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1. Active Control and Sustained Oscillations in actSIS Epidemic Dynamics

   Zhou, Yunxiu; Levin, Simon A.; Leonard, Naomi Ehrich (December 2020, 3rd IFAC Workshop on Cyber-Physical & Human Systems)

   null (Ed.)

   An actively controlled Susceptible-Infected-Susceptible (actSIS) contagion model is presented for studying epidemic dynamics with continuous-time feedback control of infection rates. Our work is inspired by the observation that epidemics can be controlled through decentralized disease-control strategies such as quarantining, sheltering in place, social distancing, etc., where individuals can actively modify their contact rates in response to observations of the infection levels in the population. Accounting for a time lag in observations and categorizing individuals into distinct sub-populations based on their risk profiles, we show that the actSIS model manifests qualitatively different features as compared with the SIS model. In a homogeneous population of risk-averters, the endemic equilibrium is always reduced, although the transient infection level can overshoot or undershoot. In a homogeneous population of risk-tolerating individuals, the system exhibits bistability, which can also lead to reduced infection. For a heterogeneous population comprised of risk-tolerators and risk-averters, we prove conditions on model parameters for the existence of a Hopf bifurcation and sustained oscillations in the infected population. 

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2. A toy model for the relativistic Vlasov-Maxwell system

   https://doi.org/10.3934/krm.2021053  

   Ben-Artzi, Jonathan; Pankavich, Stephen; Zhang, Junyong (January 2022, Kinetic and Related Models)

   The global-in-time existence of classical solutions to the relativistic Vlasov-Maxwell (RVM) system in three space dimensions remains elusive after nearly four decades of mathematical research. In this note, a simplified "toy model" is presented and studied. This toy model retains one crucial aspect of the RVM system: the phase-space evolution of the distribution function is governed by a transport equation whose forcing term satisfies a wave equation with finite speed of propagation. 

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3. Global dynamics of a delayed model with cytokine-enhanced viral infection and cell-to-cell transmission

   https://doi.org/10.3934/math.2024788  

   Hong, Liang; Li, Jie; Rong, Libin; Wang, Xia (January 2024, AIMS Mathematics)

   Recent studies have demonstrated the superiority of cell-to-cell transmission over cell-free virus infection, and highlighted the role of inflammatory cytokines in enhancing viral infection. To investigate their impacts on viral infection dynamics, we have proposed an HIV infection model incorporating general incidence rates, these infection modes, and two time delays. We derived the basic reproduction number and showed that it governs the existence and local stability of steady states. Through the construction of appropriate Lyapunov functionals and application of the LaSalle invariance principle, we established the global asymptotic stability of both the infection-free and infected steady states. 

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4. Global System for Atmospheric Modeling: Model Description and Preliminary Results

   https://doi.org/10.1029/2021MS002968  

   Khairoutdinov, Marat_F; Blossey, Peter_N; Bretherton, Christopher_S (June 2022, Journal of Advances in Modeling Earth Systems)

   Abstract The extension of a cloud‐resolving model, the System for Atmospheric Modeling (SAM), to global domains is described. The resulting global model, gSAM, is formulated on a latitude‐longitude grid. It uses an anelastic dynamical core with a single reference profile (as in SAM), but its governing equations differ somewhat from other anelastic models. For quasihydrostatic flows, they are isomorphic to the primitive equations (PE) in pressure coordinates but with the globally uniform reference pressure playing the role of actual pressure. As a result, gSAM can exactly maintain steady zonally symmetric baroclinic flows that have been specified in pressure coordinates, produces accurate simulations when initialized or nudged with global reanalyses, and has a natural energy conservation equation despite the drawbacks of using the anelastic system to model global scales. gSAM employs a novel treatment of topography using a type of immersed boundary method, the Quasi‐Solid Body Method, where the instantaneous flow velocity is forced to stagnate in grid cells inside a prescribed terrain. The results of several standard tests designed to evaluate the accuracy of global models with and without topography as well as results from real Earth simulations are presented. 

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5. Human adenovirus serotype 5 infection dysregulates cysteine, purine, and unsaturated fatty acid metabolism in fibroblasts

   https://doi.org/10.1096/fj.202402726R  

   Sanchez, Bailey‐J_C; Ortiz, Rudy_M; Grasis, Juris_A (March 2025, The FASEB Journal)

   Abstract Viral infections can cause cellular dysregulation of metabolic reactions. Viruses alter host metabolism to meet their replication needs. The impact of viruses on specific metabolic pathways is not well understood, even in well‐studied viruses, such as human adenovirus. Adenoviral infection is known to influence cellular glycolysis and respiration; however, global effects on overall cellular metabolism in response to infection are unclear. Furthermore, few studies have employed an untargeted approach, combining emphasis on viral dosage and infection. To address this, we employed untargeted metabolomics to quantify the dynamic metabolic shifts in fibroblasts infected with human adenovirus serotype 5 (HAdV‐5) at three dosages (0.5, 1.0, and 2.0 multiplicity of infection [MOI]) and across 4 time points (6‐, 12‐, 24‐, and 36‐h post‐infection [HPI]). The greatest differences in individual metabolites were observed at 6‐ and 12‐h post‐infection, correlating with the early phase of the HAdV‐5 infection cycle. In addition to its effects on glycolysis and respiration, adenoviral infection downregulates cysteine and unsaturated fatty acid metabolism while upregulating aspects of purine metabolism. These results reveal specific metabolic pathways dysregulated by adenoviral infection and the associated dynamic shifts in metabolism, suggesting that viral infections alter energetics via profound changes in lipid, nucleic acid, and protein metabolism. The results revealed previously unconsidered metabolic pathways disrupted by HAdV‐5 that can alter cellular metabolism, thereby prompting further investigation into HAdV mechanisms and antiviral targeting. 

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