Antiviral research最新文献

{"title":"Research progress of vimentin in viral infections","authors":"Jiawei Zheng ,&nbsp;Xue Li ,&nbsp;Guoqing Zhang ,&nbsp;Ying Ren ,&nbsp;Linzhu Ren","doi":"10.1016/j.antiviral.2025.106121","DOIUrl":"10.1016/j.antiviral.2025.106121","url":null,"abstract":"<div><div>Vimentin, a type III intermediate filament protein, has become a focal point in the research of viral infections. It participates in multiple crucial processes during the viral life cycle and the host's antiviral response. During viral entry, it may function as a receptor or co-receptor and interact with viral entry proteins, also influencing endocytic pathways. Furthermore, vimentin engages with replication complexes and modulates the intracellular environment in viral replication. Moreover, vimentin plays significant roles in immune responses and inflammatory reactions during viral infections. This review thoroughly analyzes the recent progress in understanding vimentin's functions during viral infections, covering aspects such as viral entry, replication, and the immune response to achieve a cohesive comprehension of the underlying mechanisms. The antiviral strategies based on vimentin are also discussed, aiming to promote the development of more effective preventive and treatment strategies for viral diseases.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106121"},"PeriodicalIF":4.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The efficiency of high-throughput screening (HTS) and in-silico data analysis during medical emergencies: Identification of effective antiviral 3CLpro inhibitors","authors":"Debora Zian ,&nbsp;Daniela Iaconis ,&nbsp;Simone Nenci ,&nbsp;Alessandra Crusco ,&nbsp;Sanjeevani Tawde ,&nbsp;Mariangela Sodano ,&nbsp;Rocco Vitalone ,&nbsp;Ameya Raje ,&nbsp;Martina Palamini ,&nbsp;Daniele Carettoni ,&nbsp;Angela Molteni ,&nbsp;Candida Manelfi ,&nbsp;Valerio Tazzari ,&nbsp;Andrea Rosario Beccari ,&nbsp;Paolo Malune ,&nbsp;Stefania Maloccu ,&nbsp;Annalaura Paulis ,&nbsp;Angela Corona ,&nbsp;Salvatore Nieddu ,&nbsp;Silvano Coletti ,&nbsp;MariaPia Catalani","doi":"10.1016/j.antiviral.2025.106119","DOIUrl":"10.1016/j.antiviral.2025.106119","url":null,"abstract":"<div><div>The COVID-19 pandemic highlighted the importance of accelerating the drug discovery process. The 3-chymotrypsin-like protease (3CLpro) is a critical enzyme in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral replication process and was quickly identified as a prime target for drug development. This study leverages High-Throughput Screening (HTS) to identify novel 3CLpro inhibitors. We screened a different library of 325,000 compounds, leading to the discovery of two new chemical scaffolds with selective inhibitory activity against 3CLpro. <em>In-silico</em> analysis and further experimental validation, elucidated the binding modes and mechanisms of action, revealing a covalent inhibitor targeting the catalytic pocket and two allosteric inhibitors affecting the monomer/dimer equilibrium of 3CLpro. The identified compounds demonstrated significant antiviral activity in vitro, reducing SARS-CoV-2 replication in VeroE6 and Calu-3 cell lines. This study highlights the potential of combining HTS and computational approaches to accelerate the discovery of effective antiviral agents, suggesting a workflow to support the research and the design of effective therapeutic strategies.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"237 ","pages":"Article 106119"},"PeriodicalIF":4.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of entecavir-induced reduction of HBV DNA integration","authors":"Danny Ka-Ho Wong ,&nbsp;Ning Chow ,&nbsp;Hoi Tang Ma ,&nbsp;Ka Yan Wong ,&nbsp;Lung-Yi Mak ,&nbsp;Wai-Kay Seto ,&nbsp;Man-Fung Yuen","doi":"10.1016/j.antiviral.2025.106120","DOIUrl":"10.1016/j.antiviral.2025.106120","url":null,"abstract":"<div><div>Nucleos(t)ide analogues (NUC) treatment can reduce the extent of HBV DNA integration in chronic hepatitis B (CHB) patients. However, the mechanism by which NUC reduces HBV integration is unclear. This study investigated the effects of entecavir (ETV), one of the commonly used NUC, on cells with HBV integration. Full genome-length HBV DNA was inserted into HepG2 cell genome using the sleeping beauty transposon system. The resulting cells, named HepG2/SB/HBV, was subjected to ETV treatment. In ETV-treated HepG2/SB/HBV, intracellular HBV DNA was reduced by 2-fold. When treated with ETV, HepG2/SB/HBV had an impaired cell survival (25% reduction in cell proliferation rate when compared with untreated cells; p = 0.043). The median integration frequency in untreated HepG2/SB/HBV was 16 integration sites per 10⁵ cells, which was reduced to 14.8 integration sites per 10⁵ cells when treated with ETV. Analysis of the expression of apoptosis and mitosis markers showed that ETV-treated HepG2/SB/HBV had a reduced expression of mitosis markers phospho-cell division control-2 (p-cdc-2) and phospho-histone H3 (p-histone H3), but that of the apoptotic markers [Poly-ADP-ribose-polymerase] (PARP) and caspase-3 were not affected. In conclusion, ETV suppressed cell proliferation of hepatoma cells with HBV integration via interference of mitosis and reduced expression of p-histone H3, thereby reducing the number of HBV-integrated hepatocytes. This may be the mechanism by which HBV integration is reduced in CHB patients who received ETV therapy.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"237 ","pages":"Article 106120"},"PeriodicalIF":4.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M49L and other drug resistance mutations emerging in individuals after administration of ensitrelvir in Japanese clinical settings","authors":"Akira Inoue ,&nbsp;Takaya Ichikawa ,&nbsp;Daiki Wada ,&nbsp;Shuhei Maruyama ,&nbsp;Haruka Shimazu ,&nbsp;Masami Kashihara ,&nbsp;Kazuyuki Okuda ,&nbsp;Fukuki Saito ,&nbsp;Takasuke Fukuhara ,&nbsp;Yasushi Nakamori","doi":"10.1016/j.antiviral.2025.106118","DOIUrl":"10.1016/j.antiviral.2025.106118","url":null,"abstract":"<div><div>Recent in-vitro and in-vivo studies and analysis of genomic information registered in GISAID have raised concerns about drug resistance mutations such as M49L after treatment with the 3C-like protease inhibitor ensitrelvir. The aim of this study was to identify resistance gene mutations to 3C-like protease inhibitors, including M49L mutations, in Japanese clinical settings. Genomic analysis of samples from our hospital admissions showed M49L mutations associated with ensitrelvir treatment in three cases and M49L mutation unrelated to ensitrelvir treatment in three cases. In a study of cases with persistent infection or rebound in viral load after 5 days of ensitrelvir treatment, 10 of 16 patients had M49L mutations and 5 had M49I mutations. Resistance gene mutations following treatment with ensitrelvir were shown to emerge even within individual patients who were not immunocompromised. In a study of persistent SARS-CoV-2 infection in severely immunocompromised patients, various drug resistance mutations emerged, with the M49L mutation especially showing a tendency to be a majority mutation. The current status of drug resistance mutations occurring in individuals following administration of ensitrelvir in Japanese clinical settings was clinically investigated for the first time. Considering that the barrier to resistance to ensitrelvir is lower than that to other antiviral drugs and that M49L is a unique mutation that occurs quickly, tends to become a majority mutation, and is maintained thereafter through its ability to replicate, the spread of strains that have acquired ensitrelvir resistance should be closely monitored.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106118"},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recombinant Pichinde reporter virus as a safe and suitable surrogate for high-throughput antiviral screening against highly pathogenic arenaviruses","authors":"Carolina Q. Sacramento ,&nbsp;Ryan Bott ,&nbsp;Qinfeng Huang ,&nbsp;Brett Eaton ,&nbsp;Elena Postnikova ,&nbsp;Ahmad J. Sabir ,&nbsp;Malaika D. Argade ,&nbsp;Kiira Ratia ,&nbsp;Manu Anantpadma ,&nbsp;Paul R. Carlier ,&nbsp;Hinh Ly ,&nbsp;Yuying Liang ,&nbsp;Lijun Rong","doi":"10.1016/j.antiviral.2025.106117","DOIUrl":"10.1016/j.antiviral.2025.106117","url":null,"abstract":"<div><div>Several arenaviruses, such as the Old World (OW) Lassa virus (LASV) and the New World (NW) Junin virus (JUNV), can cause severe and lethal viral hemorrhagic fevers in humans. Currently, no vaccines or specific antiviral therapies are FDA-approved for treating arenavirus infections. One major challenge for the development of new therapeutic candidates against these highly pathogenic viruses is that they are BSL-3/4 pathogens that need to be handled in high biocontainment laboratories. In this work, a recombinant non-pathogenic New World arenavirus, Pichinde virus (rPICV), was used for the development of a high-throughput screening (HTS) assay in the BSL-2 laboratory for the screening and identification of small molecule inhibitors against arenaviruses. The rPICV is a replication-competent virus expressing the firefly luciferase reporter gene in the infected cells proportionally to the infection rate. rPICV infection was optimized for an automated HTS in 384-well format with robust Z′ scores, high signal-to-background ratios, and low intrinsic variance. Screening an established library allowed for the identification of five top hit compounds, which included ribavirin, a known inhibitor of arenaviral RNA synthesis, showing good potency and selectivity in inhibiting rPICV replication. The antiviral activity of the top hit compounds was further validated against another recombinant arenavirus, the OW lymphocytic choriomeningitis virus (rLCMV) and against laboratory strains of LASV (Josiah) and JUNV (Romero). The use of rPICV in the HTS-based antiviral assay under BSL-2 condition has proven to be safe and suitable for the identification of broad-spectrum small molecule inhibitors against highly pathogenic arenaviruses.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106117"},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Screening of botanical drugs reveals the potential anti-human adenovirus activity of berberine","authors":"Junyuan Cao ,&nbsp;Hao Zhang ,&nbsp;Jixiang Zhang ,&nbsp;Jinlin Wang ,&nbsp;Chen Li ,&nbsp;Jin Ma ,&nbsp;Zhengyu Ye ,&nbsp;Yunting Zheng ,&nbsp;Hong Liu ,&nbsp;Gengfu Xiao ,&nbsp;Wenhao Dai ,&nbsp;Leike Zhang","doi":"10.1016/j.antiviral.2025.106105","DOIUrl":"10.1016/j.antiviral.2025.106105","url":null,"abstract":"<div><div>Human adenovirus (HAdV) is a significant viral pathogen that causes severe acute respiratory infections (SARIs) in children and immunocompromised patients. Currently, no specific treatment options are available for HAdV infections. This study used a green fluorescence protein-based, high-throughput screening (HTS) assay on a botanical drug library containing 3697 botanical compounds to identify agents that could inhibit HAdV. Four compounds with anti-HAdV-C5 activity in the low-micromolar range were identified and inhibited other wild-type HAdVs known to cause SARIs. Among these compounds, 13-methylberberine chloride presented the highest select index values. Berberine is a commercially available natural product-derived isoquinoline alkaloid with multiple pharmacological effects and is widely used in Asian countries. We systematically evaluated the anti-HAdV activity of six berberine-derived compounds in vitro and performed a time-of-drug-addition assay to explore their antiviral modes of action. Mechanistic studies revealed that berberine and its analogs inhibit HAdV replication by downregulating the MAPK signaling pathway, particularly ERK activation, which is crucial for viral replication and progeny production. Our findings suggest that berberine is a promising candidate for the development of anti-HAdV therapies.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"237 ","pages":"Article 106105"},"PeriodicalIF":4.5,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defining diabetic mouse as a highly susceptible preclinical model for monkeypox virus infection","authors":"Chao Shang ,&nbsp;Minghua Chen ,&nbsp;Yan Liu ,&nbsp;Xiao Li ,&nbsp;Yiquan Li","doi":"10.1016/j.antiviral.2025.106112","DOIUrl":"10.1016/j.antiviral.2025.106112","url":null,"abstract":"","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106112"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of nucleoside analogs against Wetland virus infection","authors":"Rui Wang ,&nbsp;Xi Wang ,&nbsp;Jianzhong Zhu ,&nbsp;Hao Li ,&nbsp;Wei Liu","doi":"10.1016/j.antiviral.2025.106114","DOIUrl":"10.1016/j.antiviral.2025.106114","url":null,"abstract":"<div><div>Wetland virus (WELV), a newly identified Orthonairovirus phylogenetically related to the Crimean–Congo hemorrhagic fever virus (CCHFV), has recently been shown to cause human infections. A portion of patients infected with WELV usually present with febrile diseases, accompanied by hemorrhagic and neurological symptoms. Currently, there are no reports demonstrating effective therapeutic drugs for the treatment of WELV. In this study, we evaluated the anti-WELV efficacy of five nucleoside analogs: four clinically approved drugs-ribavirin, remdesivir, molnupiravir, and sofosbuvir; and a clinical candidate 4′-fluorouridine. Ribavirin and 4′-fluorouridine strongly inhibited WELV replication <em>in vitro</em>. Remdesivir and molnupiravir showed limited antiviral activity against WELV in Huh7 cells but not in Vero cells, while sofosbuvir did not exhibit inhibitory effects. Utilizing a lethal immunocompetent mouse model of WELV infection, we found that oral administration of relatively low doses of ribavirin (25 mg/kg/day) or 4′-fluorouridine (2.5 mg/kg/day) significantly reduced the mortality of WELV-infected mice by decreasing viral titers in tissues and alleviating pathological damage. This treatment strategy retained significant efficacy even when initiated 2–4 days after infection. Additionally, we identified mutations G3033R and A3756V in the C-terminal region of the WELV L protein, which may be associated with viral resistance to ribavirin and 4′-fluorouridine. This study revealed varying degrees of anti-WELV efficacy among different nucleoside analogs and identified 4′-fluorouridine as a promising therapeutic candidate and ribavirin as a priority treatment option for WELV infection.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106114"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"25R,26-hydroxycholesterol and an oxysterol synthetic analog inhibit Varicella zoster Virus replication","authors":"Andrea Civra ,&nbsp;Matteo Costantino ,&nbsp;Domiziana Porporato ,&nbsp;Rachele Francese ,&nbsp;Manuela Donalisio ,&nbsp;Giuseppe Poli ,&nbsp;Maura Marinozzi ,&nbsp;David Lembo","doi":"10.1016/j.antiviral.2025.106113","DOIUrl":"10.1016/j.antiviral.2025.106113","url":null,"abstract":"<div><div>Varicella-zoster Virus (VZV) is a relevant pathogen belonging to the <em>herpesviridiae</em> family. Primary VZV infection causes chickenpox, and results in latent infection of sensory ganglia. Later in life, VZV can reactivate causing herpes zoster (HZ), which can be associated with severe complications in immunocompromised individuals. Currently, the available antivirals used to treat VZV infection target the DNA replication stage; however, resistance to these drugs has been reported in both immunocompromised and immunocompetent patients. For this reason, the identification of new antiviral molecules against VZV infection is a priority. Recently our research group demonstrated that the endogenous oxysterol 25R,26-hydroxycholesterol (25R,26OHC, more commonly named 27-hydroxycholesterol) and an oxysterol synthetic analog named PFM067 inhibit herpes simplex virus (HSV) replication. In this study we explored the antiviral activity of 25-hydroxycholesterol (25OHC), 25R,26OHC, and PFM067 against VZV. We demonstrated that 25R,26OHC and PFM067 exert antiviral activity against VZV with an EC₅₀ in the low micromolar range and are able to significantly reduce the area of the viral plaques. Moreover, 25R,26OHC and PFM067 can inhibit the egress of viral glycoprotein gE from the cis-Golgi compartment, similarly to what demonstrated by our group for HSV-2. Additionally, we show that 25R,26OHC and PFM067 act synergistically when used in combination with acyclovir (ACV). The promising antiviral activity of 25R,26OHC and PFM067, along with their different mechanism of action compared to ACV, makes these molecules suitable candidates for further investigation of the molecular target of oxysterols.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106113"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antiviral mechanisms and preclinical evaluation of amantadine analogs that continue to inhibit influenza A viruses with M2S31N-based drug resistance","authors":"Ian Tietjen ,&nbsp;Daniel C. Kwan ,&nbsp;Annett Petrich ,&nbsp;Roland Zell ,&nbsp;Ivi Theodosia Antoniadou ,&nbsp;Agni Gavriilidou ,&nbsp;Christina Tzitzoglaki ,&nbsp;Michail Rallis ,&nbsp;David Fedida ,&nbsp;Francesc X. Sureda ,&nbsp;Cato Mestdagh ,&nbsp;Lieve Naesens ,&nbsp;Salvatore Chiantia ,&nbsp;F. Brent Johnson ,&nbsp;Antonios Kolocouris","doi":"10.1016/j.antiviral.2025.106104","DOIUrl":"10.1016/j.antiviral.2025.106104","url":null,"abstract":"<div><div>To better manage seasonal and pandemic influenza infections, new drugs are needed with enhanced activity against amantadine- and rimantadine-resistant influenza A virus (IAV) strains containing the S31N variant of the viral M2 ion channel (M2^S31N). Here we tested 36 amantadine analogs against a panel of viruses containing either M2^S31N or the parental, M2 S31 wild-type variant (M2^WT). We found that several analogs, primarily those with sizeable lipophilic adducts, inhibited up to three M2^S31N-containing viruses with activities at least 5-fold lower than rimantadine, without inhibiting M2^S31N proton currents or modulating endosomal pH. While M2^WT viruses in passaging studies rapidly gained resistance to these analogs through the established M2 mutations V27A and/or A30T, resistance development was markedly slower for M2^S31N viruses and did not associate with additional M2 mutations. Instead, a subset of analogs, exemplified by 2-propyl-2-adamantanamine (<strong>38</strong>), but not 2-(1-adamantyl)piperidine (<strong>26</strong>), spiro[adamantane-2,2′-pyrrolidine] (<strong>49</strong>), or spiro[adamantane-2,2′-piperidine] (<strong>60</strong>), inhibited cellular entry of infectious IAV following pre-treatment and/or H1N1 pseudovirus entry. Conversely, an overlapping subset of the most lipophilic analogs including compounds <strong>26</strong>, <strong>49</strong>, <strong>60</strong>, and others, disrupted viral M2-M1 protein colocalization required for intracellular viral assembly and budding. Finally, a pilot toxicity study in mice demonstrated that <strong>38</strong> and <strong>49</strong> were tolerated at 30 mg/kg. Together, these results indicate that amantadine analogs act on multiple, complementary mechanisms to inhibit replication of M2^S31N viruses.</div></div>","PeriodicalId":8259,"journal":{"name":"Antiviral research","volume":"236 ","pages":"Article 106104"},"PeriodicalIF":4.5,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}