Neuropathic pain triggered by chemotherapy poses a significant clinical challenge. Investigating cell type-specific alterations through single-cell transcriptome analysis holds promise in understanding symptom development and pathogenesis. In this study, we performed single nuclei RNA (snRNA) sequencing of dorsal root ganglions (DRG) to explore the molecular mechanism underlying paclitaxel-induced neuropathic pain. Mouse exposed to repeated paclitaxel doses developed persistent pain hypersensitivity lasting at least 21 days. The snRNA sequencing unveiled seven major cell types within DRGs, with neurons further subdivided into 12 distinct subclusters using known markers. Notably, type C low-threshold mechanoreceptors (C_LTMR) exhibited the most pronounced transcriptomic changes post-paclitaxel administration. Differential gene expression and Gene Ontology (GO) analysis highlighted suppressed potassium-related currents, microtubule transport, and mitochondrial functions in C_LTMR following paclitaxel treatment. Pseudo-time analysis uncovered nine distinct states (state 1 to 9) of C_LTMR. State 1 exhibits higher prevalence in paclitaxel-treated mice and altered neurotransmission properties, likely contributing to paclitaxel-induced pain hypersensitivity. Additionally, Camk1d is involved in temperature hyperalgesia in CIPN, a key clinical symptom observed in human patients with CIPN. This comprehensive exploration sheds light on the molecular mechanisms driving paclitaxel-induced neuropathic pain, offering potential avenues for therapeutic intervention.

This study utilizes data from the China Family Panel Studies (CFPS), spanning five rounds of surveys from 2010 to 2018, as a sample. Using the deprivation index to measure income inequality among farmhouseholds, a quasi-natural experiment is established through a "progressive" difference- in-differences (DID) model to empirically examine the impact of livelihood infrastructure on income inequality among farmhouseholds, specifically focusing on the transformation of drinking water. The findings reveal that the transformation of drinking water, as a component of livelihood infrastructure, significantly reduces income inequality among farmhouseholds. The robustness of the research conclusions is validated through a series of tests, including the parallel trends test, the placebo test, and the PSM-DID. Mechanism tests indicate that the transformation of drinking water primarily reduces income inequality among farmhouseholds by enhancing their household health capital and psychological capital. Furthermore, further analysis demonstrates an inverted U-shaped non-linear relationship between the impact of drinking water transformation on income inequality and the per capita net income of households. The impact of drinking water transformation on income inequality is more pronounced among households with land ownership and households where the head engages in farming activities.

This study investigates the role of circular RNAs (circRNAs) in the context of Varicella-Zoster Virus (VZV) lytic infection. We employ two sequencing technologies, short-read sequencing and long-read sequencing, following RNase R treatment on VZV-infected neuroblastoma cells to identify and characterize both cellular and viral circRNAs. Our large scanning analysis identifies and subsequent experiments confirm 200 VZV circRNAs. Moreover, we discover numerous VZV latency-associated transcripts (VLTs)-like circRNAs (circVLTslytic), which contain multiple exons and different isoforms within the same back-splicing breakpoint. To understand the functional significance of these circVLTslytic, we utilize the Bacteria Artificial Chromosome system to disrupt the expression of viral circRNAs in genomic DNA location. We reveal that the sequence flanking circVLTs' 5' splice donor plays a pivotal role as a cis-acting element in the formation of circVLTslytic. The circVLTslytic is dispensable for VZV replication, but the mutation downstream of circVLTslytic exon 5 leads to increased acyclovir sensitivity in VZV infection models. This suggests that circVLTslytic may have a role in modulating the sensitivity to antiviral treatment. The findings shed new insight into the regulation of cellular and viral transcription during VZV lytic infection, emphasizing the intricate interplay between circRNAs and viral processes.

Neuropathic pain triggered by chemotherapy poses a significant clinical challenge. Investigating cell type-specific alterations through single-cell transcriptome analysis holds promise in understanding symptom development and pathogenesis. In this study, we performed single nuclei RNA (snRNA) sequencing of dorsal root ganglions (DRG) to explore the molecular mechanism underlying paclitaxel-induced neuropathic pain. Mouse exposed to repeated paclitaxel doses developed persistent pain hypersensitivity lasting at least 21 days. The snRNA sequencing unveiled seven major cell types within DRGs, with neurons further subdivided into 12 distinct subclusters using known markers. Notably, type C low-threshold mechanoreceptors (C\_LTMR) exhibited the most pronounced transcriptomic changes post-paclitaxel administration. Differential gene expression and Gene Ontology (GO) analysis highlighted suppressed potassium-related currents, microtubule transport, and mitochondrial functions in C\_LTMR following paclitaxel treatment. Meanwhile, Gene Set Enrichment Analysis (GSEA) suggested increased Interleukin 17 production in C\_LTMR after paclitaxel exposure. Pseudo-time analysis uncovered nine distinct states (state 1 to 9) of C\_LTMR. State 1 exhibits higher prevalence in paclitaxel-treated mice and altered neurotransmission properties, likely contributing to paclitaxel-induced pain hypersensitivity. This comprehensive exploration sheds light on the molecular mechanisms driving paclitaxel-induced neuropathic pain, offering potential avenues for therapeutic intervention.### Competing Interest StatementThe authors have declared no competing interest.

Approximately 20% of patients with shingles develop postherpetic neuralgia (PHN). We investigated the role of gut microbiota in shingle- and PHN-related pain. Patients with shingles or PHN exhibited significant alterations in their gut microbiota with microbial markers predicting PHN development among patients with shingles. Functionally, fecal microbiota transplantation from patients with PHN to mice heightened pain sensitivity. Administration of Roseburia intestinalis, a bacterium both depleted in patients with shingles and PHN, alleviated peripheral nerve injury-induced pain in mice. R. intestinalis enhanced vagal neurotransmission to the nucleus tractus solitarius (NTS) to suppress the central amygdala (CeA), a brain region involved in pain perception. R. intestinalis-generated butyrate activated vagal neurons through the receptor, G protein-coupled receptor 41 (GPR41). Vagal knockout of Gpr41 abolished the effects of R. intestinalis on the NTS-CeA circuit and reduced pain behaviors. Overall, we established a microbiota-based model for PHN risk assessment and identified R. intestinalis as a potential pain-alleviating probiotic.

BACKGROUND:In the past decades, extensive research has been conducted to identify new drug targets for the treatment of Herpes simplex virus type 1 (HSV-1) infections. However, the emergence of drug-resistant HSV-1 strains remains a major challenge. This necessitates the identification of new drugs with novel mechanisms of action. Lanatoside C (LanC), a cardiac glycoside (CG) approved by the US Food and Drug Administration (FDA), has demonstrated anticancer and antiviral properties. Nevertheless, its potential as an agent against HSV-1 infections and the underlying mechanism of action are currently unknown.PURPOSE:This study aimed to investigate the antiviral activity of LanC against HSV-1 and elucidate its molecular mechanisms.METHODS:The in vitro antiviral activity of LanC was assessed by examining the levels of viral genes, proteins, and virus titers in HSV-1-infected ARPE-19 and Vero cells. Immunofluorescence (IF) analysis was performed to determine the intracellular distribution of NRF2. Additionally, an in vivo mouse model of HSV-1 infection was developed to evaluate the antiviral activity of LanC, using indicators such as intraepidermal nerve fibers (IENFs) loss and viral gene inhibition.RESULTS:Our findings demonstrate that LanC significantly inhibits HSV-1 replication both in vitro and in vivo. The antiviral effect of LanC is mediated by the perinuclear translocation of NRF2.CONCLUSIONS:LanC exhibits anti-HSV-1 effects in viral infections, which are associated with the intracellular translocation of NRF2. These findings suggest that LanC has the potential to serve as a novel NRF2 modulator in the treatment of viral diseases.

Herpetic-related neuralgia (HN) caused by varicella-zoster virus (VZV) infection is one of the most typical and common neuropathic pain in the clinic. However, the potential mechanisms and therapeutic approaches for the prevention and treatment of HN are still unclear. This study aims to provide a comprehensive understanding of the molecular mechanisms and potential therapeutic targets of HN. We used an HSV-1 infection-induced HN mouse model and screened the differentially expressed genes (DEGs) in the DRG and spinal cord using an RNAseq technique. Moreover, bioinformatics methods were used to figure out the signaling pathways and expression regulation patterns of the DEGs enriched. In addition, quantitative real-time RT-PCR and western blot were carried out to further confirm the expression of DEGs. HSV-1 inoculation in mice resulted in mechanical allodynia, thermal hyperalgesia, and cold allodynia, following the infection of HSV-1 in both DRG and spinal cord. Besides, HSV-1 inoculation induced an up-regulation of ATF3, CGRP, and GAL in DRG and activation of astrocytes and microglia in the spinal cord. Moreover, 639 genes were upregulated, 249 genes were downregulated in DRG, whereas 534 genes were upregulated and 12 genes were downregulated in the spinal cord of mice 7 days after HSV-1 inoculation. GO and KEGG enrichment analysis suggested that immune responses and cytokine-cytokine receptor interaction are involved in DRG and spinal cord neurons in mice after HSV-1 infection. In addition, CCL5 and its receptor CCR5 were significantly upregulated in DRG and spinal cord upon HSV-1 infection in mice. And blockade of CCR5 exhibited a significant analgesic effect and suppressed the upregulation of inflammatory cytokines in DRG and spinal cord induced by HSV-1 infection in mice. HSV-1 infection-induced allodynia and hyperalgesia in mice through dysregulation of immune response and cytokine-cytokine receptor interaction mechanism. Blockade of CCR5 alleviated allodynia and hyperalgesia probably through the suppression of inflammatory cytokines. Therefore, CCR5 could be a therapeutic target for the alleviation of HSV-1 infection-induced HN.

带状疱疹后神经痛(postherpetic neuralgia,PHN)是由水痘-带状疱疹病毒(varicella zoster virus,VZV)感染所引起的常见并发症,多见于老年人和免疫功能低下者,严重影响病人的身心健康和生活质量.尚未明确的致病机制让PHN治疗效果欠佳,缺乏有效模拟PHN的动物模型更让PHN发病机制的研究止步不前.本文主要综述目前PHN动物模型构建的研究进展,重点介绍由VZV与单纯疱疹病毒1型(herpes simplex virus 1,HSV-1)诱导的PHN动物模型的建立方法和疼痛行为学表现.旨在比较现有PHN动物模型的研究概况,为进一步阐明PHN致病机制提供有效的研究工具,同时也为PHN动物模型的选择和改良提供参考.

Circular RNA (circRNA), a newly identified important component of the transcriptome, is formed by covalently bonded single-stranded RNA through back splicing (1) or other unknown mechanisms. It has been reported that circRNA plays important biological functions including microRNA (miRNA) sponges, parental gene expression regulators, and the translation template (2–5). Viral circRNAs have been recently identified from cells infected with different DNA viruses, such as Epstein-Barr virus (EBV) (6, 7), Kaposi’s sarcoma-associated herpesvirus (KSHV) (8), human papillomaviruses (HPVs) (9), and human cytomegalovirus (HCMV) (10). Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARSCoV-2), has become a worldwide pandemic and poses a high threat to global health. We unprecedentedly identified viral circRNAs from cells that were infected by different coronaviruses, including SARS-CoV-2, SARS-CoV, and Middle East respiratory syndrome (MERS)-CoV (11). However, the biogenesis of circRNAs from coronavirus is still unknown. Murine hepatitis virus (MHV), a betacoronavirus, has been used in a mouse model to study human coronaviruses (12). Gribble et al. (13) reported that an RNA proofreading exoribonuclease, nsp14-ExoN, encoded by the MHV genome contributes to RNA recombination. In their study, deep transcriptome sequencing (RNA-seq) was performed on murine DBT cells infected either with wild-type MHV (MHV-WT) or with nsp14-ExoN inactive mutant MHV (MHV-ExoN2) (Table 1). We hypothesized that nsp14-ExoN may mediate the biogenesis of MHV circRNAs. To systematically test this hypothesis, we analyzed RNA from MHV-WTor MHV-ExoN2-infected cells and virioncontaining supernatants. Currently used methods of identifying circRNA are established on the examination of the back-splicing junction (BSJ) (14). ViReMa is one such tool that can quickly and sensitively identify viral RNA splicing junctions, including forward-splicing junctions (FSJs) and BSJs from next-generation sequencing data (15). Therefore, we applied ViReMa to assess the abundance of MHV-derived BSJs and FSJs and mapped the breakpoints to their respective genomic locations (Fig. 1A to D). In summary, there are two significant hot spots of FSJs and BSJs: (i) distant splicing between the 39 and the 59 ends of the genome corresponding to the N gene and the untranslated region (UTR) and (ii) local splicing in regions of MHV. The statistical analysis of genome coverage shows that about 23,043,062 to 56,476,922 nucleotides of each sample were mapped to the MHV genome (Table 1), suggesting that the numbers of MHV RNA molecules in the samples are comparable. To assess the effect of nsp14-ExoN loss of function, we calculated the junction Editor Haidong Gu, Wayne State University Copyright © 2023 Yang et al. This is an openaccess article distributed under the terms of the Creative Commons Attribution 4.0 International license. Address correspondence to Qiyi Tang, qiyi.tang@howard.edu, or Hua Zhu, hua.zhu@rutgers.edu. The authors declare no conflict of interest.

Human cytomegalovirus (HCMV) is a widespread pathogen that poses significant risks to immunocompromised individuals. Its genome spans over 230 kbp and potentially encodes over 200 open-reading frames. The HCMV transcriptome consists of various types of RNAs, including messenger RNAs (mRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), with emerging insights into their biological functions. HCMV mRNAs are involved in crucial viral processes, such as viral replication, transcription, and translation regulation, as well as immune modulation and other effects on host cells. Additionally, four lncRNAs (RNA1.2, RNA2.7, RNA4.9, and RNA5.0) have been identified in HCMV, which play important roles in lytic replication like bypassing acute antiviral responses, promoting cell movement and viral spread, and maintaining HCMV latency. CircRNAs have gained attention for their important and diverse biological functions, including association with different diseases, acting as microRNA sponges, regulating parental gene expression, and serving as translation templates. Remarkably, HCMV encodes miRNAs which play critical roles in silencing human genes and other functions. This review gives an overview of human cytomegalovirus and current research on the HCMV transcriptome during lytic and latent infection.

This review mainly introduced the research progresses in the establishment of postherpetic neuralgia (PHN) animal model at home and abroad, with emphasis on the establishment methods and pain behaviors of PHN animal model induced by varicella zoster virus (VZV) or herpes simplex virus 1 (HSV1). The aims of this paper were to compare the current research status of PHN animal model, and to provide effective research tool for further elucidating the pathogenic mechanism of PHN, and reference for selecting and improving the PHN animal model.

Chemotherapy-induced peripheral neuropathy (CIPN) is the most common side-effect of anti-cancer therapy. To date, there are no clinically effective analgesics that could prevent and treat CIPN. However, the exact pathogenesis of CIPN is still unclear. In the present study, we use the paclitaxel-induced peripheral neuropathy (PIPN) model, aiming to better understand the transcriptomic level of the Dorsal root ganglia (DRG) neurons in rats with PIPN. mRNA from each DRG sample was reverse transcribed to cDNA and sequenced using next-generation high throughput sequencing technology. Quantitative RT-PCR verification was used to confirm the identified Differentially expressed genes (DEGs) in the DRG of PIPN rats. RNAseq results have identified 384 DEGs (adjusted P-value < 0.05; fold change ≥ 2) in the DRG of rats 14 days after paclitaxel injection in total, including 97 up-regulated genes, and 287 down-regulated genes. GO analysis revealed that these DEGs were majorly involved in neuropeptide activity, chemokine receptor activity, defense response, and inflammatory response. Kyoto Encyclopedia of Gene and Genomes analysis showed that neuroactive ligand-receptor interaction and cytokine-cytokine receptor interaction were involved in sensory neurons of rats with PIPN. Besides, comparison analysis identified that 11 DEGs in the PIPN model are shared with either inflammatory pain (Ces1d, Cfd, Retn, and Fam150b) or neuropathic pain (Atf3, Csrp3, Ecel1, Gal, Sprr1a, Tgm1, and Vip). Quantitative RT-PCR results also confirmed the validation of the RNAseq data. These results suggested that neuroactive ligand-receptor interaction and cytokine-cytokine receptor interaction are majorly involved in sensory neurons of rats with PIPN. Immune, inflammatory responses and neuron functional changes are the major pathogenesis of PIPN. Paclitaxel-induced peripheral neuropathy has shared characteristics with both inflammatory pain and neuropathic pain.

Chemotherapy-induced peripheral neuropathy is one of the most common side effects of anticancer therapy. It is anticipated that chemotherapies with different mechanisms of action may affect somatosensory neurons differently. This study aimed to explore similar and differential etiologies of oxaliplatin- and paclitaxel-induced neuropathy by comparing the transcriptomes of dorsal root ganglia (DRGs). We retrieved our previously published transcriptome data of DRGs extracted from vehicle-, oxaliplatin- and paclitaxel-treated rats (GSE160543), to analyze in parallel the differentially expressed genes (DEGs) and Gene ontology (GO) terms enrichment. We found that both oxaliplatin and paclitaxel treatments consistently produced mechanical allodynia, thermal hyperalgesia, and cold hyperalgesia in rats. Compared to vehicle, 320 and 150 DEGs were identified after oxaliplatin and paclitaxel treatment, respectively. Only 17 DEGs were commonly dysregulated by the two reagents. Activating transcription factor 3 (Atf3), a marker of nerve injury, was elevated only after paclitaxel treatment. GO analysis suggested that paclitaxel treatment was associated with neuronal changes characterized by numerous terms that are related to synaptic transmission, while oxaliplatin was more likely to affect dividing cells (e.g., the glia) and neuroinflammation. Notably, 29 biological processes GO terms were commonly enriched in response to both drugs. However, 28 out of 29 terms were oppositely modulated. This study suggests that distinct mechanisms underly paclitaxel- and oxaliplatin-induced neuropathy. Paclitaxel might directly affect somatosensory neurons while oxaliplatin primarily targets dividing cells and immune cells.

Background Induced by varicella zoster virus (VZV), postherpetic neuralgia (PHN) is one of the common complications of herpes zoster (HZ) with refractory pain. Animal models play pivotal roles in disclosing the pain mechanisms and developing effective treatments. However, only a few rodent models focus on the VZV-associated pain and PHN. Objective To summarize the establishment and characteristics of popular PHN rodent models, thus offer bases for the selection and improvement of PHN models. Design In this review, we retrospect two promising PHN rodent models, VZV-induced PHN model and HSV1-induced PHN model in terms of pain-related evaluations, their contributions to PHN pathogenesis and pharmacology. Results Significant difference of two PHN models is the probability of virus proliferation; 2) Most commonly used pain evaluation of PHN model is mechanical allodynia, but pain-induced anxiety and other behaviours are worth noting; 3) From current PHN models, pain mechanisms involve changes in virus gene and host gene expression, neuroimmune–glia interactions and ion channels; 4) antiviral drugs and classical analgesics serve more on the acute stage of herpetic pain. Conclusions Different PHN models assessed by various pain evaluations combine to fulfil more comprehensive understanding of PHN.

信息不对称理论在经济理论研究、指导经济运行和生活实际应用方面具有重大意义.基于高职学生学习理解信息不对称,理论不到位、不透彻和难以应用的三大难题,文章以信息不对称教学实践为案例,试图帮助学生和教学工作者更为深刻了解、认识信息不对称理论及其在教学实践、生活实践中的应用,以期帮助学生形成自学能力、编织知识网络、重塑知识库以及提高经济理论实际应用能力.

Abstract Objective. Herpetic-related neuralgia (HN) caused by varicella-zoster virus (VZV) infection is one of the most typical and common neuropathic pain in the clinic. However, due to the lack of an animal model to simulate HN, the potential mechanisms and therapeutic approaches for the prevention and treatment of HN are still unclear. This study aims to provide a comprehensive understanding of the molecular mechanisms and potential therapeutic targets of HN. Methods. We used an HSV-1 infection-induced HN mouse model and screened the differentially expressed genes (DEGs) in the DRG and spinal cord using an RNAseq technique. Moreover, the bioinformatics methods were used to figure out the signaling pathways and expression regulation patterns of the DEGs enriched. In addition, quantitative real-time RT-PCR and western blot was carried out to further confirm the expression of DEGs. Results. HSV-1 inoculation in mice resulted in mechanical allodynia, thermal hyperalgesia, and cold allodynia, following the infection of HSV-1 in both DRG and spinal cord. Besides, HSV-1 inoculation induced an up-regulation of ATF3, CGRP, and GAL in DRG and activation of astrocytes and microglia in the spinal cord. Moreover, 639 genes were up-regulated, 249 genes were down-regulated in DRG, whereas 534 genes were up-regulated, and 12 genes were down-regulated in the spinal cord of mice 7 days after HSV-1 inoculation. GO and KEGG enrichment analysis suggested that immune responses and cytokine-cytokine receptor interaction are involved in DRG and spinal cord neurons in mice after HSV-1 infection. In addition, CCL5 and its receptor CCR5 were significantly up-regulated in DRG and spinal cord upon HSV-1 infection in mice. And blockade of CCR5 exhibited a significant analgesic effect and suppressed the up-regulation of inflammatory cytokines in DRG and spinal cord induced by HSV-1 infection in mice. Conclusions. We reported a reliable HN model with HSV-1 infection-induced allodynia and hyperalgesia in mice through dysregulation of immune response and cytokine-cytokine receptor interaction mechanism.

HCMV infects 40% to 100% of the human population globally and may be a life-threatening pathogen in immunocompromised individuals. CircRNA is a family of unique RNA that is the most newly found and remains unknown in many aspects.

数形结合法是数学领域运用几何方法解决代数问题的重要方法.经济学教学实践中一些结论往往需要复杂的数学知识,这会加大高职学生学习难度.尝试运用数形结合方法分析经济学的经典消费者结论,回答需求曲线为什么是直线、弹性临界值为什么为1以及运用弹性解释"谷贱伤农"的合理性这三个教学知识点,帮助学生重塑消费者需求理论框架.通过运用该方法,课堂教学有效地帮助学生理解经济学基本概念及理论,培养学生运用数形结合的方法解决现实经济问题的能力,进而提高学生学习兴趣,达到良好教学效果.

BACKGROUND:Postherpetic neuralgia (PHN) is a common complication after herpes zoster infection. While conventional dorsal column temporary spinal cord stimulation (tSCS) has been shown as an effective treatment option for this pain condition, recent data suggests ipsilateral temporary spinal nerve root stimulation (tSNRS) as a safe alternative for treating PHN. However, there is no direct clinical comparison between the newer tSNRS and the traditional tSCS.OBJECTIVES:The current retrospective study aimed to describe the technical factors and the therapeutic efficacy of tSNR for patients with unilateral PHN and to compare these parameters with those treated with tSCS.STUDY DESIGN:Retrospective cohort study.SETTING:Single-center study in a large academic hospital.METHODS:One hundred sixty patients with unilateral PHN who underwent 7-14 days of tSCS (n = 109) or tSNRS (n = 51) treatment were included. Technical factors between the 2 groups, such as procedure time, radiation dosage, number of electrodes used, number of stimulation parameter adjustments, and average cost, were compared. Treatment efficacy, measured by analgesic coverage, pain visual analog scale (VAS), total analgesic agent consumption, Pittsburgh sleep quality index (PSQI), and physical and mental quality of life, were also compared between the 2 groups at baseline, post-procedure, and 3 months after stimulation treatment.RESULTS:Patients who underwent tSNRS reported significant improvement in pain level, sleep quality, and overall quality of life immediately postprocedure and during the follow-up period. This therapeutic effect was comparable to the tSCS group. Moreover, tSNRS achieved this therapeutic effect with a fewer number of implanted electrodes and stimulation adjustments than tSCS. The precision and consistency of the tSNRS technique were associated with a significant overall lower cost, a shorter procedure time, and less intraoperative radiation exposure in the tSNRS group than in those who received tSCS.LIMITATIONS:The current retrospective cohort study was limited by its relatively short follow-up period. Also, the selection of stimulation techniques was not randomized.CONCLUSIONS:While tSNRS provides similar therapeutic efficacy compared to tSCS for patients with unilateral PHN; it offers several technical advantages. These advantages include shorter procedure time, less radiation exposure, fewer implanted electrodes, more effective stimulation, and lower overall cost.

目的 探讨毛花苷丙体外抗单纯疱疹病毒Ⅰ型(HSV-1)的作用.方法 采用CCK8法计算毛花昔丙的半数有毒浓度(TC50).细胞病变效应(CPE)和病毒滴度评价毛花苷丙的抗HSV-1作用.实时荧光定量PCR(RT-qPCR)和蛋白免疫印迹法探究毛花苷丙对HSV-1基因组转录、蛋白质合成的作用.结果0.1 μmol·L-1(TC50=0.32 μmol·L-1)毛花苷丙可显著抑制HSV-1诱导的CPE.病毒滴度随着毛花苷丙处理浓度的增加显著下降(P＜0.05),与CPE趋势一致.RT-qPCR和Western blot结果显示,HSV-1即刻早期基因(IE)ICP0、早期基因(E)UL23、潜伏相关基因LAT、糖蛋白G编码基因US4和病毒蛋白ICP0的表达均能被毛花昔丙抑制(P＜0.05),且抑制呈剂量依赖性.毛花昔丙预处理可以抑制HSV-1诱导的CPE,且抑制呈剂量依赖性.结论 毛花昔丙通过抑制HSV-1基因组转录和蛋白质合成抵抗HSV-1感染,可以作为抗HSV-1的新型候选药物.