Biology subjects

Leijten, L. M.

Publications and source records attributed to Leijten, L. M..

4 recordsLinked to original sources

bioRxiv2025

Mass mortality at penguin mega-colonies due to avian cholera confounds H5N1 HPAIV surveillance in Antarctica

In the austral summer 2023/2024, H5N1 high pathogenicity avian influenza virus (HPAIV) was reported for the first time in Antarctica. Concerns of HPAIV causing high mortality of seabirds and mammals prompted immediate efforts to track its spread and impact on endemic wildlife. In March 2024, we visited the Danger Islands archipelago, that hosts two mega-colonies of Adelie penguins, and observed an unusual mortality estimated in thousands of Adelie penguins and other species. Swabs and tissues were collected for molecular detection of infectious agents from 49 carcasses, and additional tissues for histology from a selection of 9 carcasses. We unexpectedly detected Pasteurella multocida DNA in 46 of 49 individuals, and diagnosed avian cholera, and not HPAI, as the cause of death of most of these animals. By metagenomics, we retrieved the genomic sequences of the Pasteurella multocida strain which caused the epizootic, and the phylogenetic analysis showed a close relation with strains previously reported in the Southern Ocean area. This study confirms avian cholera as a relevant cause of mortality in the Antarctic region, and overall highlights the importance of considering avian cholera in the differential diagnoses during mortality events in Antarctica, even with the concurrent circulation of HPAIV.

microbiology↗

bioRxiv2025

The expanding avian influenza panzootic: skua die-off in Antarctica

High pathogenicity avian influenza virus of subtype H5 (H5 HPAIV), clade 2.3.4.4b, invaded Antarctica in 2023. Here we show that H5 HPAIV caused high mortality in a breeding colony of skuas at one of ten sites we visited in March 2024. By combined virological and pathological analyses, we found that H5 HPAIV caused multi-organ necrosis and rapid death in skuas. Taken together with recent data, skuas in Antarctica are at risk of continued mortality from H5 HPAIV infection, threatening their already small populations. Conversely, because of their wide distribution and ecological relevance, skuas may play a substantial role in spread of the virus across Antarctica. Transdisciplinary surveillance is needed in coming years to monitor the impact of this poultry-origin disease on Antarcticas unique wildlife.

microbiology↗

bioRxiv2024

A 2022 avian H5N1 influenza A virus from clade 2.3.4.4b attaches to and replicates better in human respiratory epithelium than a 2005 H5N1 virus from clade 2.3.2.1

BackgroundHighly pathogenic avian influenza (HPAI) H5 viruses of the A/Goose/Guangdong/1/1996 (GsGd) lineage pose significant global risks to wildlife, domestic animals, and humans. Recent cross-species transmission events to mammals, including humans, highlight this risk. Critical determinants for cross-species and intra-species transmission include the ability to attach to and replicate in respiratory epithelial cells. Although these factors have been studied for HPAI H5N1 viruses in the past, limited studies are available for currently circulating strains. MethodsWe compared level of adaptation to human respiratory tract of a HPAI H5N1 clade 2.3.4.4b (H5N12022) virus with those of well characterized HPAI H5N1 clade 2.1.3.2 (H5N12005) and seasonal H3N22003 viruses by three methods. First, we compared pattern of virus attachment by virus histochemistry. Second, we compared efficiency of infection and replication, as well as innate immune responses in human respiratory epithelium in vitro. Lastly, we compared polymerase complex activity in a minigenome assay. FindingsThe H5N12022 virus attached more abundantly to and replicated more efficiently in cells of the human respiratory tract compared to H5N12005 and H3N2 viruses. This increased replication was not associated with an increased polymerase activity of H5N12022 virus compared to H3N22003 virus. The efficient replication of H5N12022 virus infection induced a robust innate immune response almost comparable to H3N22003. InterpretationThe pattern of virus attachment and replication efficiency of a HPAI H5N12022 virus resembled that of H3N22003 virus more closely than a HPAI H5N12005. This could contribute to an increased risk for both human infection and virus adaptations to humans. FundingThe Netherlands Organization for Health Research and Development Research in contextO_ST_ABSEvidence before this studyC_ST_ABSHighly pathogenic avian influenza (HPAI) H5 viruses of the A/Goose/Guangdong/1/1996 (GsGd) lineage (clade 2.3.4.4b) have the ability to spread to a wide range of domesticated and wild mammalian species, including humans. Cross species transmission and transmission among humans requires-- among other factors--efficient infection of epithelial cells in the respiratory epithelium of the upper respiratory tract. Added value of this studyIn our study we show that a recent clade 2.3.4.4b HPAI H5N1 virus attached to and replicated more efficiently in respiratory epithelium than a clade 2.1.3.2 H5N1 virus that circulated in 2005. Implications of all the available dataThese data suggest that there might be an increased risk of human infections with the currently circulating 2.3.4.4b HPAI H5N1 viruses, which might facilitate opportunities for human adaptation.

microbiology↗

bioRxiv2024

Neuroinvasive and neurovirulent potential of SARS-CoV-2 in the acute and post-acute phase of intranasally inoculated ferrets

Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) can cause systemic disease, including neurological complications, even after mild respiratory disease. Previous studies have shown that SARS-CoV-2 infection can induce neurovirulence through microglial activation in the brains of patients and experimentally inoculated animals, which are models representative for moderate to severe respiratory disease. Here, we aimed to investigate the neuroinvasive and neurovirulent potential of SARS-CoV-2 in intranasally inoculated ferrets, a model for subclinical to mild respiratory disease. The presence of viral RNA, histological lesions, virus-infected cells, and the number and surface area of microglia and astrocytes were investigated. Viral RNA was detected in various respiratory tissue samples by qPCR at 7 days post inoculation (dpi). Virus antigen was detected in the nasal turbinates of ferrets sacrificed at 7 dpi and was associated with inflammation. Viral RNA was detected in the brains of ferrets sacrificed 7 dpi, but in situ hybridization nor immunohistochemistry did not verify evidence of infection. Histopathological analysis of the brains showed no evidence for an influx of inflammatory cells. Despite this, we observed an increased number of Alzheimer type II astrocytes in the hindbrains of SARS-CoV-2 inoculated ferrets. Additionally, we detected an increased microglial activation in the olfactory bulb and hippocampus, and a decrease in the astrocytic activation status in the white matter and hippocampus of SARS-CoV-2 inoculated ferrets. In conclusion, although showed that SARS-CoV-2 has limited neuroinvasive potential in this model for subclinical to mild respiratory disease, there is evidence for neurovirulent potential. This study highlights the value of this ferret model to study the neuropathogenecity of SARS-CoV-2 and reveals that a mild SARS-CoV-2 infection can affect both microglia and astrocytes in different parts of the brain.

microbiology↗