We propose a physics-inspired mathematical model underlying the temporal evolution of competing virus variants that relies on the existence of (quasi) fixed points capturing the large time scale invariance of the dynamics. To motivate our result we first modify the time-honoured compartmental models of the SIR type to account for the existence of competing variants and then show how their evolution can be naturally re-phrased in terms of flow equations ending at quasi fixed points. As the natural next step we employ (near) scale invariance to organise the time evolution of the competing variants within the effective description of the framework. We test the resulting theory against the time evolution of COVID-19 virus variants that validate the theory empirically.
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http://dx.doi.org/10.1016/j.physa.2022.127071 | DOI Listing |
Sci Transl Med
January 2025
Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
At this stage in the COVID-19 pandemic, most infections are "breakthrough" infections that occur in individuals with prior severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure. To refine long-term vaccine strategies against emerging variants, we examined both innate and adaptive immunity in breakthrough infections. We performed single-cell transcriptomic, proteomic, and functional profiling of primary and breakthrough infections to compare immune responses from unvaccinated and vaccinated individuals during the SARS-CoV-2 Delta wave.
View Article and Find Full Text PDFFront Immunol
January 2025
Institute of Virology, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Background: The emergence of novel SARS-CoV-2 variants challenges immunity, particularly among immunocompromised kidney transplant recipients (KTRs). To address this, vaccines have been adjusted to circulating variants. Despite intensive vaccination efforts, SARS-CoV-2 infections surged among KTRs during the Omicron wave, enabling a direct comparison of variant-specific immunity following-vaccination against Omicron BA.
View Article and Find Full Text PDFMol Ther Nucleic Acids
March 2025
NYU Cardiovascular Research Center, NYU Grossman School of Medicine, New York, NY 100016, USA.
Altered protein conformation can cause incurable neurodegenerative disorders. Mutations in , the gene encoding neuroserpin, can alter protein conformation resulting in cytotoxic aggregation leading to neuronal death. Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is a rare autosomal dominant progressive myoclonic epilepsy that progresses to dementia and premature death.
View Article and Find Full Text PDFBackground: Drivers of COVID-19 severity are multifactorial and include multidimensional and potentially interacting factors encompassing viral determinants and host-related factors (i.e., demographics, pre-existing conditions and/or genetics), thus complicating the prediction of clinical outcomes for different severe acute respiratory syndrome coronavirus (SARS-CoV-2) variants.
View Article and Find Full Text PDFJ Int AIDS Soc
February 2025
AP-HP, Hôpital Bichat Claude Bernard, Service de Virologie, INSERM, IAME, Paris, France.
Introduction: Molecular surveillance is an important tool for detecting chains of transmission and controlling the HIV epidemic. This can also improve our knowledge of molecular and epidemiological factors for the optimization of prevention. Our objective was to illustrate this by studying the molecular and epidemiological evolution of the cluster including the new circulating recombinant form (CRF) 94_cpx of HIV-1, detected in 2017 and targeted by preventive actions in 2018.
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