• 한국정보통신학회:학술대회논문집
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• 한국정보통신학회 2014년도 추계학술대회
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• pp.977-980
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• 2014

polyhedron promoter, vesicular stomatitis virus G (VSVG), polyA, cytomegalovirus (CMV) promoter, enhanced green fluorescent protein (EGFP), protein transduction domain (PTD) 유전자가 포함된 재조합 베큘로바이러스를 구축하였다. 본 재조합 베큘로바이러스 시스템은 인간 섬유아세포와 여러 가지 조직에 감염하여 시험하였고 재조합된 유전자의 전달과 유전자 발현을 대조 벡터시스템과 비교하였다. 본 연구의 결과로 제작된 재조합 베큘로바이러스 시스템은 유전자의 전달과 발현에 있어서 대조 벡터시스템 보다 더욱 효과적이고 안전적이었다.

• Journal of Microbiology
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• 제42권4호
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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.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.281.1-281
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• 2000

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.281.2-281
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• 2000

No Abstract, See Full Text

• Journal of Microbiology and Biotechnology
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• 제26권10호
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• pp.1800-1807
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• 2016

To understand how human cytomegalovirus (HCMV) might change and evolve after reactivation, it is very important to understand how the nucleotide sequence of cultured HCMV changes after in vitro passaging in cell culture, and how these changes affect the genome of HCMV and the consequent variation in amino acid sequence. Strain JHC of HCMV was propagated in vitro for more than 40 passages and its biological and genetic changes were monitored. For each passage, real-time PCR was performed in order to determine the genome copy number, and a plaque assay was employed to get virus infection titers. The infectious virus titers gradually increased with passaging in cell culture, whereas the number of virus genome copies remained relatively unchanged. A linear correlation was observed between the passage number and the log₁₀ infectious virus titer per virus genome copy number. To understand the genetic basis underlying the increase in HCMV infectivity with increasing passage, the whole-genome DNA sequence of the high-passage strain was determined and compared with the genome sequence of the low-passage strain. Out of 100 mutations found in the high-passage strain, only two were located in an open reading frame. A G-T substitution in the RL13 gene resulted in a nonsense mutation and caused an early stop. A G-A substitution in the UL122 gene generated an S-F nonsynonymous mutation. The mutations in the RL13 and UL122 genes might be related to the increase in virus infectivity, although the role of the mutations found in noncoding regions could not be excluded.

• 미생물학회지
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• 제44권2호
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• pp.140-146
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• 2008

다양한 염증 질환을 유발하는 사람세포거대바이러스(Human cytomegalovirus: HCMV)는 단핵구 세포주인 THP-1 세포에서 염증반응의 중요한 매개체인 세포간부착분자-1(intercellular adhesion molecule: ICAM-1) 발현을 촉진한다. ICAM-1 발현은 자외선으로 불활화시킨 HCMV (UV-HCMV)에 의해서도 촉진되므로 이 과정에 HCMV 유전자발현은 꼭 필요하지는 않은 것 같다. HCMV에 감염된 THP-1 세포 배양액을 감염되지 않은 THP-1 세포에 처리하거나 공유하게 하였을 시 감염되지 않은 세포에서도 ICAM-1 발현이 증가하였다. 감염된 세포 배양액에 의한 ICAM-1 발현 증가는 $NF-{\kappa}B$ 경로를 거친다. UV-HCMV에 감염된 세포의 배양액은 ICAM-1 발현을 촉진시키지 못하였다. 따라서 HCMV에 의한 THP-1 세포에서 ICAM-1 발현 증가는 바이러스 유전자 발현을 필요로 하지 않지만, 감염된 세포에서 ICAM-1 발현을 촉진하는 물질을 분비하는 과정에는 바이러스 유전자 발현이 필요한 것으로 생각된다.

• 한국정보통신학회:학술대회논문집
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• 한국해양정보통신학회 2008년도 춘계종합학술대회 A
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• pp.971-975
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• 2008

Human cytomegalovirus (HCMV) provokes fatal infections in AIDS patients that have deficient immune functions and patients that have cellular immune responses repressed after bone marrow transplantation. A new candidate for therapeutic against HCMV is needed because conventional treatments as ganciclovir, acyclovir, cidofovir, and foscarnet cytosine used currently are improper due to their side effects and advent of resistant HCMV. In this study, peptide nucleic acids (PNAs) against UL54 (DNA polymerase) and UL97 (phosphotransferase) that were essential in replication of HCMV were applied in inhibition of replication of HCMV. From the results of this study, 4 PNAs $_{PNA}UL97-1$, $_{PNA}UL97-2$, $_{PNA}UL54-3$, and $_{PNA}UL54-4$ showed 3.7, 3.1, 1.7, and 1.6 folds of inhibition effect against replication of HCMV in the human fibroblast cells. These PNA suggest a novel possibility as therapeutic against HCMV.

• Journal of Microbiology and Biotechnology
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• 제15권3호
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• pp.544-550
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• 2005

To develop a highly efficient mammalian expression vector, a series of vectors were constructed based on the murine cytomegalovirus (MCMV) immediate-early (IE) promoter and human ${\beta}$-globin second intron. The resulting MCMV promoter was several-fold stronger than the HCMV promoter in various mammalian cell lines, such as the NIH3T3, Neuro-2a, 293T, and HT1080 cell lines, and was only slightly weaker than the HCMV promoter in HeLa and CHO cells. The inclusion of the human ${\beta}$-globin second intron behind the MCMV promoter or HCMV promoter markedly enhanced the promoter activity in various mammalian cell lines, and the resultant MCMV/Glo-I expression system was stronger than the HCMV promoter from 4.7- to 11.2-fold in every cell line tested. Also, the MCMV/Glo-I promoter induced a higher level of the VSV-G protein in a transiently transfected 293T cell line, which is useful for the production of recombinant retrovirus and lentivirus vectors.

• 미생물학회지
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• 제38권4호
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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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• 제38권4호
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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.