COVID-19 (Corona Virus Induced Disease-19) caused by the SARS-CoV-2 coronavirus can be a serious in pregnancy. Therefore, vaccination with modRNA vaccines was recommended depending on the immunity status for women of reproductive age and pregnant women since 2022. However, there are only preliminary data on transplacental transmission of the virus and modRNA from genetic vaccines so far.
The study population included 106 women who have given birth at the Department of Obstetrics and Gynecology, University Hospital of Würzburg during November 2020 to October 2022. In addition to medical data and vaccination history, immunohistochemical examination of the placenta was performed with antibodies against SARS-CoV-2 spike and nucleocapsid proteins. RNAscope in situ Hybridization was used to show RNA detection in positive placental tissues as a proof of concept.
Altogether, 87% of participants received at least one vaccine dose against SARS-CoV-2 and 56 women (42 vaccinated, 14 not vaccinated) contracted COVID-19. In total, 31 placentas were found positive for the spike protein. Spike positive cells were predominantly Hofbauer cells and trophoblasts. In three cases of vaccinated and then infected woman, an additional nucleocapsid staining was detected, but there was no significant difference in staining pattern in correlation to the vaccine/COVID-19 status. Interestingly, we did not find viral RNA in the investigated samples, but we could show a positive in situ Hybridization of BNT162b2 and S-encoding mRNA-1273 in two individual samples.
The spike protein of SARS-CoV-2 has been be detected in placental Hofbauer and Trophoblast cells as well as villous endothelia after infection and vaccination indicating a possible transplacental transfer or uptake. These findings may suggest a potential for transplacental transfer or cellular uptake; however, the extent, mechanisms, and clinical significance of this phenomenon remain to be fully understood. Clinical trial registration: DRKS00022506.
Copyright: © 2026 Bartmann et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Coronavirus disease 2019 (COVID-19) patients have a 1.7-fold higher arrhythmia risk with rates of cardiac complications ranging from 2% non-ICU patients to 59% in non-survivors. Atrial fibrillation (AF), the most common arrhythmia, is a frequent complication of acute and long COVID-19. The high expression of ACE2 in the heart suggested that infectious virus may underlie cardiac complications. However, we recently reported in human cardiac tissue from fatal COVID-19 cases perivascular spike protein, elevated pro-inflammatory cytokines, vascular damage, and cardiac remodeling without evidence for direct infection of cardiac cells by SARS-CoV2. Mislocalization of intercalated disc (ID) components, connexin-43 (Cx43) gap junctions and NaV1.5 sodium channels, was also evident in patients' hearts, recapitulating structural remodeling we previously identified as providing a substrate for atrial arrhythmias following an acute inflammatory insult. Therefore, we hypothesized that the inflammatory response elicited by SARS-CoV2 spike protein is sufficient to provoke atrial arrhythmias. Structural and functional assessments of WT murine hearts were performed five days following a single bolus intravenous injection of the viral spike protein. In vivo ECGs demonstrated increased atrial arrhythmia burden in spike-injected mice vs. control. Immunohistochemistry studies revealed elevated expression of inflammatory markers and evidence of vascular damage in these mice. Additionally, we observed disruption of ID ultrastructure and mislocalization of Cx43 and NaV1.5 in the atria of spike protein-injected mice. Our results suggest that vascular-leak inducing inflammatory insult from viral spike protein, and not direct infection by SARS-CoV2 results in the pathophysiology of cardiac dysfunction in fatal COVID-19.
© 2025. The Author(s).

As the COVID-19 pandemic continues to evolve, novel vaccines need to be developed that are readily manufacturable and provide clinical efficacy against emerging SARS-CoV-2 variants. Virus-like particles (VLPs) presenting the spike antigen at their surface offer remarkable benefits over other vaccine antigen formats; however, current SARS-CoV-2 VLP vaccines candidates in clinical development suffer from challenges including low volumetric productivity, poor spike antigen density, expression platform-driven divergent protein glycosylation and complex upstream/downstream processing requirements. Despite their extensive use for therapeutic protein manufacturing and proven ability to produce enveloped VLPs, Chinese Hamster Ovary (CHO) cells are rarely used for the commercial production of VLP-based vaccines.
Using CHO cells, we aimed to produce VLPs displaying the full-length SARS-CoV-2 spike. Affinity chromatography was used to capture VLPs released in the culture medium from engineered CHO cells expressing spike. The structure, protein content, and glycosylation of spikes in VLPs were characterized by several biochemical and biophysical methods. In vivo, the generation of neutralizing antibodies and protection against SARS-CoV-2 infection was tested in mouse and hamster models.
We demonstrate that spike overexpression in CHO cells is sufficient by itself to generate high VLP titers. These VLPs are evocative of the native virus but with at least three-fold higher spike density. In vivo, purified VLPs elicit strong humoral and cellular immunity at nanogram dose levels which grant protection against SARS-CoV-2 infection.
Our results show that CHO cells are amenable to efficient manufacturing of high titers of a potently immunogenic spike protein-based VLP vaccine antigen.
© 2023. Springer Nature Limited.

In a neuropathological series of 20 COVID-19 cases, we analyzed six cases (three biopsies and three autopsies) with multiple foci predominantly affecting the white matter as shown by MRI. The cases presented with microhemorrhages evocative of small artery diseases. This COVID-19 associated cerebral microangiopathy (CCM) was characterized by perivascular changes: arterioles were surrounded by vacuolized tissue, clustered macrophages, large axonal swellings and a crown arrangement of aquaporin-4 immunoreactivity. There was evidence of blood-brain-barrier leakage. Fibrinoid necrosis, vascular occlusion, perivascular cuffing and demyelination were absent. While no viral particle or viral RNA was found in the brain, the SARS-CoV-2 spike protein was detected in the Golgi apparatus of brain endothelial cells where it closely associated with furin, a host protease known to play a key role in virus replication. Endothelial cells in culture were not permissive to SARS-CoV-2 replication. The distribution of the spike protein in brain endothelial cells differed from that observed in pneumocytes. In the latter, the diffuse cytoplasmic labeling suggested a complete replication cycle with viral release, notably through the lysosomal pathway. In contrast, in cerebral endothelial cells the excretion cycle was blocked in the Golgi apparatus. Interruption of the excretion cycle could explain the difficulty of SARS-CoV-2 to infect endothelial cells in vitro and to produce viral RNA in the brain. Specific metabolism of the virus in brain endothelial cells could weaken the cell walls and eventually lead to the characteristic lesions of COVID-19 associated cerebral microangiopathy. Furin as a modulator of vascular permeability could provide some clues for the control of late effects of microangiopathy.

This study compared the immune response in mild versus fatal SARS-CoV2 infection. Forty nasopharyngeal swabs with either productive mild infection (n = 20) or negative for SARS-CoV2 (n = 20) were tested along with ten lung sections from people who died of COVID-19 which contained abundant SARS-CoV2 and ten controls. There was a 25-fold increase in the CD3+T cell numbers in the viral positive nasopharyngeal swabs compared to the controls (p < 0.001) and no change in the CD3+T cell count in the fatal COVID-19 lungs versus the controls. CD11b + and CD206+ macrophage counts were significantly higher in the mild versus fatal disease (p = 0.002). In situ analysis for SARS-CoV2 RNA found ten COVID-19 lung sections that had no/rare detectable virus and also lacked the microangiopathy typical of the viral positive sections. These viral negative lung tissues when compared to the viral positive lung samples showed a highly significant increase in CD3+ and CD8 T cells (p < 0.001), equivalent numbers of CD163+ cells, and significantly less PDL1, CD11b and CD206+ cells (p = 0.002). It is concluded that mild SARS-CoV2 infection is marked by a much stronger CD3/CD8 T cell, CD11b, and CD206 macrophage response than the fatal lung disease where viral RNA is abundant.
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