Mathematical modeling of viral infection dynamics and immune response in SARS-CoV-2: A computational framework for testing drug efficacy

2021 ◽  
Author(s):  
Surbhi Sharma ◽  
Abha Saxena ◽  
Soumita Chel ◽  
Kishalay Mitra ◽  
Lopamudra Giri
Keyword(s):  
Mathematical Modeling ◽  
Immune Response ◽  
Viral Infection ◽  
Drug Efficacy ◽  
Computational Framework ◽  
Infection Dynamics

scholarly journals Competitive exclusion during co-infection as a strategy to prevent the spread of a virus: A computational perspective

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247200
Author(s):  
Safar Vafadar ◽  
Maryam Shahdoust ◽  
Ata Kalirad ◽  
Pooya Zakeri ◽  
Mehdi Sadeghi
Keyword(s):  
Viral Infection ◽  
Waiting Times ◽  
Research Direction ◽  
Exclusion Principle ◽  
Process Change ◽  
Computational Framework ◽  
Virus Growth ◽  
Infection Dynamics ◽  
Delayed Initiation ◽  
A Cell

Inspired by the competition exclusion principle, this work aims at providing a computational framework to explore the theoretical feasibility of viral co-infection as a possible strategy to reduce the spread of a fatal strain in a population. We propose a stochastic-based model—called Co-Wish—to understand how competition between two viruses over a shared niche can affect the spread of each virus in infected tissue. To demonstrate the co-infection of two viruses, we first simulate the characteristics of two virus growth processes separately. Then, we examine their interactions until one can dominate the other. We use Co-Wish to explore how the model varies as the parameters of each virus growth process change when two viruses infect the host simultaneously. We will also investigate the effect of the delayed initiation of each infection. Moreover, Co-Wish not only examines the co-infection at the cell level but also includes the innate immune response during viral infection. The results highlight that the waiting times in the five stages of the viral infection of a cell in the model—namely attachment, penetration, eclipse, replication, and release—play an essential role in the competition between the two viruses. While it could prove challenging to fully understand the therapeutic potentials of viral co-infection, we discuss that our theoretical framework hints at an intriguing research direction in applying co-infection dynamics in controlling any viral outbreak’s speed.

scholarly journals Mathematical modeling of COVID-19 infection dynamics in Ghana: Impact evaluation of integrated government and individual level interventions

2021 ◽  
Vol 6 ◽  
pp. 381-397
Author(s):  
Duah Dwomoh ◽  
Samuel Iddi ◽  
Bright Adu ◽  
Justice Moses Aheto ◽  
Kojo Mensah Sedzro ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Impact Evaluation ◽  
Individual Level ◽  
Infection Dynamics

scholarly journals The host transcriptional response to Candidemia is dominated by neutrophil activation and heme biosynthesis and supports novel diagnostic approaches

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Julie M. Steinbrink ◽  
Rachel A. Myers ◽  
Kaiyuan Hua ◽  
Melissa D. Johnson ◽  
Jessica L. Seidelman ◽  
...  
Keyword(s):  
Immune Response ◽  
Bacterial Infection ◽  
Viral Infection ◽  
Fungal Infection ◽  
Host Response ◽  
Hospitalized Patients ◽  
Neutrophil Activation ◽  
Heme Biosynthesis ◽  
Transcriptional Analysis ◽  
Diagnostic Approaches

Abstract Background Candidemia is one of the most common nosocomial bloodstream infections in the United States, causing significant morbidity and mortality in hospitalized patients, but the breadth of the host response to Candida infections in human patients remains poorly defined. Methods In order to better define the host response to Candida infection at the transcriptional level, we performed RNA sequencing on serial peripheral blood samples from 48 hospitalized patients with blood cultures positive for Candida species and compared them to patients with other acute viral, bacterial, and non-infectious illnesses. Regularized multinomial regression was utilized to develop pathogen class-specific gene expression classifiers. Results Candidemia triggers a unique, robust, and conserved transcriptomic response in human hosts with 1641 genes differentially upregulated compared to healthy controls. Many of these genes corresponded to components of the immune response to fungal infection, heavily weighted toward neutrophil activation, heme biosynthesis, and T cell signaling. We developed pathogen class-specific classifiers from these unique signals capable of identifying and differentiating candidemia, viral, or bacterial infection across a variety of hosts with a high degree of accuracy (auROC 0.98 for candidemia, 0.99 for viral and bacterial infection). This classifier was validated on two separate human cohorts (auROC 0.88 for viral infection and 0.87 for bacterial infection in one cohort; auROC 0.97 in another cohort) and an in vitro model (auROC 0.94 for fungal infection, 0.96 for bacterial, and 0.90 for viral infection). Conclusions Transcriptional analysis of circulating leukocytes in patients with acute Candida infections defines novel aspects of the breadth of the human immune response during candidemia and suggests promising diagnostic approaches for simultaneously differentiating multiple types of clinical illnesses in at-risk, acutely ill patients.

Do fish erythrocytes have a potential role in the immune response orchestration after viral infection and DNA vaccination

2013 ◽  
Vol 34 (6) ◽  
pp. 1669-1670
Author(s):  
M. Ortega-Villaizan ◽  
A. Martínez-López ◽  
P. García-Valtanen ◽  
A.H. Teruel ◽  
L. Perez ◽  
...  
Keyword(s):  
Immune Response ◽  
Viral Infection ◽  
Potential Role ◽  
Dna Vaccination

scholarly journals Epigenetic Changes in the Regulation of Nicotiana tabacum Response to Cucumber Mosaic Virus Infection and Symptom Recovery through Single-Base Resolution Methylomes

Viruses ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 402 ◽  
Author(s):  
Chenguang Wang ◽  
Chaonan Wang ◽  
Wenjie Xu ◽  
Jingze Zou ◽  
Yanhong Qiu ◽  
...  
Keyword(s):  
Immune Response ◽  
Nicotiana Tabacum ◽  
Viral Infection ◽  
Cucumber Mosaic Virus ◽  
Mosaic Virus ◽  
Developmental Stages ◽  
Reduced Representation ◽  
Reduced Representation Bisulfite Sequencing ◽  
Symptom Recovery

Plants have evolved multiple mechanisms to respond to viral infection. These responses have been studied in detail at the level of host immune response and antiviral RNA silencing (RNAi). However, the possibility of epigenetic reprogramming has not been thoroughly investigated. Here, we identified the role of DNA methylation during viral infection and performed reduced representation bisulfite sequencing (RRBS) on tissues of Cucumber mosaic virus (CMV)-infected Nicotiana tabacum at various developmental stages. Differential methylated regions are enriched with CHH sequence contexts, 80% of which are located on the gene body to regulate gene expression in a temporal style. The methylated genes depressed by methyltransferase inhibition largely overlapped with methylated genes in response to viral invasion. Activation in the argonaute protein and depression in methyl donor synthase revealed the important role of dynamic methylation changes in modulating viral clearance and resistance signaling. Methylation-expression relationships were found to be required for the immune response and cellular components are necessary for the proper defense response to infection and symptom recovery.

scholarly journals Tumour viruses and innate immunity

2017 ◽  
Vol 372 (1732) ◽  
pp. 20160267 ◽  
Author(s):  
Sharon E. Hopcraft ◽  
Blossom Damania
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Host Cells ◽  
Oncogenic Viruses ◽  
Barr Virus ◽  
Human T Cell ◽  
Epstein Barr

Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune response. PRRs are localized to several different cellular compartments and are stimulated by viral proteins and nucleic acids. PRR activation initiates signal transduction events that ultimately result in an inflammatory response. Human tumour viruses, which include Kaposi's sarcoma-associated herpesvirus, Epstein–Barr virus, human papillomavirus, hepatitis C virus, hepatitis B virus, human T-cell lymphotropic virus type 1 and Merkel cell polyomavirus, are detected by several different PRRs. These viruses engage in a variety of mechanisms to evade the innate immune response, including downregulating PRRs, inhibiting PRR signalling, and disrupting the activation of transcription factors critical for mediating the inflammatory response, among others. This review will describe tumour virus PAMPs and the PRRs responsible for detecting viral infection, PRR signalling pathways, and the mechanisms by which tumour viruses evade the host innate immune system. This article is part of the themed issue ‘Human oncogenic viruses’.

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