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Immune boosting by B.1.1.529 (Omicron) depends on previous SARS-CoV-2 exposure.

ABSTRACT: The Omicron, or Pango lineage B.1.1.529, variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) carries multiple spike mutations with high transmissibility and partial neutralizing antibody (nAb) escape. Vaccinated individuals show protection against severe disease, often attributed to primed cellular immunity. We investigated T and B cell immunity against B.1.1.529 in triple BioNTech BNT162b2 messenger RNA-vaccinated health care workers (HCWs) with different SARS-CoV-2 infection histories. B and T cell immunity against previous variants of concern was enhanced in triple-vaccinated individuals, but the magnitude of T and B cell responses against B.1.1.529 spike protein was reduced. Immune imprinting by infection with the earlier B.1.1.7 (Alpha) variant resulted in less durable binding antibody against B.1.1.529. Previously infection-naïve HCWs who became infected during the B.1.1.529 wave showed enhanced immunity against earlier variants but reduced nAb potency and T cell responses against B.1.1.529 itself. Previous Wuhan Hu-1 infection abrogated T cell recognition and any enhanced cross-reactive neutralizing immunity on infection with B.1.1.529.

SUBMITTER: Reynolds CJ

PROVIDER: S-EPMC9210451 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature

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Immune boosting by B.1.1.529 <b>(</b>Omicron) depends on previous SARS-CoV-2 exposure.

Reynolds Catherine J CJ Pade Corinna C Gibbons Joseph M JM Otter Ashley D AD Lin Kai-Min KM Muñoz Sandoval Diana D Pieper Franziska P FP Butler David K DK Liu Siyi S Joy George G Forooghi Nasim N Treibel Thomas A TA Manisty Charlotte C Moon James C JC Semper Amanda A Brooks Tim T McKnight Áine Á Altmann Daniel M DM Boyton Rosemary J RJ Abbass Hakam H Abiodun Aderonke A Alfarih Mashael M Alldis Zoe Z Altmann Daniel M DM Amin Oliver E OE Andiapen Mervyn M Artico Jessica J Augusto João B JB Baca Georgina L GL Bailey Sasha N L SNL Bhuva Anish N AN Boulter Alex A Bowles Ruth R Boyton Rosemary J RJ Bracken Olivia V OV O'Brien Ben B Brooks Tim T Bullock Natalie N Butler David K DK Captur Gabriella G Carr Olivia O Champion Nicola N Chan Carmen C Chandran Aneesh A Coleman Tom T Couto de Sousa Jorge J Couto-Parada Xose X Cross Eleanor E Cutino-Moguel Teresa T D'Arcangelo Silvia S Davies Rhodri H RH Douglas Brooke B Di Genova Cecilia C Dieobi-Anene Keenan K Diniz Mariana O MO Ellis Anaya A Feehan Karen K Finlay Malcolm M Fontana Marianna M Forooghi Nasim N Francis Sasha S Gibbons Joseph M JM Gillespie David D Gilroy Derek D Hamblin Matt M Harker Gabrielle G Hemingway Georgia G Hewson Jacqueline J Heywood Wendy W Hickling Lauren M LM Hicks Bethany B Hingorani Aroon D AD Howes Lee L Itua Ivie I Jardim Victor V Lee Wing-Yiu Jason WJ Jensen Melaniepetra M Jones Jessica J Jones Meleri M Joy George G Kapil Vikas V Kelly Caoimhe C Kurdi Hibba H Lambourne Jonathan J Lin Kai-Min KM Liu Siyi S Lloyd Aaron A Louth Sarah S Maini Mala K MK Mandadapu Vineela V Manisty Charlotte C McKnight Áine Á Menacho Katia K Mfuko Celina C Mills Kevin K Millward Sebastian S Mitchelmore Oliver O Moon Christopher C Moon James J Muñoz Sandoval Diana D Murray Sam M SM Noursadeghi Mahdad M Otter Ashley A Pade Corinna C Palma Susana S Parker Ruth R Patel Kush K Pawarova Mihaela M Petersen Steffen E SE Piniera Brian B Pieper Franziska P FP Rannigan Lisa L Rapala Alicja A Reynolds Catherine J CJ Richards Amy A Robathan Matthew M Rosenheim Joshua J Rowe Cathy C Royds Matthew M Sackville West Jane J Sambile Genine G Schmidt Nathalie M NM Selman Hannah H Semper Amanda A Seraphim Andreas A Simion Mihaela M Smit Angelique A Sugimoto Michelle M Swadling Leo L Taylor Stephen S Temperton Nigel N Thomas Stephen S Thornton George D GD Treibel Thomas A TA Tucker Art A Varghese Ann A Veerapen Jessry J Vijayakumar Mohit M Warner Tim T Welch Sophie S White Hannah H Wodehouse Theresa T Wynne Lucinda L Zahedi Dan D Chain Benjamin B Moon James C JC

Science (New York, N.Y.) 20220715 6603

The Omicron, or Pango lineage B.1.1.529, variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) carries multiple spike mutations with high transmissibility and partial neutralizing antibody (nAb) escape. Vaccinated individuals show protection against severe disease, often attributed to primed cellular immunity. We investigated T and B cell immunity against B.1.1.529 in triple BioNTech BNT162b2 messenger RNA-vaccinated health care workers (HCWs) with different SARS-CoV-2 infectio ...[more]

PMID: 35699621

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Project description:Background & objectivesVaccination and natural infection can both augment the immune responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), but how omicron infection has affected the vaccine-induced and hybrid immunity is not well studied in Indian population. The present study was aimed to assess the durability and change in responses of humoral immunity with age, prior natural infection, vaccine type and duration with a minimum gap of six months post-two doses with either ChAdOx1 nCov-19 or BBV152 prior- and post-emergence of the omicron variant.MethodsA total of 1300 participants were included in this observational study between November 2021 and May 2022. Participants had completed at least six months after vaccination (2 doses) with either ChAdOx1 nCoV-19 or an inactivated whole virus vaccine BBV152. They were grouped according to their age (≤ or ≥60 yr) and prior exposure of SARS-CoV-2 infection. Five hundred and sixteen of these participants were followed up after emergence of the Omicron variant. The main outcome was durability and augmentation of the humoral immune response as determined by anti-receptor-binding domain (RBD) immunoglobulin G (IgG) concentrations, anti-nucleocapsid antibodies and anti-omicron RBD antibodies. Live virus neutralization assay was conducted for neutralizing antibodies against four variants - ancestral, delta and omicron and omicron sublineage BA.5.ResultsBefore the omicron surge, serum anti-RBD IgG antibodies were detected in 87 per cent participants after a median gap of eight months from the second vaccine dose, with a median titre of 114 [interquartile range (IQR) 32, 302] BAU/ml. The levels increased to 594 (252, 1230) BAU/ml post-omicron surge (P<0.001) with 97 per cent participants having detectable antibodies, although only 40 had symptomatic infection during the omicron surge irrespective of vaccine type and previous history of infection. Those with prior natural infection and vaccination had higher anti-RBD IgG titre at baseline, which increased further [352 (IQR 131, 869) to 816 (IQR 383, 2001) BAU/ml] (P<0.001). The antibody levels remained elevated after a mean time gap of 10 months, although there was a decline of 41 per cent. The geometric mean titre was 452.54, 172.80, 83.1 and 76.99 against the ancestral, delta, omicron and omicron BA.5 variants in the live virus neutralization assay.Interpretation & conclusionsAnti-RBD IgG antibodies were detected in 85 per cent of participants after a median gap of eight months following the second vaccine dose. Omicron infection probably resulted in a substantial proportion of asymptomatic infection in the first four months in our study population and boosted the vaccine-induced humoral immune response, which declined but still remained durable over 10 months.

Project description:Recently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variant B.1.1.529 (Omicron) has rapidly become the dominant strain, with an unprecedented number of mutations within its spike gene. However, it remains unknown whether these variants have alterations in their entry efficiency, host tropism, and sensitivity to neutralizing antibodies and entry inhibitors. In this study, we found that Omicron spike has evolved to escape neutralization by three-dose inactivated-vaccine-elicited immunity but remains sensitive to an angiotensin-converting enzyme 2 (ACE2) decoy receptor. Moreover, Omicron spike could use human ACE2 with a slightly increased efficiency while gaining a significantly increased binding affinity for a mouse ACE2 ortholog, which exhibits limited binding with wild-type (WT) spike. Furthermore, Omicron could infect wild-type C57BL/6 mice and cause histopathological changes in the lungs. Collectively, our results reveal that evasion of neutralization by vaccine-elicited antibodies and enhanced human and mouse ACE2 receptor engagement may contribute to the expanded host range and rapid spread of the Omicron variant. IMPORTANCE The recently emerged SARS-CoV-2 Omicron variant with numerous mutations in the spike protein has rapidly become the dominant strain, thereby raising concerns about the effectiveness of vaccines. Here, we found that the Omicron variant exhibits a reduced sensitivity to serum neutralizing activity induced by a three-dose inactivated vaccine but remains sensitive to entry inhibitors or an ACE2-Ig decoy receptor. Compared with the ancestor strain isolated in early 2020, the spike protein of Omicron utilizes the human ACE2 receptor with enhanced efficiency while gaining the ability to utilize mouse ACE2 for cell entry. Moreover, Omicron could infect wild-type mice and cause pathological changes in the lungs. These results reveal that antibody evasion, enhanced human ACE2 utilization, and an expanded host range may contribute to its rapid spread.

Project description:BackgroundThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variants have risen to dominance, which contains far more mutations in the spike protein in comparison to previously reported variants, compromising the efficacy of most existing vaccines or therapeutic monoclonal antibodies. Nanobody screened from high-throughput naïve libraries is a potential candidate for developing preventive and therapeutic antibodies.MethodsFour nanobodies specific to the SARS-CoV-2 wild-type receptor-binding domain (RBD) were screened from a naïve phage display library. Their affinity and neutralizing activity were evaluated by surface plasmon resonance assays, surrogate virus neutralization tests, and pseudovirus neutralization assays. Preliminary identification of the binding epitopes of nanobodies by peptide-based ELISA and competition assay. Then four multivalent nanobodies were engineered by attaching the monovalent nanobodies to an antibody-binding nanoplatform constructed based on the lumazine synthase protein cage nanoparticles isolated from the Aquifex aeolicus (AaLS). Finally, the differences in potency between the monovalent and multivalent nanobodies were compared using the same methods.ResultsThree of the four specific nanobodies could maintain substantial inhibitory activity against the Omicron (B.1.1.529), of them, B-B2 had the best neutralizing activity against the Omicron (B.1.1.529) pseudovirus (IC50 = 1.658 μg/mL). The antiviral ability of multivalent nanobody LS-B-B2 was improved in the Omicron (B.1.1.529) pseudovirus assays (IC50 = 0.653 μg/mL). The results of peptide-based ELISA indicated that LS-B-B2 might react with the linear epitopes in the SARS-CoV-2 RBD conserved regions, which would clarify the mechanisms for the maintenance of potent neutralization of Omicron (B.1.1.529) preliminary.ConclusionOur study indicated that the AaLS could be used as an antibody-binding nanoplatform to present nanobodies on its surface and improve the potency of nanobodies. The multivalent nanobody LS-B-B2 may serve as a potential agent for the neutralization of SARS-CoV-2 variants.

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Immune boosting by B.1.1.529 (Omicron) depends on previous SARS-CoV-2 exposure.

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Immune boosting by B.1.1.529 <b>(</b>Omicron) depends on previous SARS-CoV-2 exposure.

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Immune boosting by B.1.1.529 (Omicron) depends on previous SARS-CoV-2 exposure.

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Immune boosting by B.1.1.529 &lt;b&gt;(&lt;/b&gt;Omicron) depends on previous SARS-CoV-2 exposure.

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Immune boosting by B.1.1.529 <b>(</b>Omicron) depends on previous SARS-CoV-2 exposure.