Journal of Microbiology

Bang Ju Park

2 Articles

Human cytomegalovirus IE86 protein aa 136–289 mediates STING degradation and blocks the cGAS-STING pathway: Jun-Kyu Lee , Jung-Eun Kim , Bang Ju Park , Yoon-Jae Song; J. Microbiol. 2020;58(1):54-60. Published online January 2, 2020; DOI: https://doi.org/10.1007/s12275-020-9577-6

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We previously reported that human cytomegalovirus (HCMV) 86 kDa immediate-early 2 gene product (IE86) promotes proteasome-dependent degradation of STING. In the present study, we determined the specific residues of IE86 responsible for STING degradation using a STING-firefly luciferase fusion protein expression system for quantitative measurement of STING protein levels. IE86 amino acids (aa) 136–289 were sufficient to promote STING degradation and further induced down-regulation of 2􍿁3􍿁-cyclic GMP-AMP (cGAMP)-mediated IFN-β promoter activation. Interestingly, transactivation domains (TAD) of the IE86 protein located at the N- and C-termini were required for down-regulation of Toll/interleukin-1 receptor (TIR) domain-containing adaptor- inducing interferon β (IFN-β) (TRIF)-mediated IFN-β- and p65/RelA-induced NF-κB-dependent promoter activation while amino acids (aa) 136–289 had no significant effects. Our collective data suggest that the IE86 protein utilizes the aa 136–289 region to promote STING degradation and inhibit the cGAS-STING pathway.

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An ethanol extract of Lysimachia mauritiana exhibits inhibitory activity against hepatitis E virus genotype 3 replication: Seong Eun Jin , Jung-Eun Kim , Sun Yeou Kim , Bang Ju Park , Yoon-Jae Song; J. Microbiol. 2017;55(12):984-988. Published online December 7, 2017; DOI: https://doi.org/10.1007/s12275-017-7477-1

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Abstract PDF

Hepatitis E virus (HEV) is an etiological agent of acute hepatitis E, a self-limiting disease prevalent in developing countries. HEV can cause fulminant hepatic failure with high mortality rates in pregnant women, and genotype 3 is reported to trigger chronic hepatitis in immunocompromised individuals worldwide. Screening of plant extracts for compounds with potential anti-HEV effects led to the identification of a 70% ethanol extract of Lysimachia mauritiana (LME) that interferes with replication of the swine HEV genotype 3 replicon. Furthermore, LME significantly inhibited replication of HEV genotype 3 and expression of HEV ORF2 in infected cells without exerting cytotoxic effects. Collectively, our findings demonstrate the potential utility of LME in the development of novel antiviral drugs against HEV infection.

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