• Archives of Pharmacal Research
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• v.22 no.6
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• pp.542-548
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• 1999

The UL47 gene (b 60390-b 60388) located in the unique long region of the human cytomegalovirus (HCMV) AD169 strain genome was analyzed RNA mapping. Northern blot analysis showed that the UL47 gene was expressed at late times after infection (72 h postinfection). The 9.7-kb transcript was expressed in the infected cells but not in phosphonoformate-treated cells at 72 hpi, indicating that the UL47 gene was only expressed at late times after infection. To map the 5'-end and 3'-end of UL47 transcripts, primer at late times after infection. To map the 5'-end and 3'-end of UL47 transcripts, primer extension and RNase protection analysis were performed. Primer extension analysis revealed that the transcription initiation site of UL47 was located in 27 bp downstream (b 60323) of the TATA box motif. The sizes of UL47 ORF (approximately 2.9-kb) and UL48 ORF (approximately 6.7-kb) deduced from computer sequence analysis suggest that the expressed 9.7-kb transcript of UL47 uses the 3'-end polyadenylation signal of Ul48. The result of RNase protection determined that the 3'-end of UL47 RNA utilized the 3'-end polyadenylation signal of UL48, which is located in HCMV genome b 70082.

• Journal of Microbiology
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• v.38 no.4
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• pp.255-259
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• 2000

For rapid and sensitive measurement of antiviral activities, application of a recombinant virus containing firefly luciferase gene was attempted. Recombinant human cytomegalovirus (HCMV) containing luciferase gene driven by HCMV late gene pp28 promoter (HCMV/pp28-luc) was used to test the antiviral activities of three known compounds and the result was compared with results from the conventional plaque assay for measuring the production of infectious viruses. When human fibroblast cells were infected with HCMV/pp28-luc, luciferase activity was observed at 2 days after infection and reached maximum at 6 days after infection, whereas the production of infectious virus was maximal at 4 days after infection. The antiviral activities of ganciclovir, acyclovir, and papaverine were measured in HFF cells infected with HCMV/PP28-luc and the luciferase activity was compared with the infectious virus titers. Luciferase activity decreased as the concentration of ganciclovir or papaverine increased, while there was a slight decrease in luciferase activity with acyclovir. The level of the decrease in Luciferase activity was comparable to the level of decrease in the production of infectious virus. Therefore, the antiviral assay using recombinant virus HCMV/pp28-luc resulted in sensitivity similar to the conventional plaque assay with a significant reduction in assay time.

• Clinical and Experimental Pediatrics
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• v.60 no.8
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• pp.261-265
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• 2017

Purpose: Studies on cytomegalovirus (CMV) infections in immunocompetent children are lacking, and minimal information is available in the medical literature on hepatic manifestations and complications of CMV. The aims of this study were to evaluate the clinical characteristics, laboratory data, and prognosis of children with CMV hepatitis, and to investigate its prevalence at a single medical center in Korea over a 10-year period. Methods: One hundred thirty-two children diagnosed with CMV infection based on specific markers (anti-CMV IgM, CMV polymerase chain reaction in blood and urine, or CMV culture of urine) were included in the study. Clinical and biochemical characteristics, immunological markers, and outcomes of hepatic CMV infection were determined. Results: The median age of patients (n=132) was 8.5 months (range, 14 days-11.3 years). Peak total bilirubin and alanine aminotransferase levels in serum ranged from 0.11-21.97 mg/dL, and 5-1,517 IU/L, respectively. Alanine aminotransferase remained elevated from 2-48 weeks. Jaundice was the most common clinical feature of hepatic CMV infection during infancy. The hematologic findings revealed anemia, leukocytosis, and monocytosis in CMV-infected patients. All participants recovered without administration of ganciclovir. Conclusion: In children with CMV hepatitis, fever was the most common symptom at presentation, and jaundice was the most common clinical feature of hepatic CMV infection in infants younger than 3 months of age. Hepatic CMV infection in immunocompetent children is often a self-limited illness that does not require antiviral therapy, as most patients in this study had favorable outcomes.

• Journal of Microbiology
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• v.42 no.4
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• pp.299-304
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• 2004

To investigate the presence of infectious agents in human atherosclerotic arterial tissues. Atherosclerotic plaques were removed from 128 patients undergoing carotid endarterectomy or other bypass proce­dures for occlusive disease, and from twenty normal arterial wall samples, obtained from transplant donors with no history of diabetes, hypertension, smoking, or hyperlipidemia. Using the polymerase chain reaction (PCR) or reverse transcription-PCR, these samples were analyzed for the presence of Chlamydia pneumoniae, cytomegalovirus, enterovirus, adenovirus, herpes simplex viruses types 1 and 2, and Epstein-Barr virus. The amplicons were then sequenced, and phylogenetic analyses were per­formed. Enteroviral RNA was found in 22 of 128 atherosclerotic vascular lesions $(17.2\%),$ and C. pneu­moniae and cytomegalovirus were each found in 2 samples $(1.6\%).$ In contrast, adenovirus, herpes simplex viruses, and Epstein-Barr virus were not identified in any of the atherosclerotic samples. Enterovirus was detected in 6/24 $(25.0\%)$ aortas, 7/33 $(21.2\%)$ carotid arteries, 6/40 $(15.0\%)$ femoral arteries, and 3/31 $(9.7\%)$ radial arteries of patients with chronic renal failure. There were no infectious agents detected in any of the control specimens. Using phylogenetic analysis, the enterovirus isolates were clustered into 3 groups, arranged as echovirus 9 and coxsackieviruses Bl and B3. Enteroviral RNA was detected in $17.2\%$ of atherosclerotic plaques, but was not observed in any of the control spec­imens. This suggests a connection between enteroviral infection and atherosclerosis. These findings dif­fer from those of other studies, which found more frequent incidence of C. pneumoniae and cytomegalovirus infection in atherosclerotic plaques.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.20 no.3
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• pp.178-185
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• 2017

Purpose: To evaluate the outcomes of a hybrid prophylactic strategy to prevent cytomegalovirus (CMV) disease in pediatric liver transplantation (LT) patients. Methods: CMV DNAemia was regularly monitored by quantitative nucleic acid amplification test (QNAT) and was quantified in all children. CMV infection and disease were defined according to the International Consensus Guidelines. The hybrid strategy against CMV infection consisted of universal 3-week prophylaxis and preemptive treatment of intravenous ganciclovir regardless of the recipient's serostatus. Results: A total of 143 children who underwent living donor LT were managed using the hybrid strategy. The overall incidence of CMV infection by QNAT was 48.3% (n=69/143). The highest CMV DNAemia positivity was observed in 49.2% (n=60/122) of children in the D+/R+ group, followed by 46.7% (n=7/15) in the D+/R- group. CMV disease was noted in 26.1% (n=18/69) patients. Forty-three (62.3%) children had undergone preemptive therapy consisting of intravenous ganciclovir. No symptomatic patients developed tissue-invasive disease, resulting in no CMV-associated mortality. Conclusion: The incidence of CMV infection was high in pediatric LT patients despite the hybrid strategy. However, tissue-invasive disease in pediatric LT did not occur.

• Childhood Kidney Diseases
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• v.12 no.2
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• pp.233-238
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• 2008

It has been suspected that various infections, including cytomegalovirus(CMV) infection, are associated with IgA nephropathy. In case of CMV infection, ganciclovir is known to be a treatment of choice for severe CMV infection in general. But ganciclovir has a lot of severe toxicity, so children with normal immunity are seldom treated by ganciclovir when CMV infection is suspected. On the other hand, intravenous immunoglobulin can also be used to treat CMV infection. We report a case of CMV-associated IgA nephrophaty, who was treated with deflazacort and Intravenous immunoglobulin therapy. An 11 years old boy suffered from gross hematuria for 3 days. He had proteinuria, thrombocytopenia(104,000/$mm^3$), antiplatelet antibody(＋), impaired renal function and low serum albumin. His CMV serology was CMV-IgM/IgG(＋/-) and urine CMV-PCR was positive. The renal histological findings revealed IgA nephropathy, WHO class II. His proteinuria persisted despite of deflazacort therapy(2.5 mg/kg/day). Later, intravenous immunoglobulin(1 g/kg) was administered twice. In two years, he showed no gross and microscopic hematuria, and his laboratory findings were also normalized.

• Tuberculosis and Respiratory Diseases
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• v.64 no.4
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• pp.309-313
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• 2008

Cytomegalovirus (CMV) pneumonia is a serious opportunistic infection in an immunocompromised host such as an AIDS patient or transplant recipient undergoing immunosuppressive therapy. Diffuse alveolar hemorrhage (DAH) is a relatively uncommon condition and it occurs most often in patients with systemic autoimmune disease. However, various types of infectious pneumonia with Mycoplsma hominis, Stenotrophomonas maltophilia and Pneumocystis jirovecii have been reported to be associated with the development of DAH. The association of CMV infection with the development of DAH has rarely been reported. We experienced a case of DAH associated CMV pneumonia and the patient was successfully treated with the use of antiviral agents and steroids.

• Korean Journal of Microbiology
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• v.38 no.4
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• pp.203-203
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• 2002

Cytomegalovirus (CMV), a beta-herpesvirus with worldwide distribution, exhibits host persistence, a distinguishing characteristic of all herpesviruses. This persistence is dependent upon restricted gene expression in infected cells as well as the ability of productively infected cells to escape from normal cell-mediated anti-viral immunosurveillance. Type I (IFN-α/β) and type II (IFN-γ) interferons are major components of the innate defense system against viral infection. They are potent inducers of MHC class I and II antigens and of antigen processing proteins. Additionally, IFNS mediate direct antiviral effects through induction effector molecules that block viral infection and replications such as 2′, 5-oligoadenylate synthetase (2, 5-OAS). IFNS function through activation of well-defined signal transduction pathways that involve phosphorylation of constituent proteins and ultimate formation of active transcription factors. Recent studies have shown that a number of diverse viruses, including CMV, EBV, HPV mumps and Ebola, are capable of inhibiting IFN-mediated signal transduction through a variety of mechanisms. As an example, CMV infection inhibits the ability of infected cells Is transcribe HLA class I and II antigens as well as the antiviral effector molecules 2, 5-OAS and MxA I. EMSA studies have shown that IFN-α and IFN-γ are unable to induce complete signal transduction in the presence of CMV infection, phenomena that are associated with specific decreases in JAKl and p48. Viral inhibition of IFN signal transduction represents a new mechanistic paradigm for increased viral survival, a paradigm predicting widespread consequences in the case of signal transduction factors common to multiple cytokine pathways.

• Journal of Microbiology
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• v.38 no.4
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• pp.203-208
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• 2000

Cytomegalovirus (CMV), a beta-herpesvirus with worldwide distribution, exhibits host persistence, a distinguishing characteristic of all herpesviruses. This persistence is dependent upon restricted gene expression in infected cells as well as the ability of productively infected cells to escape from normal cell-mediated anti-viral immunosurveillance. Type I (IFN-$\alpha$/$\beta$) and type II (IFN-γ) interferons are major components of the innate defense system against viral infection. They are potent inducers of MHC class I and II antigens and of antigen processing proteins. Additionally, IFNS mediate direct antiviral effects through induction effector molecules that block viral infection and replications such as 2', 5-oligoadenylate synthetase (2, 5-OAS). IFNS function through activation of well-defined signal transduction pathways that involve phosphorylation of constituent proteins and ultimate formation of active transcription factors. Recent studies have shown that a number of diverse viruses, including CMV, EBV, HPV mumps and Ebola, are capable of inhibiting IFN-mediated signal transduction through a variety of mechanisms. As an example, CMV infection inhibits the ability of infected cells Is transcribe HLA class I and II antigens as well as the antiviral effector molecules 2, 5-OAS and MxA I. EMSA studies have shown that IFN-$\alpha$ and IFN-γ are unable to induce complete signal transduction in the presence of CMV infection, phenomena that are associated with specific decreases in JAKl and p48. Viral inhibition of IFN signal transduction represents a new mechanistic paradigm for increased viral survival, a paradigm predicting widespread consequences in the case of signal transduction factors common to multiple cytokine pathways.

• Pediatric Infection and Vaccine
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• v.31 no.1
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• pp.140-146
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• 2024

Multisystem inflammatory syndrome in children (MIS-C) is a rare complication of coronavirus disease 2019 (COVID-19), causing multi-organ damage affecting the heart, lungs, kidneys, digestive tract, and nervous system. As the cases of MIS-C have been increasing following the COVID-19 pandemic, the importance of appropriate management for MIS-C is becoming increasingly apparent. Immunomodulating agents such as anakinra, infliximab, and steroids are regarded as supplementary therapy to the first-line treatment with intravenous immunoglobulin. However, these immunomodulating therapies can potentially precipitate opportunistic infections, including those caused by cytomegalovirus (CMV), Epstein-Barr virus, and tuberculosis, or increase the risk of co-infections. Herein, we report a case of a 3-year-old boy who was treated with immunoglobulin, infliximab, and high-dose methylprednisolone for MIS-C, and subsequently developed a persistent fever lasting 32 days caused by a CMV infection.