bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2023.01.05.522845

Poor neutralizing antibody responses against SARS-CoV-2 Omicron BQ.1.1 and XBB in Norway in October 2022

Vikse, E. L.·Fossum, E.·Erdal, M. S.·Hungnes, O.·Bragstad, K.
View original source ↗Export metadata ↓

Abstract

New sub-lineages of the SARS-CoV-2 omicron variants with enhanced ability to evade existing antibody responses continue to evolve. A better understanding how susceptible emerging virus variants are to immunity induced by vaccination or infection could help predict which strains will become dominant going forward. Here we evaluate neutralizing antibodies against several clinical isolates of omicron variants including BQ.1.1 and XBB in sera from 3x mRNA vaccinated individuals and individuals with breakthrough infections with early (BA.1 or 2) or late (BA.5) omicron variants. In addition, we evaluate neutralizing antibodies in serum samples harvested from 32 individuals from the middle of October 2022, to provide a more recent estimate of immunity. As expected, serum samples harvested after breakthrough infections were more efficient at neutralizing all the omicron variants, compared to sera from non-infected individuals. While neutralization remained high against variants such as BA.2.75.2, BR.1 and BF.7, there was a marked reduction in neutralizing titers against BQ.1.1 and XBB. Similarly, most serum samples harvested in October 2022 had very low neutralizing antibodies against BQ.1.1 and XBB, suggesting that these variants and their descendants will dominate infection waves in Norway this winter season.

Source connections

Explore related subjects

immunologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Vikse, E. L., Fossum, E., Erdal, M. S., Hungnes, O., Bragstad, K.. 2023-01-05. Poor neutralizing antibody responses against SARS-CoV-2 Omicron BQ.1.1 and XBB in Norway in October 2022. https://doi.org/10.1101/2023.01.05.522845

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Ksp37 is a rapidly mobilized NK cell secretory protein that engages FGF2

A key feature of natural killer (NK) cells is their preloaded arsenal of effector molecules, allowing them to rapidly respond upon activation. In this study, we characterized a previously unexplored secretory protein, termed killer-specific secretory protein of 37 kDa (Ksp37), which is highly abundant in differentiated CD56dim NK cells. Ksp37 is rapidly secreted in a dose-dependent and JAK-1 dependent manner upon low levels of cytokine stimulation, making it a sensitive readout for NK cell activation. Following secretion, intracellular levels were rapidly replenished, preserving responsiveness to subsequent cytokine stimulation. We found that Ksp37 is stored in polarized intracellular compartments distinct from those containing canonical cytotoxic effector molecules, including granzyme B and perforin, which require stronger stimulation for release. Lastly, we identified Ksp37 as a novel binding partner of fibroblast growth factor 2 (FGF2). This opens new avenues of exploration for the role of NK cells in remodeling their extracellular environment by modulating the FGF2-FGFR1 axis, which plays a key role in tumor growth, angiogenesis and tissue repair.

immunology↗
bioRxiv2026

ACE-engineered human iPSC-derived neutrophils enhance host defense against multidrug-resistant bacterial infections

Severe neutropenia predisposes patients to life-threatening infections, while donor-dependent granulocyte transfusions are limited by availability and variable cell quality. Here, we engineered human induced pluripotent stem cells (iPSCs) to constitutively or inducibly express angiotensin-converting enzyme (ACE) and differentiated them into functional ACE-engineered neutrophils (ACE-iNeu). ACE expression enhanced granulocytic maturation, reactive oxygen species generation, inflammatory cytokine production, and antimicrobial signaling. ACE-iNeu exhibited enhanced bactericidal activity against methicillin-resistant Staphylococcus aureus and multidrug-resistant Pseudomonas aeruginosa. Following adoptive transfer into neutropenic mice, ACE-iNeu significantly reduced circulating and tissue bacterial burdens. Integrated metabolomic and transcriptomic analyses revealed ACE-associated alterations in adenine nucleotide abundance and developmental and inflammatory pathways. Together, these findings establish ACE engineering as a strategy to enhance the production and antimicrobial function of human iPSC-derived neutrophils and support further preclinical development of engineered granulocyte therapies for severe drug-resistant infections.

immunology↗
bioRxiv2026

Tetravalent dengue mRNA vaccination orchestrates balanced four-serotype immunity with durable memory and protection in mice.

An effective dengue vaccine must establish durable immunity across four dengue virus (DENV) serotypes, evade antibody-dependent enhancement (ADE), and overcome immune imprinting from prior exposure. Here, we developed TetprM-E mRNA-LNP, a tetravalent vaccine comprising LNP-formulated nucleoside-modified mRNAs encoding DENV1-4 precursor membrane-envelope (prM-E) antigens, and evaluated its immunogenicity, durability, protection and breath across serotype-specific immune backgrounds. Three immunization strategies elicited neutralizing titers greater than 1:1500 against each serotype. Passive transfer of immune sera conferred 100% survival and reduced viremia after lethal DENV2 challenge in immunocompromised mice. Vaccination induced DENV envelope (env)-specific CD8+T cells and CD4-dependent germinal-center responses. DENV env-binding antibodies persisted for 34 weeks alongside DENV env-specific memory B cells. Vaccine-elicited sera showed no measurable in vitro ADE. Although monovalent priming initially biased antibody responses, TetprM-E mRNA-LNP vaccination broadened neutralization across DENV1-4 regardless of priming serotype. Together, TetprM-E mRNA-LNP elicits broad, durable, and protective immunity despite serologic constraints from pre-existing immunity.

immunology↗