 19 (3.9)
(Table 2). Compared with no history of COVID-19, previous COVID-
disease or asthma
Diabetes mellitus 8 (1.7) 19 was associated with 22.3% (95% CI: 6.5e40.5%) higher 28-day
Heart disease 2 (0.4) antibody levels. Compared with primary immunization with ChA-
Thyroid disorder 51 (10.5) dOx1, primary immunization with BNT162b2 was associated with
Previous COVID-19, n (%) 24 (5.0) 17.1% higher 28-day antibody levels. Each increase in the fatigue
Weeks since primary immunization, 29.7 (5.7)
mean (SD)
severity scale was associated with a 5.9% (95% CI: 2.1e9.9%) in-
Compound used for primary vaccination, n (%) crease in antibody levels. Each increase in the fever severity scale
BNT162b2 (Pfizer-BioNTech) 148 (30.6) was associated with a 6.5% (95% CI: 0.1 to 13.4%) increase in
ChAdOx1 (AstraZeneca) 336 (69.4) antibody levels.
Anti-RBD IgG before booster (BAU/mL), 372 (337e410)
geometric mean (95% CI)
Anti-RBD IgG at 4 wk (BAU/mL), 18 170 (16 893e19 544) Explorative analyses
geometric mean (95% CI)
Ratio of baseline to week 4, mean (SD) 86.3 (152.5) There was no correlation between the most severe systemic
BMI, body mass index; IQR, interquartile range; RBD, receptor binding domain; SD, symptom and the ratio between 28-day and pre-booster anti-RBD
standard deviation. antibody levels (BAU/mL) (rho ¼ 0.0, p 0.97) (Fig. S3).
 A. Jorda et al. / Clinical Microbiology and Infection 29 (2023) 1188e1195
Fig. 1. Relative frequency (%) of local and systemic post-booster symptoms, use of analgetic or antipyretic medication, and medical consultation within the first 7 d after booster
vaccination.
Sensitivity analyses
Compared with the 484 patients in the main analysis, the 21
patients, who were excluded because of missing symptom report-
ing, showed significantly higher 28-day antibody levels (geometric
mean [95% CI]; 27 712 [20 391e37 661] vs. 18 170 [16 893e19 544];
geometric mean ratio ¼ 1.5 [1.1e2.1]; p 0.011).
To assess the potential impact of this imbalance on our main
results, we performed two sensitivity analyses using extreme as-
sumptions about the symptoms of the excluded patients. Assuming
that all of the 21 excluded subjects experienced any severe systemic
post-vaccination symptoms (Model 1), the correlation coefficient
between post-vaccination symptoms and 28-day antibody levels
was 0.22 (p < 0.001) (Fig. S4). Assuming that all of the 21 excluded
subjects experienced no systemic post-vaccination symptom at all
(Model 2), the correlation coefficient between post-vaccination
symptoms and 28-day antibody levels was 0.14 (p 0.001) (Fig. S4).
Discussion
This is the first study to examine the association between
reactogenicity and pre-booster and 28-day antibody levels in a
large cohort. Two previous smaller studies found no association
between symptoms and antibody levels after booster vaccination
with BNT162b2 [6]. In contrast, we observed a weak but statistically
significant correlation between the severity of systemic symptoms
and 28-day antibody levels. However, the associations were subtle
and do not suggest a clinically relevant relationship between sys-
temic symptoms and 28-day antibody levels. Furthermore, these
1191
findings indicate that absent or mild symptoms do not reflect an
inadequate immune response. Symptom severity can therefore not
be used to predict the antibody response after booster vaccination
with BNT162b2.
Notably, we observed no correlation between local post-booster
symptoms and antibody levels. Previous studies examining the
correlation between reactogenicity and immunogenicity after pri-
mary immunization with BNT162b2 also found no correlation be-
tween local symptoms and antibody levels [3,5,17,18]. It is unclear
why there is no correlation between local reactogenicity and
immunogenicity. In contrast to systemic reactogenicity, local reac-
togenicity may also be affected by injection technique or anatom-
ical aspects, such as proximity to sensory nerve endings or damage
to blood vessels caused by the injection. These confounders may
obscure the correlation between underlying immunological pro-
cesses and subjective symptoms. The lack of correlation could also
be explained by the fact that the local immunologic response differs
markedly from the systemic one. Intramuscular administration of
mRNA vaccines causes local inflammation that attracts neutrophils,
monocytes, and dendritic cells from the blood to the injection site
by the production of chemokines and other inflammatory media-
tors, such as interleukin-1b, interleukin-6, and CXCL10 [19]. This
innate immune response is likely the cause of local symptoms but
may not reflect the extent of the humoral response. Antibody
production is a feature of adaptive immunity that requires the
transport of mRNA-containing lipid nanoparticles or antigen-
expressing cells to lymph nodes, where dendritic cells and mono-
cytes contribute to antigen presentation and priming of T cells [19].
Subsequently, T follicular helper cells promote the differentiation of
1192 A. Jorda et al. / Clinical Microbiology and Infection 29 (2023) 1188e1195

Fig. 2. Relationship between local post-booster symptomsd(A) any local symptom; (B) local pain; (C) itching; (D) erythema, and anti-RBD antibody levels at baseline and 28 d. Data
are presented with box-whisker plots (median, IQR, and range). Empty circles indicate the geometric mean values. IQR, interquartile range; RBD, receptor binding domain.

B cells into antibody-producing plasma cells [20]. Co-stimulatory
mediator molecules of these cellular interactions, such as type I
interferons, TNF-alpha, and interleukin-6, also contribute to sys-
temic symptoms such as fever and may correlate more strongly
with the actual antibody response [19,21]. In addition, circulating
SARS-CoV-2 antigens have been detected in human plasma after
vaccination, which may also enhance systemic symptoms and the
humoral immune response [22].
This study has several limitations. First, the explorative nature of
this analysis does not allow for proof of causality, which makes the
interpretation of our results speculative. Second, we relied on self-
reported symptoms and did not record more challenging
symptoms such as lymphadenopathy. Considering the important
immunological role of local lymph nodes near the injection site,
qualitative data on lymph node swelling would have been desirable
but not feasible in this study design. Third, although there is reli-
able evidence of the correlation between antibody levels and pro-
tection against COVID-19 [23], the clinical relevance of subtle
differences in antibody levels among the degrees of severity of
post-booster symptoms is unclear. Fourth, we had to exclude pa-
tients who did not report their symptoms after vaccination. This
exclusion may have introduced selection bias. However, two
sensitivity analyses in which assumptions were made about the
symptoms of excluded patients showed little effect on the
 A. Jorda et al. / Clinical Microbiology and Infection 29 (2023) 1188e1195 1193

Fig. 3. Relationship between systemic post-booster symptomsd(A) any systemic symptom; (B) fatigue; (C) fever; (D) headache; (E) nausea; (F) arthralgia; (G) myalgia, and anti-
RBD antibody levels at baseline and 28 d. Data are presented with box-whisker plots (median, IQR, and range). Empty circles indicate the geometric mean values. IQR, interquartile
range; RBD, receptor binding domain.
1194 A. Jorda et al. / Clinical Microbiology and Infection 29 (2023) 1188e1195

Table 2
Multivariate linear regression analysis assessing the association between log-transformed anti-RBD antibody levels at day 28 and all included covariates

Variable Incremental per-unit change (%) Lower 95% CI Upper 95% CI p VIF
in anti-RBD levels at day 28

Age (y) 0.2 0.0 0.5 0.106 1.25

BMI (kg/m2) 1.2 0.4 1.9 0.002 1.20
Female sex (vs. male) 0.4 6.9 6.7 0.918 1.20
Fatigue (none to severe) 5.9 2.1 9.9 0.002 1.63
Fever (none to severe) 6.5 0.1 13.4 0.053 1.27
Headache (none to severe) 0.5 4.3 3.3 0.783 1.62
Arthralgia (none to severe) 2.7 2.1 7.7 0.275 2.30
Myalgia (none to severe) 1.0 5.3 3.6 0.678 2.24
Analgetic or antipyretic medication 5.3 2.6 13.8 0.193 1.39
Previous COVID-19 (vs. no history of COVID-19) 22.3 6.5 40.5 0.004 1.04
Primary immunization with BNT162b2 (vs. ChAdOx1) 17.1 9.5 25.3 <0.001 1.10
Hypertension 5.0 14.8 5.8 0.351 1.20
COPD or asthma 1.2 13.3 18.1 0.877 1.04
Diabetes 23.3 51.9 22.4 0.266 1.03
Heart disease 2.5 7.3 13.3 0.629 1.09
Thyroid disorder 6.5 26.6 19.1 0.585 1.09

BMI, body mass index; COPD, chronic obstructive pulmonary disease; RBD, receptor binding domain; VIF, variance inflation factor.

correlation between post-booster symptoms and 28-day antibody Medical Scientific Fund of the Mayor of the City of Vienna. The
levels. Fifth, the independent variables, especially the systemic funding source did not influence the study design, conduct, or
symptoms, showed a moderate degree of collinearity, which may reporting.
otherwise have affected the validity of the regression model. Sixth,
data on reactogenicity after the first two vaccinations were not
Appendix A. Supplementary data
available. We reasoned that a retrospective assessment of post-
vaccination symptom severity months later would not have resul-
Supplementary data to this article can be found online at
ted in sufficient data quality.
https://doi.org/10.1016/j.cmi.2023.05.028.

Conclusion
References
This study showed only a weak correlation between the severity
of systemic post-booster symptoms and anti-SARS-CoV-2 antibody
levels after 28 days. Although the association between reac-
togenicity and immunogenicity would be plausible based on our
immunological understanding, the weak correlation precludes the
clinically meaningful use of symptom severity for predicting
immunogenicity. Importantly, absent or mild systemic symptoms
after booster vaccination do not indicate an inadequate immune
response.
Author contributions
The primary study was conceptualized by H.R., D.S., D.A., and
M.Z.; the secondary analysis presented in this article was concep-
tualized by A.J., F.B., and M.Z.; the manuscript was written by A.J.,
F.B., and M.Z.; analyses of the data were performed by A.J. and R.R.
All authors contributed to data curation and the design of the paper,
revision as well as editing of the paper.
Transparency declaration
Conflict of interest
The authors declare that they have no conflicts of interest.
The following authors received financial support within the last
3 years: D.A. from AbbVie, Amgen, Janssen, Lilly, Merck Sharp,
Novartis, Pfizer, Roche, Sandoz, Sobi Sweden; HR from Gilead, Sci-
ence GmbH, Janssen, Merck Sharp, and Pfizer.
Funding
[10] Perkmann T, Perkmann-Nagele N, Breyer MK, Breyer-Kohansal R,
The study was funded by the Federal Austrian Ministry of Edu-
cation, Science and Research (21226.), the City of Vienna, and the
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