Development of a Gene Therapy Method for Cervical Cancer Using Attenuated Coxsackievirus B3 as a Vector System

Shim, Seunghyun; Kim, Yeon-Jung; Kim, Dae-Sun; Nam, Jae-Hwan

doi:10.4167/jbv.2011.41.2.123

Cited by 5 publications

(2 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The heart tissues were homogenized in DMEM containing penicillin (100 U/ml) and streptomycin (100 µg/ml). After centrifugation, the viral titers in the supernatants were determined by plaque-forming assay, using standard procedures (Shim et al, 2011).…”

Section: Methodsmentioning

confidence: 99%

Histone deacetylase inhibitors suppress coxsackievirus B3 growth in vitro and myocarditis induced in mice

Shim¹,

Jh²,

Mb³

et al. 2013

View full text Add to dashboard Cite

Summary. -Clinical importance of myocarditis, predominantly caused by coxsackievirus B3 (CVB3), is recently rising. However, a detailed mechanism of pathogenesis of CVB3 myocarditis still needs to be clarified. Recently, it has been reported that histone modifications including acetylation are involved in coxsackievirus replication. To examine whether the CVB3 replication requires histone acetylation, histone deacetylase (HDAC) inhibitors were employed. We found that the HDAC2 activity increased in virus-infected cells at 12 hrs p.i. and that HDAC inhibitors suppressed the virus replication in vitro. This suggests that the HDAC2 activity may be required for the virus replication. Eventually, a HDAC inhibitor trichostatin A protected against CVB3-induced myocardial injury in vivo. Our results suggest that HDAC may be a novel therapeutic target for treating viral myocarditis.Keywords: coxsackievirus B3; histone acetyltransferase; histone deacetylase; HDAC inhibitors, trichostatin A; apicidin; valproic acid; shRNA; myocarditis; mouse * Corresponding author: E-mail: jhnam@catholic.ac.kr; phone: +82-2-2164-4852.

show abstract

Section: Methodsmentioning

confidence: 99%

Histone deacetylase inhibitors suppress coxsackievirus B3 growth in vitro and myocarditis induced in mice

Shim¹,

Jh²,

Mb³

et al. 2013

View full text Add to dashboard Cite

show abstract

“…The cells were then stained with crystal violet solution (Sigma, St. Louis, MO) for 10 min at room temperature and washed with water. Plaques were counted with the naked eye and viral titers were calculated as plaque-forming units (PFU) per gram, as described previously (45).…”

Section: Plaque Assaymentioning

confidence: 99%

IK Induced by Coxsackievirus B3 Infection Transiently Downregulates Expression of MHC Class II Through Increasing cAMP

Park

Kim

et al. 2013

Viral Immunology

Self Cite

View full text Add to dashboard Cite

Major histocompatibility complex (MHC) class II expression is critical for the presentation of antigens in the immune response to viral infection. Consequently, some viruses regulate the MHC class II-mediated presentation of viral antigens as a mechanism of immune escape. In this study, we found that Coxsackievirus B3 (CVB3) infection transiently increased IK expression, which reduced the expression of MHC class II (I-A/I-E) on splenic B cells. Interestingly, CVB3-induced IK elevated cAMP, a downstream molecule of the G protein-coupled receptors, which inhibited MHC class II presentation on B cells. Transgenic mice expressing truncated IK showed lower expression of MHC class II on B cells than did wild-type mice after CVB3 infection. Taken together, these results imply that IK plays a role in downregulating MHC class II expression on B cells during CVB3 infection through the induction of cAMP.

show abstract

Antiviral activity ofBifidobacterium adolescentisSPM1605 against Coxsackievirus B3

Kim

Lee

Park

et al. 2014

Biotechnology & Biotechnological Equipment

View full text Add to dashboard Cite

Bifidobacteria are considered one of the most beneficial probiotics and have been widely studied for their effects against specific pathogens. The present study investigated the antiviral activity of probiotics isolated from Koreans against Coxsackievirus B3 (CVB3). The effect of probiotic isolates against CVB3 was measured by the plaque assay and cellular toxicity of bifidobacteria in HeLa cells was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Among 13 probiotic isolates, 3 Bifidobacterium adolescentis, 2 Bifidobacterium longum and 1 Bifidobacterium pseudocatenulatum had an antiviral effect against CVB3, while the others did not show such effect. B. adolescentis SPM1605 showed the greatest inhibitory properties against CVB3. When the threshold cycle (CT) values for the treated B. adolescentis SPM1605 samples were compared to the results for the non-treated samples, it was shown that the amplified viral sequences from the CVB3 had their copy number lowered by B. adolescentis SPM1605. Moreover, the gene expression in infected HeLa cells was also inhibited by 50%. The results suggest that B. adolescentis SPM1605 suppresses CVB3 and could be used as an alternative therapy against infectious diseases caused by coxsackieviruses.

show abstract

Development of a Gene Therapy Method for Cervical Cancer Using Attenuated Coxsackievirus B3 as a Vector System

Cited by 5 publications

References 16 publications

Histone deacetylase inhibitors suppress coxsackievirus B3 growth in vitro and myocarditis induced in mice

Histone deacetylase inhibitors suppress coxsackievirus B3 growth in vitro and myocarditis induced in mice

IK Induced by Coxsackievirus B3 Infection Transiently Downregulates Expression of MHC Class II Through Increasing cAMP

Antiviral activity ofBifidobacterium adolescentisSPM1605 against Coxsackievirus B3

Contact Info

Product

Resources

About