Omicron sub-lineages BA.4/BA.5 escape BA.1 infection elicitedneutralizing immunity
Khadija Khan1,2, Farina Karim1,2, Yashica Ganga1, Mallory Bernstein1, Zesuliwe Jule1, Kajal
Reedoy1, Sandile Cele1,2, Gila Lustig3, Daniel Amoako4,5, Nicole Wolter4,6, Natasha
Samsunder3, Aida Sivro3,7, James Emmanuel San8, Jennifer Giandhari8, Houriiyah Tegally8,9,Sureshnee Pillay8, Yeshnee Naidoo8, Matilda Mazibuko1, Yoliswa Miya1, Nokuthula Ngcobo1,
Nithendra Manickchund10, Nombulelo Magula11, Quarraisha Abdool Karim3,12, Anne vonGottberg4,6, Salim S. Abdool Karim3,12, Willem Hanekom1,13, Bernadett I. Gosnell10, COMMITKZN Team§, Richard J. Lessells8, Tulio de Oliveira8,9,14, Mahomed-Yunus S. Moosa10, Alex
Sigal1,2,3,15
1

Africa Health Research Institute, Durban, South Africa. 2School of Laboratory Medicine and Medical
Sciences, University of KwaZulu-Natal, Durban, South Africa. 3Centre for the AIDS Programme of
Research in South Africa, Durban, South Africa. 4National Institute for Communicable Diseases of the
National Health Laboratory Service, Johannesburg, South Africa. 5School of Health Sciences, Collegeof Health Sciences, University of KwaZulu-Natal, KwaZulu-Natal, South Africa. 6School of Pathology,
Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. 7Departmentof Medical Microbiology, University of KwaZulu-Natal, Durban, South Africa. 8KwaZulu-Natal ResearchInnovation and Sequencing Platform, Durban, South Africa. 9Centre for Epidemic Response andInnovation (CERI), School of Data Science and Computational Thinking, Stellenbosch University,
Stellenbosch, South Africa. 10Department of Infectious Diseases, Nelson R. Mandela School of Clinical
Medicine, University of KwaZulu-Natal, Durban, South Africa. 11Department of Internal Medicine,
Nelson R. Mandela School of Medicine. University of Kwa-Zulu Natal. 12Department of Epidemiology,
Mailman School of Public Health, Columbia University, New York, NY, United States. 13Division of
Infection and Immunity, University College London, London, UK. 14Department of Global Health,
University of Washington, Seattle, USA. 15Max Planck Institute for Infection Biology, Berlin, Germany.

The SARS-CoV-2 Omicron (B.1.1.529) variant first emerged as the BA.1 sub-lineage,
with extensive escape from neutralizing immunity elicited by previous infection withother variants, vaccines, or combinations of both1,2. Two new sub-lineages, BA.4 andBA.5, are now emerging in South Africa with changes relative to BA.1, including L452R
and F486V mutations in the spike receptor binding domain. We isolated live BA.4 andBA.5 viruses and tested them against neutralizing immunity elicited to BA.1 infection
in participants who were Omicron/BA.1 infected but unvaccinated (n=24) andparticipants vaccinated with Pfizer BNT162b2 or Johnson and Johnson Ad26.CoV.2S
with breakthrough Omicron/BA.1 infection (n=15). In unvaccinated individuals, FRNT50,
the inverse of the dilution for 50% neutralization, declined from 275 for BA.1 to 36 forBA.4 and 37 for BA.5, a 7.6 and 7.5-fold drop, respectively. In vaccinated BA.1
breakthroughs, FRNT50 declined from 507 for BA.1 to 158 for BA.4 (3.2-fold) and 198 forBA.5 (2.6-fold). Absolute BA.4 and BA.5 neutralization levels were about 5-fold higher
in this group versus unvaccinated BA.1 infected participants. The observed escape of
BA.4 and BA.5 from BA.1 elicited immunity is more moderate than of BA.1 against
previous immunity1,3. However, the low absolute neutralization levels for BA.4 and BA.5,
particularly in the unvaccinated group, are unlikely to protect well against symptomatic
infection4.This may indicate that, based on neutralization escape, BA.4 and BA.5 havepotential to result in a new infection wave.

We enrolled participants in November-December 2021 during the Omicron/BA.1 infection
wave in South Africa (Table S1). We enrolled 24 SARS-CoV-2 infected unvaccinatedparticipants and 15 vaccinated participants where eight were vaccinated with Pfizer
BNT162b2 and seven with Johnson and Johnson Ad26.CoV.2S (Table S2). For this study weused blood samples collected a median of 23 days after symptoms onset (IQR 18-27 forvaccinated and 20-28 for unvaccinated participants), corresponding to a time post-symptoms
when Omicron/BA.1 neutralizing immunity developed and plateaued3. As previously described(see also Table S2), infecting virus per participant was sequenced and all successfully
sequenced viruses were Omicron/BA.13.
We observed that FRNT50 in unvaccinated participants declined from 275 for BA.1 to 36 forBA.4 (7.6-fold, 95% CI 4.9-12.0, Figure 1a) and 37 for BA.5 (7.5-fold, 95% CI 4.4-12.5, Figure1b). In contrast, in vaccinated BA.1 infected participants, FRNT50 declined from 507 to 158 forBA.4 (3.2-fold, 95% CI 2.3-4.4, Figure 1c) and 198 for BA.5 (2.6-fold, 95% CI 1.8-3.7, Figure1d). Absolute BA.4 and BA.5 neutralization levels were about 5-fold higher in the vaccinatedversus unvaccinated group (Figure 1d).
Neutralization capacity elicited to BA.1 infection in unvaccinated participants was low,
accounting for the BA.4 and BA.5 fold-drops leading to very low residual neutralization levels.
The low immunity to BA.1 is perhaps reflective of lower immunogenicity of this variant3,5. The
vaccinated group showed about 5-fold higher neutralization capacity of BA.4 and BA.5 andshould be better protected, although levels may decrease with waning. BA.4 and BA.5 show
similar escape. This is not surprising given that sequence differences between BA.4 and BA.5
are outside spike.
The escape we observe is substantially higher than what we detected for BA.2, where it wasslight and non-significant3. Given the higher escape and especially the low residual
neutralization in the unvaccinated group, we speculate that a BA.4/BA.5 infection wave is astrong possibility. However, vaccination increase neutralization capacity against theseemerging variants and would likely offer good protection against severe disease.

Materials and methods
Informed consent and ethical statement
Blood samples were obtained after written informed consent from adults with PCR-confirmed
SARS-CoV-2 infection who were enrolled in a prospective cohort study at the Africa HealthResearch Institute approved by the Biomedical Research Ethics Committee at the Universityof KwaZulu–Natal (reference BREC/00001275/2020). The Omicron/BA.1 and BA.4 was
isolated from a residual swab sample with SARS-CoV-2 isolation from the sample approvedby the University of the Witwatersrand Human Research Ethics Committee (HREC) (ref.
M210752). The sample to isolate Omicron/BA.5 was collected after written informed consent
as part of the COVID-19 transmission and natural history in KwaZulu-Natal, South Africa:
Epidemiological Investigation to Guide Prevention and Clinical Care in the Centre for the AIDS
Programme of Research in South Africa (CAPRISA) study and approved by the Biomedical
Research Ethics Committee at the University of KwaZulu–Natal (reference
BREC/00001195/2020, BREC/00003106/2021).
Data availability statement
Sequences of outgrown Omicron sub-lineages have been deposited in GISAID with accession
EPI_ISL_7886688(Omicron/BA.1),
EPI_ISL_12268495.2(Omicron/BA.4),

EPI_ISL_12268493.2 (Omicron/BA.5). Raw images of the data are available upon reasonable
request.
Reagent availability statement
Virus isolates and cell line are available from the corresponding author. A Biosafety Level 3
facility is required for laboratories receiving live SARS-CoV-2.
Competing interest statement
Salim S. Abdool Karim is a member in the COVID advisory panel for Emerging Markets at
Pfizer. The authors declare no other competing interests.
Author contributions
AS and KK conceived the study and designed the study and experiments. AvG, QAK, SSAK,
GL, ASi, and NS identified and provided virus samples. M-YSM, FK, BIG, MB, KK, TN, MM,
NM, ZM, NN, YM, ZJ, KR, and YG set up and managed the cohort and cohort data. KK, ZJ,
KR, SC, HT, JES, YG, JG, YR, AK, DA, and JB performed experiments and sequence analysis
with input from AS, TdO, RJL, and JNB. AS, KK, FK, RM, and YR interpreted data with input
from M-YSM, GG, SSAK, WH, TdO, RJL. AS and KK prepared the manuscript with input fromall authors.
Whole-genome sequencing, genome assembly and phylogenetic analysis
RNA was extracted on an automated Chemagic 360 instrument, using the CMG-1049 kit(Perkin Elmer, Hamburg, Germany). The RNA was stored at −80◦C prior to use. Libraries forwhole genome sequencing were prepared using either the Oxford Nanopore Midnight protocol
with Rapid Barcoding or the Illumina COVIDseq Assay. For the Illumina COVIDseq assay, thelibraries were prepared according to the manufacturer’s protocol. Briefly, amplicons were
tagmented, followed by indexing using the Nextera UD Indexes Set A. Sequencing libraries
were pooled, normalized to 4 nM and denatured with 0.2 N sodium acetate. An 8 pM sample
library was spiked with 1% PhiX (PhiX Control v3 adaptor-ligated library used as a control).
We sequenced libraries on a 500-cycle v2 MiSeq Reagent Kit on the Illumina MiSeq
instrument (Illumina). On the Illumina NextSeq 550 instrument, sequencing was performed
using the Illumina COVIDSeq protocol (Illumina Inc, USA), an amplicon-based next-generation
sequencing approach. The first strand synthesis was carried using random hexamers primersfrom Illumina and the synthesized cDNA underwent two separate multiplex PCR reactions.
The pooled PCR amplified products were processed for tagmentation and adapter ligation
using IDT for Illumina Nextera UD Indexes. Further enrichment and cleanup was performed
as per protocols provided by the manufacturer (Illumina Inc). Pooled samples were quantified
using Qubit 3.0 or 4.0 fluorometer (Invitrogen Inc.) using the Qubit dsDNA High Sensitivity
assay according to manufacturer’s instructions. The fragment sizes were analyzed using
TapeStation 4200 (Invitrogen). The pooled libraries were further normalized to 4nM
concentration and 25 μL of each normalized pool containing unique index adapter sets werecombined in a new tube. The final library pool was denatured and neutralized with 0.2N sodiumhydroxide and 200 mM Tris-HCL (pH7), respectively. 1.5 pM sample library was spiked with
2% PhiX. Libraries were loaded onto a 300-cycle NextSeq 500/550 HighOutput Kit v2 and run
on the Illumina NextSeq 550 instrument (Illumina, San Diego, CA, USA). For Oxford Nanopore
sequencing, the Midnight primer kit was used as described by Freed and Silander55. cDNA
synthesis was performed on the extracted RNA using LunaScript RT mastermix (New England
BioLabs) followed by gene-specific multiplex PCR using the Midnight Primer pools which
produce 1200bp amplicons which overlap to cover the 30-kb SARS-CoV-2 genome.
Amplicons from each pool were pooled and used neat for barcoding with the Oxford Nanopore
Rapid Barcoding kit as per the manufacturer’s protocol. Barcoded samples were pooled andbead-purified. After the bead clean-up, the library was loaded on a prepared R9.4.1 flow-cell.
A GridION X5 or MinION sequencing run was initiated using MinKNOW software with thebase-call setting switched off. We assembled paired-end and nanopore.fastq reads using
Genome Detective 1.132 (https://www.genomedetective.com) which was updated for theaccurate assembly and variant calling of tiled primer amplicon Illumina or Oxford Nanopore
reads, and the Coronavirus Typing Tool56. For Illumina assembly, GATK HaploTypeCaller -min-pruning 0 argument was added to increase mutation calling sensitivity near sequencing
gaps. For Nanopore, low coverage regions with poor alignment quality (<85% variant
homogeneity) near sequencing/amplicon ends were masked to be robust against primer dropout experienced in the Spike gene, and the sensitivity for detecting short inserts using a regionlocal global alignment of reads, was increased. In addition, we also used the wf_artic (ARTIC
SARS-CoV-2) pipeline as built using the nextflow workflow framework57. In some instances,mutations were confirmed visually with .bam files using Geneious software V2020.1.2(Biomatters). The reference genome used throughout the assembly process was
NC_045512.2 (numbering equivalent to MN908947.3). For lineage classification, we used thewidespread dynamic lineage classification method from the ‘Phylogenetic Assignment ofNamed Global Outbreak Lineages’ (PANGOLIN) software suite (https://github.com/hCoV2019/pangolin).
Cells
Vero E6 cells (originally ATCC CRL-1586, obtained from Cellonex in South Africa) were
propagated in complete growth medium consisting of Dulbecco's Modified Eagle Medium(DMEM) with 10% fetal bovine serum (Hyclone) containing 10mM of HEPES, 1mM sodium
pyruvate, 2mM L-glutamine and 0.1mM nonessential amino acids (Sigma-Aldrich). Vero E6
cells were passaged every 3–4 days. The H1299-E3 cell line (H1299 originally from ATCC as
CRL-5803) was propagated in growth medium consisting of complete Roswell Park Memorial
Institute (RPMI) 1640 medium with 10% fetal bovine serum containing 10mM of HEPES, 1mM
sodium pyruvate, 2mM L-glutamine and 0.1mM nonessential amino acids. Cells werepassaged every second day. The H1299-E3 (H1299-ACE2, clone E3) cell line was derived
from H1299 as described in our previous work1,6.
Virus expansion
All work with live virus was performed in Biosafety Level 3 containment using protocols for
SARS-CoV-2 approved by the Africa Health Research Institute Biosafety Committee. ACE2expressing H1299-E3 cells were seeded at 4.5 × 105 cells in a 6 well plate well and incubatedfor 18–20 h. After one DPBS wash, the sub-confluent cell monolayer was inoculated with 500
μL universal transport medium diluted 1:1 with growth medium filtered through a 0.45-μm filter.
Cells were incubated for 1 h. Wells were then filled with 3 mL complete growth medium. After
4 days of infection (completion of passage 1 (P1)), cells were trypsinized, centrifuged at 300
rcf for 3 min and resuspended in 4 mL growth medium. Then all infected cells were added to
Vero E6 cells that had been seeded at 2 × 105 cells per mL, 20mL total, 18–20 h earlier in a
T75 flask for cell-to-cell infection. The coculture of ACE2-expressing H1299-E3 and Vero E6
cells was incubated for 1 h and the flask was filled with 20 mL of complete growth medium
and incubated for 4 days. The viral supernatant from this culture (passage 2 (P2) stock) wasused for experiments.
Live virus neutralization assay
H1299-E3 cells were plated in a 96-well plate (Corning) at 30,000 cells per well 1 day preinfection. Plasma was separated from EDTA-anticoagulated blood by centrifugation at 500 rcf
for 10 min and stored at −80 °C. Aliquots of plasma samples were heat-inactivated at 56 °C
for 30 min and clarified by centrifugation at 10,000 rcf for 5 min. Virus stocks were used at
approximately 50-100 focus-forming units per microwell and added to diluted plasma.

Antibody–virus mixtures were incubated for 1 h at 37 °C, 5% CO2. Cells were infected with
100 μL of the virus–antibody mixtures for 1 h, then 100 μL of a 1X RPMI 1640 (Sigma-Aldrich,
R6504), 1.5% carboxymethylcellulose (Sigma-Aldrich, C4888) overlay was added without
removing the inoculum. Cells were fixed 18 h post-infection using 4% PFA (Sigma-Aldrich) for
20 min. Foci were stained with a rabbit anti-spike monoclonal antibody (BS-R2B12, GenScript
A02058) at 0.5 μg/mL in a permeabilization buffer containing 0.1% saponin (Sigma-Aldrich),
0.1% BSA (Sigma-Aldrich) and 0.05% Tween-20 (Sigma-Aldrich) in PBS. Plates wereincubated with primary antibody overnight at 4 °C, then washed with wash buffer containing
0.05% Tween-20 in PBS. Secondary goat anti-rabbit HRP conjugated antibody (Abcam
ab205718) was added at 1 μg/mL and incubated for 2 h at room temperature with shaking.
TrueBlue peroxidase substrate (SeraCare 5510-0030) was then added at 50 μL per well andincubated for 20 min at room temperature. Plates were imaged in an ImmunoSpot Ultra-V S602-6140 Analyzer ELISPOT instrument with BioSpot Professional built-in image analysis(C.T.L).
Statistics and fitting
All statistics and fitting were performed using custom code in MATLAB v.2019b. Neutralization
data were fit to:
Tx=1/1+(D/ID50).
Here Tx is the number of foci normalized to the number of foci in the absence of plasma on
the same plate at dilution D and ID50 is the plasma dilution giving 50% neutralization. FRNT50= 1/ID50. Values of FRNT50 <1 are set to 1 (undiluted), the lowest measurable value. We notethat the most concentrated plasma dilution was 1:25 and therefore FRNT50 < 25 wereextrapolated. To calculate confidence intervals, FRNT50 or fold-change in FRNT50 per
participant was log transformed and arithmetic mean plus 2 std and arithmetic mean minus 2
std were calculated for the log transformed values. These were exponentiated to obtain theupper and lower 95% confidence intervals on the geometric mean FRNT 50 or the fold-change
in FRNT50 geometric means.
Acknowledgements
This study was supported by the Bill and Melinda Gates award INV-018944 (AS), National
Institutes of Health award R01 AI138546 (AS), and South African Medical Research Council
Award 6084COAP2020 (AS). The funders had no role in study design, data collection andanalysis, decision to publish, or preparation of the manuscript.

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COMMIT-KZN Team
Rohen Harrichandparsad24, Kobus Herbst1,25, Prakash Jeena26, Thandeka Khoza1, Henrik
Kløverpris1,27, Alasdair Leslie1,11, Rajhmun Madansein28, Nombulelo Magula29, Nithendra
Manickchund13, Mohlopheni Marakalala1,11, Matilda Mazibuko1, Mosa Moshabela30,
Ntombifuthi Mthabela1, Kogie Naidoo8, Zaza Ndhlovu1, 31, Thumbi Ndung’u1,16,31,32, NokuthulaNgcobo1, Kennedy Nyamande33, Vinod Patel34, Theresa Smit1, Adrie Steyn1,35 & Emily
Wong1,35.
24Department of Neurosurgery, University of KwaZulu-Natal, Durban, South Africa. 25South

African Population Research Infrastructure Network, Durban, South Africa. 26Department ofPaediatrics and Child Health, University of KwaZulu-Natal, Durban, South Africa.
27Department of Immunology and Microbiology, University of Copenhagen, Copenhagen,Denmark. 28Department of Cardiothoracic Surgery, University of KwaZulu-Natal, Durban,
South Africa. 29Department of Medicine, King Edward VIII Hospital and University of KwaZulu
Natal, Durban, South Africa.30College of Health Sciences, University of KwaZulu-Natal,
Durban, South Africa. 31Ragon Institute of MGH, MIT and Harvard, Boston, USA. 32HIV
Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZuluNatal, Durban, South Africa. 33Department of Pulmonology and Critical Care, University of
KwaZulu-Natal, Durban, South Africa. 34Department of Neurology, University of KwaZuluNatal, Durban, South Africa.35Division of Infectious Diseases, University of Alabama at
Birmingham, USA.

All participants infected in BA.1 infection wave in South Africa
VaccinatedUnvaccinatedBA.1 vs.BA.4 virusbBA.1 vs. BA.5 virus

FRNT50

a

BA.1

BA.4

BA.1

BA.5

BA.1

BA.5

d

FRNT50

c

BA.1

BA.4

e

**

**

BA.1

BA.5

BA.4

FRNT50*Figure 1: Escape of BA.4 and BA.5 from Omicron/BA.1 elicited immunity. Neutralization of BA.4(a) or BA.5 (b) compared to BA.1 virus by immunity elicited through BA.1 infection in n=24 unvaccinatedparticipants. Neutralization of BA.4 (c) or BA.5 (d) compared to BA.1 virus by immunity elicited throughBA.1 infection in n=15 participants vaccinated either with Pfizer BNT162b2 (n=8) or Johnson and Johnson
Ad26.CoV2.S (n=7). Numbers are geometric mean titer (GMT) FRNT50 . Dashed line is most concentrated
plasma tested. (e) Neutralization of BA.1, BA.4, and BA.5 in the n=15 Omicron/BA.1 infected vaccinatedcompared to the n=24 Omicron/BA.1 infected unvaccinated participants. Numbers are GMT FRNT50 and error
bars are GMT 95% confidence intervals. Data is from 2 (BA.4, BA.5) or 3 (BA.1) independent experiments
done on different days. p-values were determined by a two-sided Wilcoxon rank sum test and represented as*0.05-0.01, **0.01-0.001.

Table S1: Summary of participant details

Age
FemaleVaccination to symptom onset (days)
Symptom onset to collection (days)
Required supp. O2
Hospitalized
Duration of hospitalization (days)

All
39

Vaccinated
15 (38%)

Unvaccinated
24 (62%)35 (27-55)
25 (64%)23 (19-27)
7 (18%)
27 (69%)7 (3-11)37 (32-60)
9 (60%)
135 (111-195)
23 (18-27)
2 (13%)
8 (53%)
3.5 (2.5-14.5)

31.5 (26-49)
16 (67%)23 (20-28)
5 (21%)
19 (79%)8 (3-11)

Table S2: Participant characteristics and vaccination status
Date of
Symp. to sample
SubSupp.
#
Age
Sex
Vacc. type
vacc.
Date symp. onset(days)
lineage
Seq. GISAID ID
O2
Hosp.
1
30-39
M
AD26.COV2
MAR-2021
DEC-2021
23
BA.1
EPI_ISL_9967759
No
No
2
30-39
M
AD26.COV2*
NOV-2021
NOV-2021
22
BA.1
EPI_ISL_9967761
No
No
3
50-59
F
BNT162b2
JUL-2021
DEC-202127
BA.1
EPI_ISL_8604915
No
No
4
30-39
F
AD26.COV2
MAY-2021
DEC-2021
13
BA.1
EPI_ISL_8604910
No
No
5
20-29
F
AD26.COV2
SEP-2021
DEC-202127
BA.1
EPI_ISL_9967760
No
Yes
6
10-19
F
BNT162b2
JUL-2021
DEC-2021
12
BA.1
EPI_ISL_8604906
No
Yes
7
20-29
F
NOV-2021
24
N/A
N/A
No
Yes
8
30-39
M
DEC-2021
23
BA.1
EPI_ISL_8604919
No
Yes
9
40-49
F
DEC-202128
BA.1
EPI_ISL_8604901
No
Yes
10 20-29
M
DEC-2021
13
BA.1
EPI_ISL_8604908
No
Yes
11 20-29
F
DEC-2021
22
BA.1
EPI_ISL_8604913
NoNo
12 20-29
F
DEC-2021
22
BA.1
EPI_ISL_8604912
NoYes
13 30-39
M
BNT162b2
JUL-2021
NOV-202128
BA.1
EPI_ISL_8604916
NoYes
14 20-29
M
NOV-2021
15
N/A
N/A
No
Yes
15 60-69
F
BNT162b2
JUL-2021
DEC-202125
BA.1
EPI_ISL_8604920
NoYes
16 60-69
M
BNT162b2
DEC-2021
DEC-2021
10
BA.1
EPI_ISL_8578311
NoNo
17 30-39
M
DEC-2021
19
BA.1
EPI_ISL_8604923
NoNo
18 60-69
F
DEC-2021
23
BA.1
EPI_ISL_8578312
Yes
Yes
19 30-39
M
DEC-202127
BA.1
EPI_ISL_8604924
NoYes
20 20-29
F
DEC-2021
24
BA.1
EPI_ISL_8604911
NoYes
21 20-29
M
DEC-2021
21
BA.1
EPI_ISL_8604922
NoNo
22 30-39
F
AD26.COV2
AUG-2021
DEC-2021
23
BA.1
EPI_ISL_8693907
No
Yes
23 20-29
F
DEC-2021
10
BA.1
EPI_ISL_8604902
NoNo
24 50-59
M
BNT162b2
AUG-2021
DEC-2021
18
N/A
N/A
No
Yes
25 30-39
F
AD26.COV2
APR-2021
DEC-2021
24
BA.1
EPI_ISL_8604914
NoNo
26 50-59
F
AD26.COV2
JUL-2021
DEC-2021
23
N/A
N/A
No
No
27 50-59
F
DEC-2021
28
N/A
N/A
Yes
Yes
28 80-89
F
BNT162b2
JUL-2021
JAN-2022
22
N/A
N/A
Yes
Yes
29 60-69
M
BNT162b2
JUL-2021
DEC-2021
32
N/A
N/A
Yes
Yes
30 40-49
M
DEC-2021
13
BA.1
EPI_ISL_8604909
NoNo
31 30-39
F
DEC-2021
22
N/A
N/A
Yes
Yes
32 50-59
F
DEC-2021
36
BA.1
EPI_ISL_8578347
NoYes
33 20-29
F
DEC-2021
18
N/A
N/A
No
Yes
34 30-39
F
DEC-2021
30
N/A
N/A
No
Yes
35 50-59
F
DEC-202127
BA.1
EPI_ISL_8578342
Yes
Yes
36 20-29
F
DEC-2021
23
N/A
N/A
No
Yes
37 50-59
F
DEC-2021
30
N/A
N/A
No
Yes
38 30-39
M
DEC-2021
31
N/A
N/A
No
Yes
39 50-59
F
DEC-2021
30
N/A
N/A
Yes
Yes
Symp. Symptoms date. Supp O2: participant required supplemental oxygen during the study. Hosp.: participant hospitalized during the study. N/A: Not available;sequencing failed, usually due to insufficient virus substrate. *Boosted with Ad26.CoV2.S in Nov-2021.