Virology最新文献

{"title":"Differential induction of PD-L1 expression in cells infected with feline infectious peritonitis virus and feline enteric coronavirus","authors":"Alexandria Zabiegala,&nbsp;Yunjeong Kim,&nbsp;Kyeong-Ok Chang","doi":"10.1016/j.virol.2025.110734","DOIUrl":"10.1016/j.virol.2025.110734","url":null,"abstract":"<div><div>Feline infectious peritonitis (FIP) is a fatal systemic disease of cats, which is caused by FIP virus (FIPV), a virulent biotype of feline coronavirus (FCoV). In a small number of cats infected with feline enteric coronavirus (FECV), virus mutation may emerge that enable infection of monocytes and macrophages, leading to the development of FIP. This cell tropism shift, along with impaired T cell response, plays a critical role in FIP development. Programmed cell death protein (PD-1) and its ligands (PD-L1 and PD-L2) play crucial roles in immune responses as an immune checkpoint system. The PD-1 axis downregulates T cell response and is reported to be involved in immune evading mechanisms of various viruses. In this study, we used two virus strains FIPV-1146 and FECV-1683 corresponding to FIPV and FECV biotypes, respectively, to study the role of PD-L1 expression as a potential mechanism for FIP development. While both viruses demonstrated robust viral replication at comparable levels, FIPV-1146, but not FECV-1683, significantly upregulated PD-L1 expression in CRFK and and Fcwf-4 cells. Infection of Fcwf-4 cells with FIPV-Black strain also increased PD-L1 levels. Co-culture studies using Jurkat cells and Fcwf-4 cells infected with FIPV-1146 or FECV-1683 showed that PD-L1 induction by FIPV-1146 attenuated T cell activation. The cell signaling profiling assays showed that FIPV-1146, but not FECV-1683, induced the type I IFN synthesis, which is a well-known regulator for PD-L1 expression. The elevated PD-L1 levels by FIPV may lead to dampened T cell response, allowing persistent infection in macrophages and development of the FIP clinical disease.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"614 ","pages":"Article 110734"},"PeriodicalIF":2.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145446935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular biology of Cotton Leafroll Dwarf Virus (CLRDV) and potential application of CRISPR-Cas technology for developing virus-resistant cotton","authors":"Sriharsha V. Lankireddy ,&nbsp;Saikrishna Lekkala ,&nbsp;Archana Khadgi ,&nbsp;Venkateswara R. Sripathi ,&nbsp;Madhusudhana R. Janga","doi":"10.1016/j.virol.2025.110730","DOIUrl":"10.1016/j.virol.2025.110730","url":null,"abstract":"<div><div>Cotton leafroll dwarf virus (CLRDV) poses an increasing threat to global cotton production. Transmitted by the cotton aphid (<em>Aphis gossypii</em>) in a persistent, circulative manner, CLRDV exhibits a wide geographical distribution, with documented presence in South America, Africa, Asia, and the USA. Infection can result in either cotton blue disease (CBD) in South America or cotton leafroll dwarf disease (CLRDD) in the USA, both of which are associated with CLRDV. The considerable genetic diversity and frequent recombination events within CLRDV populations contribute to this symptom variability and complicate both diagnosis and management. While resistant cultivars have reduced disease impact in South America, these lines remain susceptible to emerging US strains, underscoring the urgent need for region-specific resistance breeding. Current molecular diagnostics rely on RT-PCR, but there is a need for rapid, field-deployable detection tools. Recent advances, such as CRISPR-Cas13a based SHERLOCK assays, offer sensitive and specific detection of CLRDV, with potential for on-site applications. Efficient screening techniques, supported by next-generation sequencing and transcriptomics, are essential for identifying novel resistance sources and elucidating virus-host interactions. CRISPR-based genome editing holds significant promise, as demonstrated in other crops. Targeted disruption of host susceptibility genes using CRISPR-Cas9, or direct degradation of viral genomes with RNA-targeting systems such as Cas12/Cas13, could offer durable, broad-spectrum resistance. By integrating molecular virology, high-throughput genomics, and precision gene editing, this review outlines a roadmap for translating these advances into sustainable, field-level solutions for CLRDV management and long-term cotton productivity.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"614 ","pages":"Article 110730"},"PeriodicalIF":2.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Viral diversity in vertebrates from Alto Pantanal, Mato Grosso, 2019","authors":"Janeth Aracely Ramirez Pavon ,&nbsp;Nilvanei Aparecido da Silva Neves ,&nbsp;Anderson de Oliveira Martins ,&nbsp;João Batista Pinho ,&nbsp;Vilma Juscineide de Souza ,&nbsp;Sandro Patroca da Silva ,&nbsp;Ana Cecília Ribeiro Cruz ,&nbsp;Daniele Barbosa de Almeida Medeiros ,&nbsp;Márcio Roberto Teixeira Nunes ,&nbsp;Renata Dezengrini Slhessarenko","doi":"10.1016/j.virol.2025.110729","DOIUrl":"10.1016/j.virol.2025.110729","url":null,"abstract":"<div><div>The Alto Pantanal is a key yet unexplored Brazilian wetland for studying vertebrate viral profiles. This study presents viral taxonomic profiles from vertebrate sera sampled in May, June and October of 2019 in Porto São Luiz and Pirizal, Alto Pantanal. A total of 13 frogs, 19 bats, 23 caimans, 36 equids, 20 domestic hens, 140 birds and 16 humans were sampled. After nucleic acid extraction, individual samples were pooled by species and subjected to a metagenomic approach. Viral reads accounted for less than 0.2 % in each pool, except in domestic hens (35.8 %), yielding an overall viral abundance variation among pools of 48.83 %. In total, twenty-nine viral genomic sequences were retrieved from five pools. In equids, two coding-complete genomes were identified belonging to species <em>Copiparvovirus ungulate8</em> and <em>Mutorquevirus equid2</em>. In domestic hens, four coding-complete genomes of species <em>Alpharetrovirus avileu</em> were detected, along with partial genomes of three gyroviroviruses of species <em>Gyrovirus homsa1</em>, <em>Gyrovirus galga1</em> and a putative novel unclassified gyrovirus. In humans, 15 genomes of known human anelloviruses were identified, as well as partial sequences of <em>Orthoflavivirus ilheusense</em> and <em>Erythroparvovirus primate</em> species. In caimans, a partial genome belonging to genus <em>Betadintovirus</em> was detected. In frogs, one partial sequence of a putative novel pegivirus, and a coding-complete sequence of an unclassified retrovirus (Rhinella marina endogenous retrovirus) were found. These findings provide valuable insights into viral circulation within the diverse Pantanal biome, and support viral genomic surveillance efforts in the region.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"614 ","pages":"Article 110729"},"PeriodicalIF":2.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145420121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the contribution of hemagglutinin-neuraminidase to the endocytic entry of Newcastle Disease Virus","authors":"Ran Zhao,&nbsp;Zongxi Han,&nbsp;Huixin Li,&nbsp;Yuhao Shao,&nbsp;Junfeng Sun,&nbsp;Shengwang Liu","doi":"10.1016/j.virol.2025.110741","DOIUrl":"10.1016/j.virol.2025.110741","url":null,"abstract":"<div><div>Entry of Newcastle disease virus (NDV) into target cells via caveolae-mediated endocytosis has been presented. However, the viral factors that mediate the endocytic entry and fusion in intracellular endosomes remain poorly understood. Herein, the potential contributions of HN stalk region and second receptor biding site (site II) located at the globular head region on the endocytosis of NDV and the viral-cell membrane fusion in endosomes were investigated. HN protein mutants with substitutions at positions 89 and 94 in the stalk region and at position 516 in site II were firstly constructed. We demonstrated that mutations in HN stalk region restricted its interaction with F protein and fusion promotion activity. While mutation in HN site II resulted in slightly decreased fusion promotion activity without affected the HN-F interactions. Further evaluation of receptor binding and entry capacities with HN mutant NDVs obtained by reverse genetics demonstrated that both mutations at stalk region and site II reduced the binding abilities of NDV to receptors. Interestingly, site II in HN was not responsible for the endocytic entry of NDV and subsequent viral-cell membrane fusion in endosomes. While the residues at 89 and 94 in HN stalk region were involved in the fusion of NDV in endosomes. Of particular note, the acidic condition was indispensable for efficiently fusion triggering of NDV within endosomes. Besides, residues at 89 and 94 in HN were conserved in different genotypes of NDVs and the endocytic entry of NDV into cells was not determined by viral virulence and genotype.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"614 ","pages":"Article 110741"},"PeriodicalIF":2.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145526707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the surface topology of respiratory syncytial virus particles that form on the surface of virus-infected cells","authors":"Chris E. Jeffree ,&nbsp;Thong Beng Lu ,&nbsp;Boon-Huan Tan ,&nbsp;Richard J. Sugrue","doi":"10.1016/j.virol.2025.110732","DOIUrl":"10.1016/j.virol.2025.110732","url":null,"abstract":"<div><div>The surface topology of virus filaments on respiratory syncytial virus (RSV)-infected cells was examined using field emission gun-scanning electron microscopy (FEG-SEM) and atomic force microscopy (AFM). FEG-SEM analysis of the surface of RSV-infected cells labelled with anti-F and anti-G protein antibodies revealed the presence of virus filaments and clusters of the F and G proteins distributed intermittently along their surface of the virus filaments. RSV-infected cells thinly coated with chromium were imaged using FEG-SEM and revealed a distinct structured surface topology consisting of closely packed surface domains. The G protein clusters were only associated within a subset of these domains which suggested that this structured topology was mainly derived from the host cell. Imaging of RSV-infected cells using AFM was undertaken as a different but complementary approach to the FEG-SEM analysis. Imaging using AFM revealed a similar structured surface topology on the virus filaments to that observed in the FEG-SEM analysis, indicating the consistency in the appearance of the virus surface topology using these different methods. Collectively, this study provides the first detailed imaging of the surface topology of the virus filaments as they form on RSV-infected cells. The imaging data is consistent with the envelopment of the virus filaments by cellular membrane microdomains and the concentration of the virus glycoproteins in other microdomains at specific locations on the virus filaments. Collectively, these data further highlight the complexity of the spatial organisation within the viral envelope during virus assembly.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"614 ","pages":"Article 110732"},"PeriodicalIF":2.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145526708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptome analysis of Crandell Rees Feline Kidney (CRFK) cells infected with Feline calicivirus strain 023 (FCV 023)","authors":"Ruiming Zhang ,&nbsp;Hongwei Zhu ,&nbsp;Guangrong Zhao ,&nbsp;Xiu Xue ,&nbsp;Xin Yu ,&nbsp;Yang Liu ,&nbsp;Jiayu Yu ,&nbsp;Linlin Jiang ,&nbsp;Jianlong Zhang ,&nbsp;Xingxiao Zhang","doi":"10.1016/j.virol.2025.110716","DOIUrl":"10.1016/j.virol.2025.110716","url":null,"abstract":"<div><div><em>Vesivirus felis</em> (Feline calicivirus, FCV) is a widely prevalent viral pathogen in domestic cats, commonly associated with upper respiratory tract infections. However, the transcriptomic responses of host cells to FCV infection remain largely uncharacterized. In this study, an <em>in vitro</em> FCV infection model was established using Crandell-Rees Feline Kidney (CRFK) cells. High-throughput RNA sequencing (RNA-Seq) was performed at 4, 8, and 12 h post-infection (hpi) to investigate the dynamics of host gene expression. Differentially expressed genes (DEGs) were identified and subjected to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) network analyses. A total of 829, 5,432, and 6342 DEGs were detected at 4, 8, and 12 hpi, respectively. Key enriched pathways were associated with metabolic processes, endoplasmic reticulum stress, cytoskeletal remodeling, apoptosis, and immune responses, including the activation of Ubiquitin-mediated proteolysis, Apoptosis signaling, Adherens junctions, and the MAPK, NF-κB, and Toll-like receptor signaling pathways. This study provides a comprehensive transcriptomic landscape of FCV-infected CRFK cells and identifies key molecular mechanisms involved in virus-host interactions, offering potential targets for antiviral therapy.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"613 ","pages":"Article 110716"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145331457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effects of berberine hydrochloride on porcine epidemic diarrhea virus in vitro and in vivo","authors":"Mengkai Cai ,&nbsp;Zhi Wei ,&nbsp;Zhu Wu ,&nbsp;Zaizhong Zhang ,&nbsp;Weilin Xu ,&nbsp;Guihong Zhang ,&nbsp;Zezhong Zheng ,&nbsp;Lang Gong ,&nbsp;Meidi Li","doi":"10.1016/j.virol.2025.110711","DOIUrl":"10.1016/j.virol.2025.110711","url":null,"abstract":"<div><div>Porcine epidemic diarrhea virus (PEDV) causes severe economic losses in swine, necessitating the development of novel antiviral strategies. In this study, we evaluated the inhibitory effects of berberine hydrochloride (BBH) on PEDV in vitro and in vivo. PEDV-infected Vero-E6 cells were treated with BBH, followed by assays for cell viability, viral RNA levels, and protein expression. PEDV-infected piglets were administered BBH, and clinical signs, intestinal morphology, and viral load were assessed. In vitro, BBH (≤120 μM) exhibited low cytotoxicity and inhibited PEDV replication in a dose-dependent manner, markedly reducing viral titers and nucleocapsid (N) protein expression. Time-of-addition assays showed inhibition across multiple stages of the viral life cycle, with pronounced effects on viral attachment and internalization. Mechanistically, BBH suppressed the autophagy marker LC3-II in a dose- and time-dependent manner, and its antiviral activity was partially reversed by the autophagy activator rapamycin, indicating that autophagy suppression contributes to its effect. In PEDV-challenged suckling piglets, oral BBH (40 mg/kg/day) notably improved survival (66.7 % vs. 0 % in controls), alleviated diarrhea, reduced viral shedding in anal swabs, lowered viral load in intestinal tissues (duodenum, jejunum, ileum), and mitigated histopathological damage. Collectively, these results demonstrate that <span>BBH</span> exerts potent anti-PEDV activity through inhibition of viral entry/replication and modulation of autophagy modulation, supporting its potential as an adjunctive therapy against PEDV.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"613 ","pages":"Article 110711"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of baseline humoral immunity on treatment outcomes with molnupiravir in the MOVe-OUT randomized, controlled trial","authors":"Matthew G. Johnson,&nbsp;Julie M. Strizki,&nbsp;David W. Hilbert,&nbsp;Ying Zhang,&nbsp;Patricia Carmelitano,&nbsp;Michelle L. Brown,&nbsp;Dominik J. Wolf,&nbsp;Amanda Paschke,&nbsp;Carisa S. De Anda","doi":"10.1016/j.virol.2025.110710","DOIUrl":"10.1016/j.virol.2025.110710","url":null,"abstract":"<div><h3>Background</h3><div>In the large, randomized, placebo-controlled MOVe-OUT trial, molnupiravir reduced hospitalization/death in unvaccinated, high-risk adults with mild-to-moderate COVID-19. We investigated humoral immune responses and the impact of anti-SARS-CoV-2 antibodies in MOVe-OUT.</div></div><div><h3>Methods</h3><div>All participants prospectively underwent serum testing for total antibodies (combined IgA, IgG, and/or IgM) to the SARS-CoV-2 nucleocapsid protein and neutralizing antibodies to the spike protein. For participants with a positive baseline anti-nucleocapsid test, samples were retrospectively tested for subtype-specific IgM and IgG anti-nucleocapsid antibodies. Residual baseline samples from all participants were also retrospectively tested for anti-spike IgG antibodies. Clinical and virologic outcomes according to baseline antibody status were determined.</div></div><div><h3>Results</h3><div>Fewer participants in the molnupiravir (239/709, 33.7 %) than the placebo arm (259/699, 37.1 %) were positive for any baseline anti–SARS-CoV-2 antibody; anti-spike antibodies only, the specific pattern potentially indicating prior vaccination, were detected in 13.8 % molnupiravir-treated and 15.2 % placebo participants. Molnupiravir reduced the risk of hospitalization/death through day 29 in participants who were seronegative at baseline (molnupiravir 40/470 [8.5 %], placebo 64/440 [14.5 %], 95 % confidence interval for the risk difference: −10.3 % to −1.9 %). Post-baseline, most participants exhibited anti–SARS-CoV-2 antibodies by day 10; by day 29, anti-nucleocapsid antibodies were detected in 93.2 % of molnupiravir-treated and 94.9 % of placebo participants and neutralizing anti-SARS-CoV-2 antibodies in 80.8 % and 82.8 %, respectively.</div></div><div><h3>Conclusion</h3><div>Anti–SARS-CoV-2 antibodies at baseline, more common with placebo, provided protection against poor clinical outcomes. Potentially undisclosed vaccination unlikely impacted the overall trial outcomes. Molnupiravir treatment did not significantly affect development of humoral immunity to SARS-CoV-2 infection. ClinicalTrials.gov: <span><span>NCT04575597</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"613 ","pages":"Article 110710"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145350851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Specificity of Drosophila innubila Nudivirus infection in Drosophila cell culture","authors":"Kent M. Mulkey,&nbsp;Taiye S. Adewumi,&nbsp;Robert L. Unckless","doi":"10.1016/j.virol.2025.110709","DOIUrl":"10.1016/j.virol.2025.110709","url":null,"abstract":"<div><div>Viral host range is an important aspect of both viral biology but also the pragmatic issue of producing viral stocks for experimentation. Host range is important both in terms of the species a virus can infect (taxonomy), and the types of host cells the virus can infect (tropism). Nudiviruses are large DNA viruses that infect several arthropods and are generally poorly studied. Several nudiviruses infect <em>Drosophila</em> species including the <em>Drosophila innubila</em> Nudivirus (DiNV). We aimed to identify cell lines that support the replication of DiNV both for the sake of understanding host range, and to develop a system for large scale production of the virus for infection. We utilized cell lines from the focal host, <em>D. innubila</em>, as well as available cell lines from <em>D. virilis</em> and <em>D. melanogaster</em> and inoculated with both a wild-collected pool of “naïve” virus and a <em>D. innubila</em> cell culture-adapted isolate. We found that virus from wild caught flies infected cells from the 3 cell lines and replicated its genome, but the passage 1 fluids from these infections were unable to reinfect upon introduction to new cells. In contrast, a cell culture-adapted strain of DiNV infected the same <em>Drosophila</em> cells (though relatively poorly in <em>D. melanogaster</em> cells) and produced infectious progeny that infected new cells. Thus, our cell culture-adapted virus developed the ability to infect broadly <em>and</em> produce infectious virions.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"613 ","pages":"Article 110709"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative viral dynamics: Methods for parameter estimation","authors":"Angela Tower ,&nbsp;Katherine Owens ,&nbsp;Shadisadat Esmaeili ,&nbsp;Joshua T. Schiffer ,&nbsp;Daniel B. Reeves ,&nbsp;Elissa J. Schwartz","doi":"10.1016/j.virol.2025.110631","DOIUrl":"10.1016/j.virol.2025.110631","url":null,"abstract":"<div><div>Fitting mathematical models of viral dynamics to serial, quantitative viral load data provides inferences on the mechanisms in virus infection. This process can reveal the speed and magnitude of viral replication, cell proliferation and death, immune responses, and/or treatment efficacy. Viral dynamics modeling involves developing conceptual models, translating them into equations, and applying the appropriate statistical tools to determine the optimal parameters such that the model recapitulates observations from human and animal infections. In this review, we outline the theoretical foundations needed to understand model fitting, parameter estimation, and what it means to achieve a good fit. We provide examples and explain the strengths and limitations of three commonly used model fitting approaches: individual fitting, population mixed effects fitting, and feature fitting. We briefly review fitting algorithms and highlight powerful available computer software packages that can be used for fitting and parameter estimation. We discuss different model types, parameter identifiability, and how future modeling efforts can leverage advances in multi-dimensional data. Finally, we conclude with simple guidelines for choosing the best approach based on available data and scientific questions.</div></div>","PeriodicalId":23666,"journal":{"name":"Virology","volume":"613 ","pages":"Article 110631"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}