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Biology subjects

Christ, W.

Publications and source records attributed to Christ, W..

9 recordsLinked to original sources

An ONT sequencing framework for hantavirus genome assembly, variant analysis, and defective viral genome characterization from whole-segment amplicons

Orthohantaviruses are zoonotic, tri-segmented negative-sense RNA viruses of rodents and other small mammals that can cause severe human disease. Whole genome sequencing remains difficult because of low viral loads, high sequence diversity, and an inherent instability of the viral L segment. Current tiled amplicon and hybrid-capture approaches do not capture the heterogeneity of virus populations, including defective viral genomes (DVGs), which have never been described for hantaviruses. Here, we present an Oxford Nanopore Technologies sequencing framework based on universal reverse transcription primers targeting the conserved genome termini of orthohantaviruses and a single species-specific primer pair per segment, enabling amplification and sequencing of complete S, M, and L segments. We also developed an accompanying bioinformatic pipeline that performs reference-guided assembly of hantavirus genomes, consensus generation, variant calling, and DVG classification using the newly developed ORCHID classification pipeline. We applied this approach to diverse Puumala virus strains from infected cell cultures and bank voles, to representative Old World and New World orthohantaviruses, and to highly pathogenic New World viruses in vivo. In all cases we were able to accurately reconstruct full hantavirus genomes. Notably, we found that hantavirus populations contain highly abundant DVGs and conserved L segment deletions, whereas the S and M segments remained largely intact. Together, this work provides a low-cost, broadly applicable and easily customisable workflow for hantavirus genomics and reveals DVGs as a previously unrecognized feature of hantavirus populations.

microbiology↗

Drug repurposing high-throughput screen identifies candidate antiviral compounds against Puumala Orthohantavirus

Hantaviruses are zoonotic negative-sense RNA viruses that cause two severe diseases; haemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS) for which no approved antiviral therapies are available. To identify host-directed modulators of hantavirus infection in the available annotated drug space, we performed a drug repurposing screen in A549 cells and HUVECs, using live Puumala virus (PUUV). We identified and validated 70 drugs with antiviral activity across these 2 different cell systems. Functional clustering confirmed the known infection-inhibitory effect of several group of compounds, including inhibitors of heat shock proteins, mTOR pathway or nucleotide synthesis. In addition, we also identified compounds yet unexplored as antivirals against Hantaviruses, such as certain antibiotics. This dataset provides a systematic map of host pathways influencing PUUV infection and highlights candidate compounds and cellular processes that warrant further investigation.

cell biology↗

Small aberrant viral genomes induce the innate immune response to arenaviruses

Arenaviruses are a family of negative-sense RNA viruses mainly found in rodents in which they cause chronic asymptomatic infections. Some arenaviruses, however, can occasionally infect humans and cause pathogenic viral haemorrhagic fevers. These viral haemorrhagic fevers are associated with a massively dysregulated immune response characterized by excessive release of pro-inflammatory cytokines resulting in hyperinflammatory immunopathology. Here, we systematically characterize the immune response of human cells to a wide panel of mammalian arenaviruses and identify a clear distinction between New World viruses, which uniformly induce a robust interferon response, and Old World viruses, which do not induce any significant host response. This innate immune response is primarily driven by RIG-I-mediated RNA sensing and might be aided by differences in viral interferon antagonist expression patterns. Furthermore, we identified differences in quantity and type of non-standard viral genomes produced in unpassaged Old World and New World virus infections. Finally, we demonstrate that small non-standard viral RNA expression by New World viruses are key drivers of the innate immune response and might help explain how the host response can shape viral disease phenotypes and inform triage of patients.

microbiology↗

Discovery of a novel inhibitor of macropinocytosis with antiviral activity

Several viruses hijack various forms of endocytosis in order to infect host cells. Here, we report the discovery of a new molecule with antiviral properties that we named virapinib, which limits viral entry by macropinocytosis. The identification of virapinib derives from a chemical screen using High-Throughput Microscopy, where we identified new chemical entities capable of preventing infection with a pseudotype virus expressing the spike (S) protein from SARS-CoV-2. Subsequent experiments confirmed the capacity of virapinib to inhibit infection by SARS-CoV-2, as well as by additional viruses, such as Monkeypox virus and TBEV. Mechanistic analyses revealed that the compound inhibited macropinocytosis, limiting this entry route for the viruses. Importantly, virapinib has no significant toxicity to host cells. In summary, we present a new molecule that inhibits viral entry via the endocytic route, offering a new alternative to prevent viral infection.

pharmacology and toxicology↗

SARS-CoV-2 variant-specific differences in inhibiting the effects of the PKR-activated integrated stress response

The integrated stress response (ISR) is a eukaryotic cell pathway that triggers translational arrest and the formation of stress granules (SGs) in response to various stress signals, including those caused by viral infections. The SARS-CoV-2 nucleocapsid protein has been shown to disrupt SGs, but SARS-CoV-2 interactions with other components of the pathway remains poorly characterized. Here, we show that SARS-CoV-2 infection triggers the ISR through activation of the eIF2-kinase PKR while inhibiting a variety of downstream effects. In line with previous studies, SG formation was efficiently inhibited and the induced eIF2 phosphorylation only minimally contributed to the translational arrest observed in infected cells. Despite ISR activation and translational arrest, expression of the stress-responsive transcripts ATF4 and CHOP was not induced in SARS-CoV-2 infected cells. Finally, we found variant-specific differences in the activation of the ISR between ancestral SARS-CoV-2 and the Delta and Omicron BA.1 variants in that Delta infection induced weaker PKR activation while Omicron infection induced higher levels of p-eIF2 and greatly increased SG formation compared to the other variants. Our results suggest that different SARS-CoV-2 variants can affect normal cell functions differently, which can have an impact on pathogenesis and treatment strategies.

microbiology↗

SARS-CoV-2 and HSV-1 Induce Amyloid Aggregation in Human CSF

The corona virus (SARS-CoV-2) pandemic and the resulting long-term neurological complications in patients, known as long COVID, have renewed the interest in the correlation between viral infections and neurodegenerative brain disorders. While many viruses can reach the central nervous system (CNS) causing acute or chronic infections (such as herpes simplex virus 1, HSV-1), the lack of a clear mechanistic link between viruses and protein aggregation into amyloids, a characteristic of several neurodegenerative diseases, has rendered such a connection elusive. Recently, we showed that viruses can induce aggregation of purified amyloidogenic proteins via the direct physicochemical mechanism of heterogenous nucleation (HEN). In the current study, we show that the incubation of HSV-1 and SARS-CoV-2 with human cerebrospinal fluid (CSF) leads to the amyloid aggregation of several proteins known to be involved in neurodegenerative diseases, such as: APLP1 (amyloid beta precursor like protein 1), ApoE, clusterin, 2-macroglobulin, PGK-1 (phosphoglycerate kinase 1), ceruloplasmin, nucleolin, 14-3-3, transthyretin and vitronectin. Importantly, UV-inactivation of SARS-CoV-2 does not affect its ability to induce amyloid aggregation, as amyloid formation is dependent on viral surface catalysis via HEN and not its ability to replicate. Additionally, viral amyloid induction led to a dramatic drop in the soluble protein concentration in the CSF. Our results show that viruses can physically induce amyloid aggregation of proteins in human CSF and result in soluble protein depletion, and thus providing a potential mechanism that may account for the association between persistent and latent/reactivating brain infections and neurodegenerative diseases. Significance StatementViruses have generally been excluded from the etiology of amyloid pathologies based on the assumption that amyloid formation requires a proteinaceous conformational template (a prion) to form. Here we show that neuroinvasive viruses induce amyloid aggregation of a plethora of proteins in human CSF even after UV inactivation. Our work illustrates that viruses can induce amyloid aggregation of endogenous human proteins in their native environment by acting as physical catalysts of amyloid nucleation and phase transition. Demonstrating this direct mechanistic link, which is independent of templating, can help better understand the link between viruses and neurodegenerative disorders, especially in the post-COVID-19 era.

microbiology↗

Clinical grade ACE2 effectively inhibits SARS-CoV-2 Omicron infections

The recent emergence of the SARS-CoV-2 variant Omicron has caused considerable concern due to reduced vaccine efficacy and escape from neutralizing antibody therapeutics. Omicron is spreading rapidly around the globe and is suspected to account for most new COVID-19 cases in several countries, though the severity of Omicron-mediated disease is still under debate. It is therefore paramount to identify therapeutic strategies that inhibit the Omicron SARS-CoV-2 variant. Here we report using 3D structural modelling that Spike of Omicron can still associate with human ACE2. Sera collected after the second mRNA-vaccination did not exhibit a protective effect against Omicron while strongly neutralizing infection of VeroE6 cells with the reference Wuhan strain, confirming recent data by other groups on limited vaccine and convalescent sera neutralization efficacy against Omicron. Importantly, clinical grade recombinant human soluble ACE2, a drug candidate currently in clinical development, potently neutralized Omicron infection of VeroE6 cells with markedly enhanced potency when compared to reference SARS-CoV-2 isolates. These data show that SARS-CoV-2 variant Omicron can be readily inhibited by soluble ACE2, providing proof of principle of a viable and effective therapeutic approach against Omicron infections.

molecular biology↗

Longitudinal characterization of humoral and cellular immunity in hospitalized COVID-19 patients reveal immune persistence up to 9 months after infection

BackgroundInsights into early, specific humoral and cellular responses to infection with SARS-CoV-2, as well as the persistence and magnitude of resulting immune memory is important amidst the ongoing pandemic. The combination of humoral and cellular immunity will most likely contribute to protection from reinfection or severe disease. MethodsHere, we conducted a longitudinal study on hospitalized moderate and severe COVID-19 patients from the acute phase of disease into convalescence at five- and nine-months post symptom onset. Utilizing flow cytometry, serological assays as well as B cell and T cell FluoroSpot assays, we assessed the magnitude and specificity of humoral and cellular immune memory during and after human SARS-CoV-2 infection. FindingsDuring acute COVID-19, we observed an increase in germinal center activity, a substantial expansion of antibodysecreting cells, and the generation of SARS-CoV-2-neutralizing antibodies. Despite gradually decreasing antibody levels, we show persistent, neutralizing antibody titers as well as robust specific memory B cell responses and polyfunctional T cell responses at five- and nine-months after symptom onset in both moderate and severe COVID-19 patients. Long-term SARS-CoV-2 specific responses were marked by preferential targeting of spike over nucleocapsid protein. ConclusionsOur findings describe the initiation and, importantly, persistence of cellular and humoral SARS-CoV-2 specific immunological memory in hospitalized COVID-19 patients long after recovery, likely contributing towards protection against reinfection.

immunology↗

Expansion of SARS-CoV-2-specific Antibody-secreting Cells and Generation of Neutralizing Antibodies in Hospitalized COVID-19 Patients

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in late 2019 and has since become a global pandemic. Pathogen-specific antibodies are typically a major predictor of protective immunity, yet B cell and antibody responses during COVID-19 are not fully understood. Here, we analyzed antibody-secreting cell (ASC) and antibody responses in twenty hospitalized COVID-19 patients. The patients exhibited typical symptoms of COVID-19, and presented with reduced lymphocyte numbers and increased T cell and B cell activation. Importantly, we detected an expansion of SARS-CoV-2 nucleocapsid protein-specific ASCs in all twenty COVID-19 patients using a multicolor FluoroSpot assay. Out of the 20 patients, 16 had developed SARS-CoV-2-neutralizing antibodies by the time of inclusion in the study. SARS-CoV-2-specific IgA, IgG and IgM antibody levels positively correlated with SARS-CoV-2-neutralizing antibody titers, suggesting that SARS-CoV-2-specific antibody levels may reflect the titers of neutralizing antibodies in COVID-19 patients during the acute phase of infection. Lastly, we showed that interleukin 6 (IL-6) and C-reactive protein (CRP) concentrations were higher in serum of patients who were hospitalized for longer, supporting the recent observations that IL-6 and CRP could be used to predict COVID-19 severity. Altogether, this study constitutes a detailed description of clinical and immunological parameters in twenty COVID-19 patients, with a focus on B cell and antibody responses, and provides tools to study immune responses to SARS-CoV-2 infection and vaccination.

immunology↗