SARS-CoV-2 is responsible for the coronavirus disease 2019 (COVID-19) pandemic, infecting millions of people and causing hundreds of thousands of deaths. The Spike glycoproteins of SARS-CoV-2 mediate ...viral entry and are the main targets for neutralizing antibodies. Understanding the antibody response directed against SARS-CoV-2 is crucial for the development of vaccine, therapeutic, and public health interventions. Here, we perform a cross-sectional study on 106 SARS-CoV-2-infected individuals to evaluate humoral responses against SARS-CoV-2 Spike. Most infected individuals elicit anti-Spike antibodies within 2 weeks of the onset of symptoms. The levels of receptor binding domain (RBD)-specific immunoglobulin G (IgG) persist over time, and the levels of anti-RBD IgM decrease after symptom resolution. Although most individuals develop neutralizing antibodies within 2 weeks of infection, the level of neutralizing activity is significantly decreased over time. Our results highlight the importance of studying the persistence of neutralizing activity upon natural SARS-CoV-2 infection.
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Antibodies against SARS-CoV-2 Spike correlate with COVID-19 severityRBD-specific IgM and IgA decline more rapidly than IgGSARS-CoV-2 neutralizing antibodies are elicited within 2 weeks of infectionNeutralizing antibodies decline significantly after resolution of the infection
Prévost et al. report a cross-sectional study on a cohort of 106 COVID-19 patients and show that most infected individuals are able to elicit a sustained antibody response over time. However, plasma neutralizing capacity wanes after infection resolution, but its implication on protection from re-infection remains unknown.
Lymphocytic choriomeningitis virus (LCMV) is an old-world arenavirus capable of causing severe diseases in humans. Despite the extensive use of LCMV in studying immune responses to viral infection, ...very little is known about its entry pathway. As an enveloped virus, the main determinant of LCMV entry is the viral glycoprotein, which allows for the fusion of the viral membrane with that of the target cell, upon specific triggers. While the exact triggers for LCMV GP are currently unknown, low pH and interaction with a yet to be identified host-encoded receptor are likely involved in the activation of the GP fusion activity. This thesis finds that a triad of histidine residues on LCMV’s GP is absolutely critical for infection. Since mutation of the histidine triad had no effect on GP synthesis and did not completely abrogate its ability to bind to cells, our data suggest that the histidine triad are important for a step after virus internalization, potentially allowing low pH sensing. In addition, through the use of engineered soluble GPs, pulldown experiments, and mass spectrometry, various LCMV receptor candidates were identified. These candidates were further validated in order to identify crucial host proteins involved in LCMV entry. This study finds that LCMV GP interacts strongly with the Neuropilin proteins NRP1 and NRP2, and these cellular proteins may play a role in LCMV’s entry pathway during infection.
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