Omicron variant BA.1, BA.5, BQ.1.1, and XBB.1.5 Neutralizing Antibodies Following BNT162b2 BA.4/5 versus mRNA-1273 BA.1 Bivalent Vaccination

doi:10.21203/rs.3.rs-2846541/v1

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Omicron variant BA.1, BA.5, BQ.1.1, and XBB.1.5 Neutralizing Antibodies Following BNT162b2 BA.4/5 versus mRNA-1273 BA.1 Bivalent Vaccination

https://doi.org/10.21203/rs.3.rs-2846541/v1

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Neutralization of Omicron subvariants by different bivalent vaccines have not been well evaluated. This study characterized neutralization against Omicron subvariants in 98 individuals receiving dialysis or with a kidney transplant receiving the BNT162b2 (BA.4/BA.5) or mRNA-1273 (BA.1) bivalent COVID-19 vaccine. Neutralization against Omicron BA.1, BA.5, BQ.1.1, and XBB.1.5 increased by 8-fold one month following bivalent vaccination. In comparison to wild-type (D614G), neutralizing antibodies against Omicron-specific variants were 7.3-fold lower against BA.1, 8.3-fold lower against BA.5, 45.8-fold lower against BQ.1.1, and 48.2-fold lower against XBB.1.5. Viral neutralization was not significantly different by bivalent vaccine type for wild-type (D614G) (P=0.48), BA.1 (P=0.21), BA.5 (P=0.07), BQ.1.1 (P=0.10), nor XBB.1.5 (P=0.10). Hybrid immunity conferred higher neutralizing antibodies against all Omicron subvariants. Given that both BNT162b2 (BA.4/BA.5) and mRNA-1273 (BA.1) induced similar neutralization against all Omicron subvariants, this suggests that bivalent vaccines confer protection even when they are antigenically divergent from the circulating variant.

Health sciences/Diseases/Infectious diseases/Viral infection

Health sciences/Diseases/Kidney diseases

COVID-19

Serology

Vaccine

Chronic Kidney Disease

Dialysis

Bivalent

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes Coronavirus Disease 2019 (COVID-19), has undergone continuous evolution leading to the emergence of novel variants of concern with high rates of breakthrough infections. Therefore, bivalent vaccines targeting the ancestral wild-type (D614G) spike and B.1.1.529 (Omicron) subvariants were approved for use.^1-3 Chronic kidney disease is a major risk factor for severe COVID-19⁴ and those receiving hemodialysis are at increased risk for exposure to SARS-CoV-2.⁵ Although patients with chronic kidney disease demonstrate robust antibody response to third-dose vaccination, new Omicron subvariants including BQ.1.1 and XBB.1.5 demonstrate immune-evasive potential.^6,7 Therefore, we evaluated the neutralizing antibody response to Omicron subvariants following bivalent COVID-19 vaccination in 98 patients receiving hemodialysis and kidney transplant recipients. Given that the mRNA-1273 bivalent vaccine targets BA.1 while BNT162b2 targets BA.4/5, we examined differences in neutralizing antibody levels against BA.1, BA.5, BQ.1.1, and XBB.1.5 induced by the different bivalent vaccines using a spiked-pseudotyped lentiviral neutralization assay.

Baseline characteristics of the 98 participants stratified by bivalent vaccine type were well balanced (Extended Data Table 1). Median age was 69 years and 34% were female. The bivalent COVID-19 vaccine was the fifth overall dose in 92%, with 73% (72/98) receiving mRNA-1273 while 27% (26/98) received BNT162b2.

In samples taken prior to receipt of the bivalent vaccine, the median time from the most recent COVID-19 vaccine dose was 236 days (interquartile [IQR] 189–290). Following receipt of the bivalent vaccine dose, serum samples were taken at a median of 25 days (IQR 24–27). Among participants, 26% (25/98) had prior confirmed COVID-19, as determined by RT-PCR or rapid antigen testing, while 41% (40/98) had a positive anti-nucleocapsid antibody before bivalent vaccination.

Neutralizing antibodies increased a median of 4.5-fold (IQR 11.5) for wild-type, 8.8-fold (IQR 41.0) for BA.1, 7.8-fold (IQR 53) for BA.5, 8.5-fold for BQ.1.1 (IQR 66.2), and 8.1-fold (IQR 194) for XBB.1.5 following bivalent vaccination. The proportion of patients with detectable neutralization increased significantly from baseline to one-month post-vaccination for all subvariants (p<0.001 for all): wild-type: 95% to 99%, BA.1: 76% to 93%, BA.5: 74% to 96%, BQ.1.1: 55% to 84%, XBB.1.5: 48% to 81% (Fig 1; Extended Data Fig. 1 and Table 2). Compared to the wild-type strain, median neutralizing antibody levels were attenuated by 7.3-fold for BA.1 (IQR 17.5), 8.3-fold for BA.5 (IQR 19.2), 45.8-fold for BQ.1.1 (IQR 170.3), and 48.2-fold (IQR 376.7) against XBB.1.5 (Extended Data Table 3).

While absolute neutralizing antibody levels were higher among those receiving the BNT162b2 vaccine, one month following bivalent vaccination, these differences were not statistically different by vaccine type for wild-type (P=0.48), BA.1 (P=0.21), BA.5 (P=0.069), BQ.1.1 (P=0.10), or XBB.1.5 (P=0.099) subvariants after adjustment for pre-specified covariates (Fig 2a; Extended Data Fig. 2 and Table 4).

There was no significant difference in neutralizing antibodies against any subvariant when comparing participants who had received the bivalent vaccine as the fourth dose (n=8) versus the fifth dose (n=90) (Extended Data Fig. 3 and Table 5).

We observed that participants with prior COVID-19 as determined by rapid antigen testing or RT-PCR, had higher absolute neutralizing antibody titers against all variants of concern following bivalent vaccination in comparison to those without prior COVID-19, although this was only statistically higher for BA.5 (P=0.023), BQ.1.1 (P=0.0017), and XBB.1.5 (P=0.049) (Extended Data Table 6). When we determined prior COVID-19 infection instead by positive anti-nucleocapsid antibody rather than clinical infection to detect asymptomatic COVID-19, Omicron-specific neutralizing antibodies were significantly higher among those with a positive anti-nucleocapsid antibody against wild-type (P=0.047), BA.1 (P=0.0048), BA.5 (P=0.029), BQ.1.1 (P=0.018), and XBB.1.5 (P=0.014) (Fig. 2b).

One month following bivalent vaccination, kidney transplant recipients (n=15) had significantly lower absolute neutralizing antibody levels than hemodialysis patients (n=83) against BA.1 (P=0.044), BQ.1.1 (P=0.015), and XBB.1.5 (P=0.025), but not wild-type (P=0.42) or BA.5 (P=0.063) (Fig. 2C). Increases in neutralizing antibody levels from baseline were significantly lower in kidney transplant recipients than hemodialysis for wild-type (p<0.001), BA.1 (P=0.008), BA.5 (P=0.010), BQ.1.1 (P=0.030) and XBB.1.5 (P=0.010) (Extended Data Table 7).

Following bivalent vaccination, binding IgG antibodies for anti-spike increased from 1.16 (IQR 0.77, 1.65) to 1.76 (IQR 1.52,1.86) 1-month post-vaccination and anti-RBD increased from 0.45 (IQR 0.18, 0.97) to 1.24 (IQR 0.80, 1.53) 1-month post-vaccination (p<0.0001 for both) (Extended Data Fig. 4).

In this study of patients with kidney disease receiving bivalent COVID-19 vaccines, we found that neutralizing antibody response against Omicron subvariants increased approximately eight-fold following vaccination. However, concerns have emerged regarding immune escape with newer Omicron subvariants.^8,9 Consistent with this, we observed a 46-fold decrease in viral neutralization against BQ.1.1 and 48-fold decrease against XBB.1.5 in comparison to wild-type. Consistent with other reports, we found that hybrid immunity enhanced neutralizing antibody response.¹⁰ In addition, while BNT162b2 elicited higher absolute neutralizing antibodies in comparison to mRNA-1273 against all Omicron subvariants, these differences were not statistically significant after accounting for confounders including prior COVID-19, number of vaccine doses, and patient type. Given that XBB.1.5 is presently the dominant circulating Omicron subvariant worldwide, this suggests that boosters targeting earlier subvariants may provide similar protection. Our results are consistent with a case series of dialysis patients, where bivalent vaccination increased anti-spike IgG 2.5 fold which correlated with BA.4/5 neutralization.¹¹

Other studies have found not found a higher peak neutralizing antibody response with bivalent vaccines in comparison to monovalent vaccines, and suggested a role for immunologic imprinting wherein prior antigenic exposure primes B cell memory and limits the development of memory B cells and neutralizing antibodies against newer subvariants.^8,12 Kidney transplant recipients generally had both lower increases and absolute lower neutralizing antibodies levels post-vaccination which is unsurprising given that transplant recipients are known to have attenuated humoral response to COVID-19 vaccination.¹³ The number of prior vaccine doses (4 versus 5) did not meaningfully influence neutralizing antibody levels both prior to and following bivalent vaccination.

Strengths of this study include that it is the first to compare neutralizing antibody response against current circulating Omicron subvariants with bivalent vaccines targeting BA.1 versus BA.4/5. We had anti-nucleocapsid serology and clinical information available on all participants, allowing us to account for multiple factors including prior COVID-19 in our analysis.

This study does have limitations. We did not evaluate cellular immunity, although prior studies have suggested that spike-specific CD8 + and CD4 + T-cell response increased only modestly after bivalent mRNA boosting.¹⁴ In addition, while neutralizing antibody levels correlate with vaccine effectiveness,^15,16 the clinical implications of these findings on preventing COVID-19 require confirmation at a population-level, and there is evidence that bivalent vaccine effectiveness declines after one month.¹⁷ Finally, we were not able to evaluate the mRNA-1273 BA.4/5 bivalent vaccine as it was not approved in our jurisdiction during the study period.

In conclusion, we found that bivalent vaccines increased neutralizing antibodies against Omicron subvariants, although neutralizing antibody titers were significantly attenuated against BQ.1.1 and XBB.1.5. We found that both BNT162b2 and mRNA-1273 bivalent vaccines elicited a similar neutralizing antibody response against Omicron subvariants including BQ.1.1 and XBB.1.5, suggesting that variant modified bivalent vaccines may confer protection against emerging circulating Omicron subvariants despite antigenic divergence.

This was a prospective observational cohort study involving individuals age ≥ 18 receiving hemodialysis or with a kidney transplant receiving the mRNA-1273 bivalent vaccine (Original and Omicron BA.1) or BNT162b2 bivalent vaccine (Original and Omicron BA.4/BA.5). The study was conducted between July 25, 2022 and November 30, 2022. The protocol for this study has been published previously. ¹⁸ Only participants unable to provide informed consent due to cognitive impairment or a language barrier if a translator was unavailable were excluded. Demographics, vaccination status, comorbidities, and medications were obtained from electronic patient records. Serum samples were taken prior to and one month following bivalent vaccination to evaluate neutralizing antibody levels against Omicron subvariants. Serum samples were collected in a serum separator tube and allowed to clot for 30 minutes and centrifuged for 10 minutes at 3000 × g at room temperature. Levels of binding IgG antibodies to each of the antigens (produced by the National Research Council of Canada) were normalized to reference standards included on each plate and expressed as relative ratios or World Health Organization International Standard units (BAU/mL).

Spiked-Pseudotyped Lentiviral Neutralization

The spiked-pseudotyped lentiviral neutralization assay was performed in HEK293T-ACE2/TMPRSS2 cells was performed as described previously.¹³ Lentiviral virus-like particles were generated from co-transfection of the viral packaging (psPAX2, Addgene, #12260), the ZsGreen and luciferase reporter construct (pHAGE-CMV-Luc2-IRES-ZsGreen-W, provided by Jesse Bloom), and the spike protein constructs: wild-type (D614G), Omicron BA.1, BA.5, BQ.1.1, XBB.1.5 subvariants available at http://nbcc.lunenfeld.ca/resources), into HEK293TN cells (System Biosciences [LV900A-1]). To construct HDM_XBB.1.5, a human codon-optimized cDNA encoding the XBB.1 spike variant (Twist Bioscience) was first inserted into the mammalian expression plasmid HDM (a gift from Jesse Bloom), and modified to include the F486P mutation starting from the cDNA fragment encoding the XBB.1.5 RBD. Viral supernatants were harvested, clarified, and filtered through 0.45-µm filters prior to storage at -80°C. A viral titer assay was performed by infecting HEK293T-ACE2/TMPRSS2 cells, followed by a luciferase assay to determine the relative luciferase unit (1:10 to 1:250 dilution of virus stock, depending on the virus titers of each variant). For the neutralization assay, diluted patient sera samples (1:22.5) were prepared and serially diluted by 3-fold over 7 dilutions, followed by incubation with diluted pseudovirus for 1 hour at 37°C prior to addition to HEK293T-ACE2/TMPRSS2 cells. Cells were lysed 48-hours post infections using the Bright-Glo Luciferase Assay System (Promega), and the luminescence signals were detected using a PerkinElmer EnVision instrument. HEK293TN and HEK293T-ACE2/TMPRSS2 cells are maintained at 85% confluency for no more than 25 passages. The inhibitory dilution with 50% virus neutralization (ID50) was calculated in GraphPad Prism version 9.5.0 using a nonlinear regression algorithm (log[inhibitor] versus normalized response - variable slope). In patients with an absence of 50% neutralization with undiluted serum, a log₁₀ ID₅₀ of zero was considered the threshold for detectable viral neutralization.

SARS-CoV-2 Binding IgG Antibodies

Binding IgG antibodies against the full-length spike protein (anti-spike), its receptor binding domain (anti-RBD), and anti-nucleocapsid antibodies were measured on an automated enzyme-linked immunosorbent assay platform described previously.¹⁹ Binding antibody levels were reported as relative ratios to a synthetic standard included as a calibration curve on each assay plate. Thresholds for binding antibody seroconversion were determined by aggregating data from negative controls and calculating the mean + 3 standard deviations (SD) and were measured at a 1:160 (0.0625µL/well) dilution. Seroconversion thresholds were 0.186, 0.19, and 0.164 for anti-RBD, anti-spike, and anti-nucleocapsid antibodies, respectively.

Statistical Analysis

Descriptive statistics were used to describe baseline characteristics. Neutralizing antibodies were analyzed through linear mixed-effects models with random intercepts and fixed covariates adjusting for vaccine time point, bivalent vaccine type, number of COVID-19 vaccine doses (four versus five), kidney transplant recipients versus dialysis patients, and anti-nucleocapsid antibody status. With two-sided testing, P = 0.05 was considered statistically significant. We performed all analyses using R version 4.0.5 (R Project for Statistical Computing).

Ethics Statement

This study was approved by the respective Institutional Review Boards at Sunnybrook Health Sciences Centre, Unity Health Toronto, and Michael Garron Hospital.

Disclosures:

Adeera Levin reports being a scientific advisor to, or member of, AstraZeneca, Bayer, Boehringer-Ingelheim, Canadian Journal of Kidney Health and Disease, Canadian Institutes of Health Research, Certa, Chinook Therapeutics, Johnson and Johnson, Kidney Foundation of Canada, National Institutes of Health (NIH), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Otsuka, Reata, Retrophin, and The George Institute; receiving research funding from AstraZeneca, Boehringer-Ingelheim, Canadian Institute of Health Research, Janssen, Johnson and Johnson, Kidney Foundation of Canada, Merck, NIDDK, NIH, Ortho Biotech, Otsuka, and Oxford Clinical Trials; and having consultancy agreements with Amgen, AstraZeneca, Bayer, Boehringer-Ingelheim, Johnson and Johnson/Jansen, Reata, and Retrophin (unrelated to the submitted work). Darren Yuen reports being a scientific co-founder and consultant for Fibrocor Therapeutics; receiving speaking honoraria and/or consultancy fees from AstraZeneca, GlaxoSmithKline, and Vivace Therapeutics (unrelated to the submitted work). Jeffrey Perl reported receiving speaking honoraria and consultancy fees from Baxter Healthcare; grants from Agency for Healthcare Research and Quality grant support; speaking honoraria from Fresenius Medical Care, AstraZeneca, Davita Healthcare, and US Renal Care; and consultancy fees from LiberDi Dialysis (unrelated to the submitted work). Jerome Leis has received payment for expert testimony upon request of hospitals of the Ontario Hospital Association, Ministry of Attorney General of Ontario, and Seneca College (unrelated to the submitted work). Anne-Claude Gingras has received research funds from a research contract with Providence Therapeutics Holdings, Inc for other projects, participated in the COVID-19 Immunity Task Force Immune Science and Testing working party, chaired the CIHR Institute of Genetics Advisory Board, and chairs the SAB of the National Research Council of Canada Human Health Therapeutics Board. Matthew Oliver and Michelle Hladunewich are contracted Medical Leads at the Ontario Renal Network, Ontario Health. Matthew Oliver is owner of Oliver Medical Management Inc., which licenses Dialysis Management Analysis and Reporting System software. He has received honoraria for speaking from Baxter Healthcare (unrelated to the submitted work). Michelle Hladunewich reports receiving grants from Pfizer for a study in focal segmental glomerulosclerosis, Ionis, Calliditas and Chinook for studies in Immunoglobulin A nephropathy, and Roche for a preeclampsia study (unrelated to the submitted work). No other competing interests were declared.

Acknowledgements

This study is supported by the COVID-19 Immunity Task Force grant 2122-HQ-000071 to A.L., M.J.O, and M.H which is funded by the Government of Canada. The Canadian Institutes of Health Research supports lentivirus assay development through CoVaRR-Net (Coronavirus Variants Rapid Response Network). The equipment used is housed in the Network Biology Collaborative Centre at the Lunenfeld-Tanenbaum Research Institute, a facility supported by Canada Foundation for Innovation funding (grant CFI 33474), by the Ontario Government, Genome Canada, and Ontario Genomics (OGI-139). K.Y. is supported by the University of Toronto Department of Medicine Eliot Phillipson Clinician Scientist Training Program, Banting and Best Diabetes Centre Postdoctoral Fellowship, and KRESCENT Postdoctoral Fellowship. The KRESCENT program is co-sponsored by the Kidney Foundation of Canada, the Canadian Society of Nephrology, and the Canadian Institute of Health Research. D.A.Y. is supported by a Canada Research Chair, Tier 2, in Fibrotic Injury. A.C.G. is supported by the Canadian Institutes of Health Research (FDN 143301) and a Canada Research Chair, Tier 1, in Functional Proteomics and is a pillar lead for CoVaRR-Net. The antibody measurements and initial data analysis were performed by Bhavisha Rathod, Geneviève Mailhot, Mahya Fazel-Zarandi, Jenny Wang, Kento Abe and Adrian Pasculescu. We would like to thank Gail Klein and Mandana Rahimi for valuable assistance in coordinating this study.

Author Contributions

K.Y., Q.H., A.C.G. and M.H. designed the study. A.K, F.Q., Q.H. performed the data extraction, curation and analysis. K.Y, A.K., F.Q., Q.H. and Y.J. performed the data analysis. K.Y. and M.H. wrote the first draft of the manuscript. All authors contributed to the writing and reviewed and approved the final report.

Data Sharing Statement

All or portions of the de-identified data are available upon reasonable request to the corresponding author, Michelle Hladunewich.

ORCID

Kevin Yau https://orcid.org/0000-0001-8653-6778

Darren Yuen https://orcid.org/0000-0002-0054-6607

Anne-Claude Gingras https://orcid.org/0000-0002-6090-4437

Michelle Hladunewich https://orcid.org/ 0000-0001-9227-4292

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Yes there is potential Competing Interest. Adeera Levin reports being a scientific advisor to, or member of, AstraZeneca, Bayer, Boehringer-Ingelheim, Canadian Journal of Kidney Health and Disease, Canadian Institutes of Health Research, Certa, Chinook Therapeutics, Johnson and Johnson, Kidney Foundation of Canada, National Institutes of Health (NIH), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Otsuka, Reata, Retrophin, and The George Institute; receiving research funding from AstraZeneca, Boehringer-Ingelheim, Canadian Institute of Health Research, Janssen, Johnson and Johnson, Kidney Foundation of Canada, Merck, NIDDK, NIH, Ortho Biotech, Otsuka, and Oxford Clinical Trials; and having consultancy agreements with Amgen, AstraZeneca, Bayer, Boehringer-Ingelheim, Johnson and Johnson/Jansen, Reata, and Retrophin (unrelated to the submitted work). Darren Yuen reports being a scientific co-founder and consultant for Fibrocor Therapeutics; receiving speaking honoraria and/or consultancy fees from AstraZeneca, GlaxoSmithKline, and Vivace Therapeutics (unrelated to the submitted work). Jeffrey Perl reported receiving speaking honoraria and consultancy fees from Baxter Healthcare; grants from Agency for Healthcare Research and Quality grant support; speaking honoraria from Fresenius Medical Care, AstraZeneca, Davita Healthcare, and US Renal Care; and consultancy fees from LiberDi Dialysis (unrelated to the submitted work). Jerome Leis has received payment for expert testimony upon request of hospitals of the Ontario Hospital Association, Ministry of Attorney General of Ontario, and Seneca College (unrelated to the submitted work). Anne-Claude Gingras has received research funds from a research contract with Providence Therapeutics Holdings, Inc for other projects, participated in the COVID-19 Immunity Task Force Immune Science and Testing working party, chaired the CIHR Institute of Genetics Advisory Board, and chairs the SAB of the National Research Council of Canada Human Health Therapeutics Board. Matthew Oliver and Michelle Hladunewich are contracted Medical Leads at the Ontario Renal Network, Ontario Health. Matthew Oliver is owner of Oliver Medical Management Inc., which licenses Dialysis Management Analysis and Reporting System software. He has received honoraria for speaking from Baxter Healthcare (unrelated to the submitted work). Michelle Hladunewich reports receiving grants from Pfizer for a study in focal segmental glomerulosclerosis, Ionis, Calliditas and Chinook for studies in Immunoglobulin A nephropathy, and Roche for a preeclampsia study (unrelated to the submitted work). No other competing interests were declared.

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Omicron variant BA.1, BA.5, BQ.1.1, and XBB.1.5 Neutralizing Antibodies Following BNT162b2 BA.4/5 versus mRNA-1273 BA.1 Bivalent Vaccination

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Abstract

Figures

Introduction

Discussion

Methods

Spiked-Pseudotyped Lentiviral Neutralization

SARS-CoV-2 Binding IgG Antibodies

Statistical Analysis

Ethics Statement

Declarations

References

Additional Declarations

Supplementary Files

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