Human cytomegalovirus (HCMV) profoundly reprograms host transcription and RNA metabolism, yet its impact on transcription start site (TSS) regulation of host genes remains poorly understood. Here, we employed NanoCap Analysis of Gene Expression sequencing (NanoCAGE-seq) to investigate HCMV-driven changes in alternative TSS usage across the host transcriptome. We identified widespread TSS switching, with ribosomal protein genes (RPGs) emerging as a highly enriched category. Alternative TSS usage produced isoforms with distinct 5’untranslated regions (UTRs), thereby altering cis-regulatory elements that shape translational efficiency. Integrative transcriptomic and proteomic analyses revealed a paradoxical accumulation of RPG proteins despite transcriptional downregulation during infection. Using 5’ Rapid Amplification of cDNA Ends (5’RACE), we characterized four RPGs of RPL4, RPS11, RPS23, and RPS24 that generated 5’UTR variants through alternative TSS usage. Notably, isoforms containing a 5’terminal oligopyrimidine (5’TOP) motif were significantly enriched, correlating with mTOR activation induced by HCMV. Functional assays with bicistronic reporter constructs in HEK293 cells and infection models in human embryonic lung fibroblasts demonstrated that the RPL4 5’TOP isoform exhibited enhanced mTORC1-driven translation compared with non-5’TOP counterparts. Importantly, RPL4 upregulation facilitated viral protein synthesis and boosted production of infectious virions. Together, our findings reveal that dynamic TSS switching of RPGs provides a simple, yet effective, mechanism for fine-tuning mTORC1-responsive translation. By co-opting host transcriptional and translational programs, HCMV enhances ribosome function to optimize the cellular environment for productive viral replication.

Following the publication of the above article, a concerned author drew to the Editor's attention that there appeared to be splicing events (and breaks in the continuity) of certain of the gels shown for the GST‑pulldown experiments in Fig. 1 on p. 2170, and the co‑immunoprecipitation experiments shown in Fig. 2 on p. 2171. After assessing their data, the authors have responded to the office to explain that they integrated data from repeated analyses into these figures, rather than the data all being generated from the same experiments. The authors also presented all their original data to the Editorial Office for our perusal, and wished to point out that the data in question were only intended to show qualitative results, and did not form part of the main analysis of the study; nor did the results from these experiments have a major impact on the reported conclusions. After volunteering to repeat these experiments, the authors were given authorization to do so by the Editor, and the revised versions of Figs. 1 and 2 (with revised figure legends) are shown opposite. The revised figures have both resolved the presentational difficulties associated with the original figures, and confirmed the original findings as presented in the published paper. All the authors approve of the publication of this corrigendum, and are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this; furthermore, they apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 13: 2167-2174, 2016; DOI: 10.3892/mmr.2016.4778].

Congenital human cytomegalovirus (HCMV) infection is a major cause of abnormalities and disorders in the central nervous system (CNS) and/or the peripheral nervous system (PNS). However, the complete pathogenesis of neural differentiation disorders caused by HCMV infection remains to be fully elucidated. Stem cells from human exfoliated deciduous teeth (SHEDs) are mesenchymal stem cells (MSCs) with a high proliferation and neurogenic differentiation capacity. Since SHEDs originate from the neural crest of the early embryonic ectoderm, SHEDs were hypothesized to serve as a promising cell line for investigating the pathogenesis of neural differentiation disorders in the PNS caused by congenital HCMV infection. In this work, SHEDs were demonstrated to be fully permissive to HCMV infection and the virus was able to complete its life cycle in SHEDs. Under neurogenic inductive conditions, HCMV infection of SHEDs caused an abnormal neural morphology. The expression of stem/neural cell markers was also disturbed by HCMV infection. The impairment of neural differentiation was mainly due to a reduction of intracellular cholesterol levels caused by HCMV infection. Sterol regulatory element binding protein-2 (SREBP2) is a critical transcription regulator that guides cholesterol synthesis. HCMV infection was shown to hinder the migration of SREBP2 into nucleus and resulted in perinuclear aggregations of SREBP2 during neural differentiation. Our findings provide new insights into the prevention and treatment of nervous system diseases caused by congenital HCMV infection.

Human cytomegalovirus (HCMV) is a herpes virus with a long replication cycle. HCMV encoded long non-coding RNA termed RNA2.7 is the dominant transcript with a length of about 2.5kb, accounting for 25% of total viral transcripts. Studies have shown that HCMV RNA2.7 inhibits apoptosis caused by infection. The effect of RNA2.7 on other forms of cell death is still unclear. In this work, we found that RNA2.7 deletion significantly decreased the viability of HCMV-infected cells, while treatment with ferroptosis inhibitor Fer-1 rescued the infection-induced cell death, demonstrating an anti-ferroptosis role of RNA2.7. The results further showed that RNA2.7 inhibited ferroptosis via enhancing Ferritin Heavy Chain 1 (FTH1) and Solute Carrier Family 7 Member 11 (SLC7A11) expression in Erastin treated cells without involving other viral components. Pooled Genome-wide CRISPR screening revealed zinc finger protein 395 (ZNF395) as a new regulator repressing the expression of FTH1 and SLC7A11. HCMV RNA2.7 promoted proteasome-mediated degradation of ZNF395 that resulted in upregulation of FTH1 and SLC7A11 to inhibit ferroptosis, therefore maintain survival in host cells and complete replication of virus.

The eukaryotic ribosome is a large ribonucleoprotein complex consisting of four types of ribosomal RNA (rRNA) and approximately 80 ribosomal proteins (RPs), forming the 40S and 60S subunits. In all living cells, its primary function is to produce proteins by converting messenger RNA (mRNA) into polypeptides. In addition to their canonical role in protein synthesis, RPs are crucial in controlling vital cellular processes such as cell cycle progression, cellular proliferation, differentiation, DNA damage repair, genome structure maintenance, and the cellular stress response. Viruses, as obligate intracellular parasites, depend completely on the machinery of the host cell for their replication and survival. During viral infection, RPs have been demonstrated to perform a variety of extra-ribosomal activities, which are especially important in viral disease processes. These functions cover a wide range of activities, ranging from controlling inflammatory responses and antiviral immunity to promoting viral replication and increasing viral pathogenicity. Deciphering the regulatory mechanisms used by RPs in response to viral infections has greatly expanded our understanding of their functions outside of the ribosome. Furthermore, these findings highlight the promising role of RPs as targets for the advancement of antiviral therapies and the development of novel antiviral approaches. This review comprehensively examines the many functions of RPs outside of the ribosome during viral infections and provides a foundation for future research on the host–virus interaction.

Pancreatic cancer (PC) is known for its high degree of heterogeneity and exceptionally adverse outcome. While disulfidptosis is the most recently identified form of cell death, the predictive and therapeutic value of disulfidptosis-related genes (DRGs) for PC remains unknown. RNA sequencing data with the follow-up information, were retrieved from the TCGA and ICGC databases. Consensus clustering analysis was conducted on patient data using R software. Subsequently, the LASSO regression analysis was conducted to create a prognostic signature for foreseeing the outcome of PC. Differences in relevant pathways, mutational landscape, and tumor immune microenvironment were compared between PC samples with different risk levels. Finally, we experimentally confirmed the impact of DSG3 on the invasion and migration abilities of PC cells. All twenty DRGs were found to be hyperexpressed in PC tissues, and fourteen of them significantly associated with PC survival. Using consensus clustering analysis based on these DRGs, four DRclusters were identified. Additionally, altogether 223 differential genes were evaluated between clusters, indicating potential biological differences between them. Four gene clusters (geneClusters) were recognized according to these genes, and a 10-gene prognostic signature was created. High-risk patients were found to be primarily enriched in signaling pathways related to the cell cycle and p53. Furthermore, the rate of mutations was markedly higher in high-risk patients, besides important variations were present in terms of immune microenvironment and chemotherapy sensitivity among patients with different risk levels. DSG3 could appreciably enhance the invasion and migration of PC cells. This work, based on disulfidoptosis-related genes (DRGs), holds the promise of classifying PC patients and predicting their prognosis, mutational landscape, immune microenvironment, and drug therapy. These insights could boost an improvement in a better comprehension of the role of DRGs in PC as well as provide new opportunities for prognostic prediction and more effective treatment strategies.

Circular RNA (circRNA) exists extensively and plays essential roles in serving as microRNA (miRNA) or protein sponges and protein scaffolding in many organisms. However, the profiles and potential functions of the virus-encoded circRNA, including human cytomegalovirus (HCMV)-encoded circular RNAs, remain unclear. In the present study, HCMV-encoded circRNAs profile in human embryonic lung fibroblasts (HELF) with lytic infection was investigated using RNA deep sequencing and bioinformatics analysis. In total, 629 HCMV-encoded circRNAs were identified with various expression patterns in our results. The full sequences and alternative splicings of circUS12, circUL55, and circUL89 were verified by reverse transcriptase-PCR (RT-PCR) with divergent primers followed and Sanger sequencing. Transcription of circUL89 was validated by Northern blot. The HCMV-encoded circRNA-miRNA network analyses revealed the potential function of HCMV-encoded circRNAs during HCMV infection in HELFs. Collectively, HCMV infection deduced abundant HCMV-associated circRNAs during infection, and the HCMV-encoded circRNAs might play important roles in benefiting HCMV infection.

Human cytomegalovirus (HCMV) is a ubiquitous pathogen belongs to betaherpesvirus subfamily. RNA2.7 is a highly conserved long non-coding RNA accounting for more than 20% of total viral transcripts. In our study, functions of HCMV RNA2.7 were investigated by comparison of host cellular transcriptomes between cells infected with HCMV clinical strain and RNA2.7 deleted mutant. It was demonstrated that RNA polymerase II (Pol II)-dependent host gene transcriptions were significantly activated when RNA2.7 was removed during infection. A 145 ​nt-in-length motif within RNA2.7 was identified to inhibit the phosphorylation of Pol II Serine-2 (Pol II S2) by reducing the interaction between Pol II and phosphorylated cyclin-dependent kinase 9 (pCDK9). Due to the loss of Pol II S2 phosphorylation, cellular DNA pre-replication complex (pre-RC) factors, including Cdt1 and Cdc6, were significantly decreased, which prevented more cells from entering into S phase and facilitated viral DNA replication. Our results provide new insights of HCMV RNA2.7 functions in regulation of host cellular transcription.

Human cytomegalovirus (HCMV), a herpesvirus family member, is a large, complex enveloped virus. The activation of liver X receptor (LXR) can significantly inhibit the replication of HCMV and weaken the virulence of progeny virus (unpublished data). Our results showed activated LXR affected some important viral protein expression and reduced cholesterol content in HCMV infected cells and virus particles. To further clarify the influence of activated LXR on HCMV replication, HCMV assembly and maturation processes were studied by transmission electron microscopy (TEM) in HCMV infected foreskin fibroblasts treated with LXR agonist GW3965. Results showed that activated LXR could reduce the envelope integrity of maturating virions. The functional stage of activated LXR on viral envelope integrity was mainly at virus assembly compartment (VAC) mediated envelopment but not structurally complete virus nucleocapsid formation and the egress of nucleocapsid from the nucleus to the cytoplasm mediated by nuclear egress complex. Reduced cholesterol synthesis and viral protein expression might interfere with the VAC-mediated envelopment. The nucleocapsid and tegument proteins enter the VAC area for the secondary envelope, which was interfered with and resulted in the defective particle, thereby affecting the amount and infectivity of the mature virus. The results indicate that inhibition of HCMV maturation is one mechanism of activated LXR inhibiting virus replication in infected cells.

Objective:To investigate the clinical features, therapy and prognosis of human cytomegalovirus(HCMV)pneumonia in pediatric patients, and to analyze the diagnosis value of detecting HCMV DNA in bronchoalveolar lavage fluid(BALF)by real-time PCR.Methods:The clinical characteristics of 58 pediatric inpatients who were HCMV DNA positive in BALF were retrospectively reviewed.All the patients were from Shengjing Hospital of China Medical University from January 2015 to December 2019.Clinical, radiologic, laboratory and microbiologic data was collected for each patient.The study cohort was divided into HCMV productive infection and latent infection consisting of 22 and 36 patients respectively, based on the HCMV active infection in lung or not.Receiver operating characteristic(ROC)curve was used to assess utility of detecting HCMV DNA in BALF and establish a threshold for diagnosis.Results:(1)Compared with patients in latent infection group, the children in productive infection group had a lower age of onset( P<0.05), a higher proportion of male( P<0.05), and more prolonged hospitalization stay( P<0.05). Pulmonary rales, hypoxemia and higher AST, CK, LDH in serum were easier to detect in productive infection group( P<0.05). Higher HCMV DNA copies in BALF was also detected( P<0.01). Patients in productive infection group had significantly more exposure to additional oxygen treatment or mechanical ventilation and systemic hormone therapy( P<0.05), while with poorer outcomes( P<0.05). (2) ROC curve analysis showed that the AUC for HCMV DNA in BALF in diagnosis of HCMV pneumonia was 0.708 with a threshold of 8.83×10 3 copies/mL, a sensitivity of 77.27%, and a specificity of 58.33%. Conclusion:Those who are diagnosed HCMV pneumonia have a lower age of onset with higher male proportion.These children suffered severer clinical signs.The patients with HCMV DNA copies higher than 8.83×10 3 copies/mL in BALF would be more likely to be diagnosed as HCMV pneumonia.

环状RNA(circRNA)是非编码RNA的家族成员,具有稳定性、特异性和高度保守性等特点,可参与调控多种疾病的发生,与恶性肿瘤的关系最为密切.口腔鳞状细胞癌(OSCC)目前呈现年轻化趋势,预后较差,易复发.因此,研究circRNA在OSCC中的作用十分必要,且关于circRNA与疾病诊断、治疗和预后的研究也具有较高的临床转化价值.本文对circRNA在OSCC中的表达及作用的最新研究进展和诊断治疗价值进行综述.

目的 了解沈阳地区不同年龄段患者中人巨细胞病毒?(HCMV)?的感染状况.方法 选择疑似HCMV感染患者123616例,采用荧光定量PCR技术检测HCMV?DNA,化学发光免疫分析法检测血清HCMV?IgM和IgG抗体,收集患者临床诊断信息.结果 HCMV?DNA、IgM抗体、IgG抗体阳性率分别为12.48％、2.34％、95.58％.>28?d～1岁组患儿HCMV?DNA阳性率?(31.52％)、IgM抗体阳性率?(9.86％)?最高.不同体液HCMV?DNA阳性率不同,尿HCMV?DNA阳性率?(14.61％)?大于血清?(2.36％)?和肺泡灌洗液?(2.17％).HCMV?DNA阳性率与IgM抗体阳性率呈正相关,HCMV?DNA阳性患者中,HCMV?IgM抗体阳性者病毒载量高于IgM抗体阴性者.HCMV感染的临床诊断包括肺炎、神经系统损害、肝炎、血液病等.结论 不同年龄段患者的HCMV感染状况存在差异.婴儿是HCMV易感人群,HCMV感染后主要累及肺脏、肝脏、神经系统等.多种体液样本HCMV?DNA检测以及HCMV?DNA与IgM抗体联合检测对HCMV检测和诊治有重要的意义.

自20世纪初，新发与再发传染病(ERI)疫情不断出现，已经对人类生命安全和健康造成重大威胁，也对社会稳定和经济发展造成了严重危害。ERI感染性强、传播速度快，还具有高度不确定性及难以预测性，已经成为公共卫生系统面对的巨大挑战。本文对ERI进行综述，以期加强公众对ERI的认识，为今后有效应对ERI提供参考。

目的 筛选并鉴定年龄≥60岁老年口腔鳞癌(OSCC)病人的癌组织及正常组织中的非编码小RNA(microRNA)的表达,分析其在OSCC发生中的临床意义.方法 收集44例老年OSCC标本,23例正常口腔组织标本进行芯片检测,筛选与OSCC密切相关的micro RNA.采用Taqman定量PCR方法检测OSCC组织与正常组织中 microRNA-200家族(miR-200a、miR-200b、miR-200c、miR-141 和 miR-429)及 U78的转录水平,对检测结果进行统计学分析,并采用生物信息学工具对其生物学功能进行预测分析.结果 芯片及Taqman定量PCR结果证实,与正常口腔组织相比,OSCC组织中microRNA-200家族各microRNAs及U78的表达水平均有显著升高.生物信息学分析结果提示,microRNA-200家族microRNAs可靶向调控β-链蛋白和转化生长因子β2等与肿瘤发生发展密切相关的基因.多元线性回归分析表明,U78的表达量与肿瘤组织病理分级具有明显相关性(P = 0.023),与临床分期及有无临床转移等临床指征无相关性.结论 microRNA-200家族及U78作为生物诊断指标可用于辅助诊断OSCC.

It must grow the awareness that contagious have never been far away from mankind. and the threats have always been next to us. Taking the laboratory detections of severe acute respiratmy syndrome coronavirus 2 (SARS-CoV-Z) as an example, this article mainly introduces the advantages and limitations of the I'eaJ-time fluorescent quantitative PCR and serological antibody detection teehnnlogy that 11an been used for laboratory detections of the etiology of Viral infectious diseases. It is hoped that the intmduetion will be helpful to the clinical diagnosis of viral infectious diseases, espet'ially COVID~19.

Objective:To investigate the epidemic situation of Epstein-Barr virus (EBV) infection in children in Shenyang and analyze the serological characteristics.Methods:The IgM antibody against EBV capsid antigen (VCA-IgM), IgG antibodies against capsid antigen (VCA-IgG), nuclear antigen IgG (EBNA-IgG) and early antigen (EA-IgG) of 26 714 pediatric patients hospitalized in Shengjing Hospital, China Medical University from August 2017 to July 2018 were detected simultaneously by LIAISON chemiluminescence analyzer.The infection stages of EBV were determined comprehensively according to the antibody spectrum of VCA-IgM, VCA-IgG and EBNA-IgG.Meanwhile, EBV antibodies were re-examined after 4-6 weeks in the patients with positive VCA-IgM only.Results:Among the 26 714 patients, a total of 2 963 cases (11.09%) were VCA-IgM positive, 15 349 cases (57.46%) were VCA-IgG positive, 14 263 cases (53.39%) were EBNA-IgG positive and 731 cases (2.74%) were EA-IgG positive.The positive rates of VCA-IgM, VCA-IgG, EBNA-IgG and EA-IgG in 15 149 boys were 10.98% (1 663/15 149 cases), 57.73% (8 745/15 149 cases), 53.49% (8 103/15 149 cases) and 2.57% (389/15 149 cases), respectively.The positive rates of VCA-IgM, VCA-IgG, EBNA-IgG and EA-IgG in 11 565 girls were 11.24% (1 300/11 565 cases), 57.10% (6 604/11 565 cases), 53.26% (6 160/11 565 cases) and 2.96% (342/11 565 cases), respectively.There was no significant difference in the positive rates of the 4 antibodies between male and female(all P>0.05). The positive rates of VCA-IgG and EBNA-IgG increased gradually with the age of children ( χ2=4 057.744, 4 776.285, all P<0.05), and those of VCA-IgG and EBNA-IgG were 87.98%(1 317/1 497 cases) and 88.78%(1 329/1 497 cases) respectively when children reached 14 years old.Typical primary infection [36.38%(1 078/2 963 cases)] and the recovery or reactivation of primary infection[43.81%(1 298/2 963 cases)] were predominant in acute infection children with positive VCA-IgM.Moreover, 95.09% (12 777/13 437 cases) of the previously infected cases had both positive VCA-IgG and positive EBNA-IgG.Of the 198 children with only positive VCA-IgM, 133(67.17%) did not show seroconversion.There was no case who had only positive EA-IgG, and 3.19% (428/13 437 cases) previously infection cases had positive EA-IgG. Conclusions:The positive rates of EBV 4 antibodies are not different between male and female children, and the past infection rate increases with age.The combined detection of antibodies can provide more detailed and reliable information for clinical diagnosis.Double serum antibodies detection can improve diagnosis accuracy; EA-IgG is an important serological marker for diagnosing reactivation of EBV infection.

Human cytomegalovirus (HCMV)–encoded microRNAs (miRNAs) are involved in posttranscriptional regulation of gene expression. Extracellular vesicles (EVs) can incorporate miRNAs. Relationship between HCMV infection and miRNAs in EVs remains unknown. EVs were isolated from supernatants of human embryonic lung fibroblasts (HELF) cells. Profiles of miRNAs in EVs were analyzed by deep sequencing. Dynamics of candidate viral miRNAs transportation via EVs was investigated using TaqMan PCR. Levels of candidate viral miRNAs in serum EVs from infants with HCMV active infection were detected and analyzed with their clinical index levels. A total of 16 HCMV miRNAs were found in EVs from infected HELF. Levels of miR-US25-1-5p and miR-UL112-3p in EVs increased at 6 h post-infection and were correlated with those in cells (for miR-US25-1-5p: r2 = 0.9375, p value < 0.05; for miR-UL112-3p: r2 = 0.7557, p value < 0.05). Viral miRNAs were transported into recipient cells at 2 h post-incubation. Moreover, levels of miR-US25-1-5p in serum EVs showed positive correlations with serum levels of γ-glutamyl transpeptidase, direct bilirubin, and total bile acid. Levels of miR-UL112-3p in serum EVs showed a positive correlation with serum levels of direct bilirubin. HCMV miRNAs could be transported to uninfected cells via EVs. Levels of miR-US25-1-5p and miR-UL112-3p in serum EVs from infants with HCMV active infection were significantly correlated with liver damage.

TORCH, which is considered as a series of pathogens, including the Toxoplasma gondii, Rubella virus, Cytomegalovirus or Herpes simplex virus, often infects the pregnant women to induce the the fetus or newborn infection by transplacental infection or exposure to contaminated genital tract secretions at delivery. Increasing evidence have been confirmed that the infection of TORCH may cause the miscarriage, premature birth, malformed fetus, stillbirth, intrauterine growth retardation, neonatal multiple organ dysfunction and other adverse pregnancy outcomes. For most TORCH-infections cases may lacking the effective treatments during pregnancy, and it is important to achieve the effacing monitoring of TORCH infections before and during pregnancy. The laboratory testing of TORCH has the great significance. However, the consensus opinions still need to improve the the standardization of TORCH testing process and the correct interpretation. Based on the characteristics of the TORCH detection method, this article gives a consensus opinion on the standardized detection and clinical application of TORCH from the laboratory perspective according to the characteristics and types of infection of different pathogens.

Antibody neutralization of cytomegalovirus (CMV) entry into diverse cell types is a key consideration for development of vaccines and immunotherapeutics. CMV entry into fibroblasts differs significantly from entry into epithelial or endothelial cells: fibroblast entry is mediated by gB and gH/gL/gO, whereas both epithelial and endothelial cell entry require an additional pentameric complex (PC) comprised of gH/gL/UL128/UL130/UL131A. Because PC-specific antibodies in CMV-seropositive human sera do not affect fibroblast entry but potently block entry into epithelial or endothelial cells, substantially higher neutralizing potencies for CMV-positive sera are observed when assayed using epithelial cells as targets than when using fibroblasts. That certain sera exhibit similar discordances between neutralizing potencies measured using epithelial vs. endothelial cells (Gerna G. et al.J Gen Virol, 89:853–865, 2008) suggested that additional mechanistic differences may also exist between epithelial and endothelial cell entry. To further explore this issue, neutralizing potencies using epithelial and endothelial cells were simultaneously determined for eight CMV-positive human sera, CMV-hyperimmune globulin, and a panel of monoclonal or anti-peptide antibodies targeting specific epitopes in gB, gH, gH/gL, or the PC. No significant differences were observed between epithelial and endothelial neutralizing potencies of epitope-specific antibodies, CMV-hyperimmune globulin, or seven of the eight human sera. However, one human serum exhibited a six-fold higher potency for neutralizing entry into epithelial cells vs. endothelial cells. These results suggest that epitopes exist that are important for epithelial entry but are less critical, or perhaps dispensable, for endothelial cell entry. Their existence should be considered when developing monoclonal antibody therapies or subunit vaccines representing limited epitopes.

Up to now, the UL16-17 region of human cytomegalovirus (HCMV) has not been well characterized at the level of mRNA and protein, especially for the Han strain, the first clinical HCMV strain in China. In previous studies, three transcripts were detected from the UL16-17 region by northern blot analysis for Merlin strain. Transcriptions of UL16 and UL17 were also studied by 5' rapid amplification of cDNA ends (5'RACE) and deep sequencing for AD169 and Towne strains, respectively. However, details of 3' end of UL16 and UL17 transcripts have never been confirmed by 3'RACE. The expressing phage of the UL16-17 region needs further research by northern blot, too. In the present study, cDNA library screening, northern blot and RACE were used to identify the transcription characteristics of the UL16-17 region. Mainly, 3 clusters of transcripts with the same 3' end were found to be expressed from the UL16-17 region in both Han and AD169 strains. The lengths of the core transcripts among the 3 clusters were 1,254nt, 718nt and 468nt, respectively. The corresponding 5' ends are at nt23119, nt23655, nt23905 in the HCMV Han genome. The consistent 3' end is located at nt24372 in the Han genome. The 1,254nt and 468nt transcripts are transcribed in early and late phases, and the 718nt transcript is transcribed only in the late phase.