• Pediatric Infection and Vaccine
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• 제12권2호
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• pp.208-212
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• 2005

포진상 습진(eczema herpeticum)은 헤르페스의 가장 심한 양상 중 하나로서, 아토피 피부염 등이 있는 피부에 HSV가 감염되어 발생하며 치명적일 수 있다. 포진상 습진은 HSV의 1차 감염 뿐만 아니라 2차 감염에 의해서도 발생할 수 있다. 포진상 습진에서 2차성 세균 감염은 흔하게 발생하는데, 황색포도상구균이 가장 흔하게 분리되는 호기성 균주이다. 포진상 습진의 치료에 중요한 점은 전신적인 항바이러스 치료를 빨리 시작하고 2차적인 세균 감염을 줄이기 위해 항균제를 사용하는 것이다. 저자들은 지속적인 아토피 피부염으로 인해 한방 치료를 받던 환아에게서 중증 포진상 습진이 발생한 2례를 화상 드레싱 및 항바이러스제 치료로 호전을 보인 경험을 하여 이를 보고하는 바이다.

• 한국미생물·생명공학회지
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• 제50권2호
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• pp.270-276
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• 2022

This study analyzed the epidemiological trends of sexually transmitted infections (STIs) according to age and sex among individuals aged 50 years or older in South Korea from September 2018 to December 2020. We found that the positivity rate for Gardnerella vaginalis was the highest in the study group, followed by the positivity rate for Ureaplasma parvum (UP). Interestingly, the positivity rates for Mycoplasma hominis and UP were higher in female participants than in male participants. The positivity rate for Treponema pallidum was very low in the female participants. During the study period, the positivity rate for herpes simplex virus 2 increased in the female participants, while the positivity rate for Candida increased in the male participants. These results show that the STI positivity rate varies according to age and sex, and a difference was observed in the average age of positive participants according to the type of STIs. We found a clear pattern of infection in the elderly population and according to sex. Our findings are expected to be used as baseline data for future research, education, and prevention of STIs in the elderly population.

• Genomics & Informatics
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• 제21권2호
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• pp.26.1-26.9
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• 2023

Stevens-Johnson syndrome (SJS) produces a severe hypersensitivity reaction caused by Herpes simplex virus or mycoplasma infection, vaccination, systemic disease, or other agents. Several studies have investigated the genetic susceptibility involved in SJS. To provide further genetic insights into the pathogenesis of SJS, this study prioritized high-impact, SJS-associated pathogenic variants through integrating bioinformatic and population genetic data. First, we identified SJS-associated single nucleotide polymorphisms from the genome-wide association studies catalog, followed by genome annotation with HaploReg and variant validation with Ensembl. Subsequently, expression quantitative trait locus (eQTL) from GTEx identified human genetic variants with differential gene expression across human tissues. Our results indicate that two variants, namely rs2074494 and rs5010528, which are encoded by the HLA-C (human leukocyte antigen C) gene, were found to be differentially expressed in skin. The allele frequencies for rs2074494 and rs5010528 also appear to significantly differ across continents. We highlight the utility of these population-specific HLA-C genetic variants for genetic association studies, and aid in early prognosis and disease treatment of SJS.

• Journal of Korean Neurosurgical Society
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• 제30권sup1호
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• pp.13-19
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• 2001

Objective : We investigated the feasibility of a double suicide gene/prodrug therapy, involving direct introduction of the herpes simplex virus Type 1 thymidine kinase(TK) gene and the Escherichia coli cytosine deaminase(CD) gene, via a recombinant adenoviral vector and ganciclovir(GCV) and/or 5-fluorocytosine(5-FC) treatment, in C6 glioma cells. Methods : Efficient gene transfer and transduction of C6 glioma cells via a recombinant adenovirus were evaluated by infecting cells with adenovirus bearing the ${\beta}$-galactosidase gene and then staining cells with 5-bromo-4-chloro-3-indolyl-13-D-galactoside. CD/TK expression in cells infected with adenovirus bearing the CD/TK gene(ad-CD/TK) was examined by immunoblotting analysis. For in vitro cytotoxicity experiments, the cells were infected with ad-CD/TK or ad-${\Delta}E1$(as a control). After addition of a variety of concentrations of GCV and 5-FU, either separately or in combination, cell viability was determined by staining the cells with crystal violet solution 6 days after infection. Result : C6 glioma cells were efficiently transduced with recombinant adenoviral vector at multiplicities of infection of 200 or more. In vitro cytotoxicity of GCV and/or 5-FC, either alone or in combination, was exclusively observed in the cells transduced with ad-CD/TK. Obvious cytotoxicity(>50% inhibition) was observed in the presence of 5-FC at concentrations greater than 30ug/ml or GCV at concentrations greater than 0.3ug/ml at a multiplicity of infection of 100. Additionally, cytotoxicity in the presence of both GCV and 5-FC was greater than that after sinlge-prodrug treatments, indicating additive effects of the prodrug treatments. Conclusion : The administration of a double-suicide gene/prodrug therapy might have great potential in the treatment of brain tumors.

• 대한약리학회지
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• 제25권1호
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• pp.115-134
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• 1989

Ganciclovir(GCV)와 Vidarabine(ara-A)을 단독으로 또는 동시에 HSV-1에 작용시켰을때 HSV-1의 복제, DNA합성 및 단백질 합성에 미치는 영향을 관찰할 목적으로 본 연구를 시행하였다. 본 실험에서는 4가지의 다른 HSV-1(Wild type KOS, $VCV^r$, $IUdR^r$, 및 $PAA^r5$)를 사용하였다. Virus복제에 미치는 항 virus약의 효과는 Vero 세포단층 배양에서 Yield reduction assay에 의해서 관찰하였다. 항 virus약의 virus DNA 합성에 미치는 영향은 NaI 밀도 구배초원심침전후 $H^3-$표지 virus DNA의 방사능에 의해서 관찰하였다. Virus 단백질의 합성에 미치는 항 virus약의 효과는 $^{35}S$를 표지한 후 polyacrylamide 겔 전기영동법, 자가방사기록법 그러고 virus bands의 음영농도주사법을 이용, 관찰하여 다음과 같은 결과를 얻었다. 1. GCV는 wild trype HSV-1 KOS와 $PAA^r5$의 복제를 강력하게 억제하였으나 $ACV^r$와 $IUdR^r$는 GCV에 대해서 중등도의 저항을 보였다. ara-A는 실험대상의 모든 HSV-(KOS, $ACV^r$, $IUdR^r$ 및 $PAA^r5$)의 복제에 대해서 거의 비슷하게 억제효과를 보였다. GCV와 ara-A 동시첨가는 KOS와 $PAA^r5$의 복제에 대해서 상승적인 억제효과를 보였고 $ACV^r$와 $IUdR^r5$의 복제에 대해서는 상가작용이하의 억제 효과를 보였다. 2. GCV또는 ara-A는 HSV-1감염 Vero세포에서 virus DNA의 합성을 유의하게 억제하였다. GCV와 ara-A의 동시첨가는 KOS 또는 $PAA^r5$ 감염세포에서 virus DNA 합성을 GCV 또는 ara-A를 단독 첨가하였을때 보다 현저하게 억제하였다. $ACV^r$ 또는 $IUdR^r$ 감염세포에서는 이런 현상을 관찰할 수 없었다. 3. Wild type HSV-1 감염세포에서 virus-단백질의 합성은 GCV, ara-A의 단독 첨가 또는 GCV와 ara-A의 동시첨가에 의해서 변경되지 않았다. Wild type HSV-1 감염말기에 GCV 또는 ara-A 단독 혹은 동시첨가에 의해서 virus 단백질의 합성은 경미하나마 유의성있게 증가하였다. Wild type HSV-1과 $PAA^r5$에 의한 단백질의 합성은 GCV 또는 ara-A 단독 첨가에 의해서 유의성있게 억제되었다. GCV또는 ara-A의 동시첨가는 GCV또는 ara-A를 단독으로 첨가했을 경우보다 단백질의 합성을 더욱 억제하였다. 이상의 실험결과로 보아 GCV와 ara-A의 동시사용은 HSV-1 혹은 ACV저항 DNA polymerase변이주인 $PAA^r5$에 대해서 상승적인 억제작용을 나타냈으며 이 효과는 virus DNA 합성 억제에 의한 것으로 생각된다. ACV저항 thymidine kinase 변이주인 $ACV^r$ 및 $IUdR^r$에 대해서는 ara-A가 유효하였다. 항 virus 약물에 의한 virus 단백질합성의 변화는 virus DNA 합성에 대한 억제효과에 인한 것으로 사려된다.

• 동의생리병리학회지
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• 제18권4호
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• pp.1061-1070
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• 2004

Chronic oral aphthae, recurrent ulcer and uveitis are the three main festations of Behcet's disease(BD). The aetiopathogenesis of Behcet's disease is still obscure, but herpes simplex virus is one of the possible casual factors. Gamchosasim-tang (Gancaoxiexin-tang), Banhasasim-tang(Banxiaxiexin-tang) and Saenggangsasim-tang( Shengjiangxiexin-tang) are traditional medication in Oriental medicine, that has been used to treat inflammatory disease. Especially, Gamchosasim-tang used to treat Behcet's disease like symptoms. ICR mice were used for this study. The earlobe of the mice were scratched with a needle, then inoculation with 1.0×10/sup 6/ plaque forming units/㎖ of HSV type I. Virus inoculation was performed twice with 10 day interval, followed by 16 weeks of observation. Using the HSV-induced Behcet's disease mouse model, kinds of Sasim-tang were administered variously before and after inoculation. In order to. classify the symptomatic mice as having Behcet's disease like symptoms. We followed the revised Japanese classification with minor modifications. Ulceration of the mice were monitored. In addition, spleen cytokine expression were measured by polymerase chain reaction, ELISA. HSV DNA was detected in HSV inoculation mice. HSV-induced mice treated with kinds of Sasim-tang showed improvement in symptom. In RT-PCR results, IFN-γ was expressed for all groups, IL-2 was expressed for the treated groups, and IL-10 was also expressed. IL-4 was expressed nothing. In ELISA, IL-2 was increased for GSST 2, BSST 2, GSST 2, GSST3 and INF-γ was increased for GSST 2, BSST 2, SSST 2, SSST 3. This model suggest the possible role of immune response to viral infection in the development and activation of Behcet's disease.

• 한국동물위생학회지
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• 제27권4호
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• pp.355-369
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• 2004

The equine herpesvirus type 1 (EHV-1) immediate-early (IE) protein is a potent transactivator responsible for the activation of both early and late genes during the course of infection and is comprised of discrete functional domains that mediate its many functions. Interaction between trans activators such as the IE protein and various components of the RNA polymerase II transcription initiation machinery has been demonstrated to be critical for transactivation. In the present report, it is addressed the hypothesis that the IE protein interacts with various components of transcription machinery to mediate transactivation of target viral genes. In these studies, it is demonstrated that in vitro transcribed and translated IE protein interacts with TFIIB-agarose conjugate but not with TFIID-agarose conjugate. Additional immunoprecipitation studies using nuclear extracts derived from EHV-1 infected RK-13 cells confirmed that the IE protein interacts strongly with TFIIB, but fails to interact with TFIID. IR2, a truncated form of the IE protein lacking the potent transactivation domain and involved in the down-regulation of the IE gene, also interacted with TFIIB but not with TFIID. Studies were also performed to ascertain if particular TBP-associated factors (TAFs) could mediate IE or IR2 binding to TFIID. In vitro transcribed and translated TAF250 added to nuclear extracts generated from EHV-1 infected cells also failed to mediate an interaction between the IE protein or the IR2 protein and TFIID. This study demonstrated that the IE protein mediates transactivation of target viral genes by a mechanism that involves TFIIB. This is in contrast to mechanisms that have been proposed for both the herpes simplex virus ICP4 and VP16 protein which have been proposed to transactivate viral genes through interactions involving both TFIIB and TFIID. This study also intimates that IR2 mediate its repressive effects during the course of EHV-1 infection by a mechanism that involves sequestration of various transcription factors.

• IMMUNE NETWORK
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• 제5권2호
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• pp.89-98
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• 2005

Background: DNA vaccination represents an anticipated approach for the control of numerous infectious diseases. Used alone, however, DNA vaccine is weak immunogen inferior to viral vectors. In recent, heterologous prime-boost vaccination leads DNA vaccines to practical reality. Methods: We assessed prime-boost immunization strategies with a DNA vaccine (minigene, $gB_{498-505}$ DNA) and recombinant vaccinia virus $(vvgB_{498-505})$ expressing epitope $gB_{498-505}$ (SSIEF ARL) of CD8+ T cells specific for glycoprotein B (gB) of herpes simplex virus (HSV). Animals were immunized primarily with $gB_{498-505}$ epitope-expressing DNA vaccine/recombinant vaccinia virus and boosted with alternative vaccine type expressing entire Ag. Results: In prime-boost protocols using vvgBw (recombinant vaccinia virus expressing entire Ag) and $vvgB_{498-505}$, CD8+ T cell-mediated immunity was induced maximally at both acute and memory stages if primed with vvgBw and boosted with $vvgB_{498-505}$ as evaluated by CTL activity, intracellular IFN-staining, and MHC class I tetramer staining. Similarly $gB_{498-505}$ DNA prime-gBw DNA (DNA vaccine expressing entire Ag) boost immunization elicited the strongest CD8+ T cell responses in protocols based on DNA vaccine. However, the level of CD8+ T cell-mediated immunity induced with prime-boost vaccination using DNA vaccine expressing epitope or entire Ag was inferior to those based on vvgBw and $vvgB_{498-505}$. Of particular interest CD8+ T cell-mediated immunity was optimally induced when $vvgB_{498-505}$ was used to prime and gB DNA was used as alternative boost. Especially CD7+ T cell responses induced by such protocol was longer lasted than other protocols. Conclusion: These facts direct to search for the effective strategy to induce optimal CD8+ T cell-mediated immunity against cancer and viral infection.

• Pediatric Infection and Vaccine
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• 제28권2호
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• pp.92-100
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• 2021

목적: 중추신경계 감염의 적절한 치료를 위해서 신속한 원인 병원체의 확인이 중요하다. 본 연구는 열이 있는 영아의 뇌척수액 검체에서 원인 병원체 검출을 위한 BioFire^® Meningitis/Encephalitis (ME) panel 검사 방법의 진단적 가치를 평가하고자 수행되었다. 방법: 2016년 1월부터 2019년 7월까지 발열을 주소로 서울대학교 어린이병원에 내원한 90일 미만의 영아로부터 채취한 뇌척수액으로 기존검사(세균 배양, Xpert^® enterovirus assay, herpes simplex virus-1 and -2 중합효소 연쇄반응 검사)를 시행한 후 -70℃ 초저온 냉동고에 보관된 검체를 대상으로 BioFire^® ME panel 검사를 시행하였다. 결과: 총 72개 검체(원인 병원체가 검출된 24개와 검출되지 않은 48개)가 포함되었다. BioFire^® ME panel 검사 결과, 기존검사로 원인 병원체가 검출되지 않은 48개의 검체 중 41개(85.4%)는 음성이었고 원인 병원체가 검출된 24개 검체 중 22개(91.7%)가 동일한 결과(enterovirus 19개, Streptococcus agalactiae 2개, Streptococcus pneumoniae 1개)를 보여 전체 일치율은 87.5% (63/72)였다. 병원체가 기존검사에서 검출되지 않았으나 BioFire^® ME panel에서 검출된 7개의 검체 중 6개에서 human parechovirus (HPeV)가 검출되었다. 결론: 열이 있는 90일 미만 영아에서 BioFire^® ME panel 검사법은 원인 병원체가 밝혀진 기존검사 결과와는 비교적 높은 일치도를 보이며, HPeV를 추가적으로 진단할 수 있었다. 향후, 소아청소년 진료 영역에서 BioFire^® ME panel 검사법을 적용할 근거를 마련하기 위한 임상적 유용성과 비용 효과에 대한 연구가 필요하다.

• Molecules and Cells
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• 제26권1호
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• pp.67-73
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• 2008

Herpetic stromal keratitis (HSK) is an inflammatory disorder induced by HSV-1 infection and characterized by T cell-dependent destruction of corneal tissues. It is not known what triggers $CD4^+$ T cell migration into the stroma of HSV-1-infected corneas. The keratocyte is a fibroblast-like cell that can function as an antigen-presenting cell in the mouse cornea by expressing MHC class II and costimulatory molecules after HSV-1 infection. We hypothesized that chemokines produced by stromal keratocytes are involved in $CD4^+$ T cell infiltration into the cornea. We found that keratocytes produce several cytokines and chemokines, including MCP-1, RANTES, and T cell activation (TCA)-3. HSV-1 infection increased the production of MCP-1 and RANTES by keratocytes, and these acted as chemoattractants for HSV-1-primed $CD4^+$ T cells expressing CCR2 and CCR5. ExpreHerpetic stromal keratitis (HSK) is an inflammatory disorder induced by HSV-1 infection and characterized by T cell-dependent destruction of corneal tissues. It is not known what triggers $CD4^+$ T cell migration into the stroma of HSV-1-infected corneas. The keratocyte is a fibroblast-like cell that can function as an antigen-presenting cell in the mouse cornea by expressing MHC class II and costimulatory molecules after HSV-1 infection. We hypothesized that chemokines produced by stromal keratocytes are involved in $CD4^+$ T cell infiltration into the cornea. We found that keratocytes produce several cytokines and chemokines, including MCP-1, RANTES, and T cell activation (TCA)-3. HSV-1 infection increased the production of MCP-1 and RANTES by keratocytes, and these acted as chemoattractants for HSV-1-primed $CD4^+$ T cells expressing CCR2 and CCR5. Expression of MCP-1 in the corneal stroma was confirmed in vivo. Finally, when HSV-1-primed $CD4^+$ T cells were adoptively transferred into wild type and MCP-1-deficient mice that had been sublethally irradiated to minimize chemokine production from immune cells, infiltration of $CD4^+$ T cells was markedly reduced in the MCP-1-deficient mice, suggesting that it is the MCP-1 from HSV-1-infected keratocytes that attracts $CD4^+$ T cells into the cornea.