• Journal of fish pathology
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• v.30 no.2
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• pp.71-78
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• 2017

The glycoprotein of novirhabdoviruses is known to play a critical role in the determination of host specificity. Viral hemorrhagic septicemia viruses (VHSVs) in different genotypes have different glycoprotein sequences and show different preferences for specific cell lines. In this study, to know whether the glycoprotein is solely responsible for the host cell preference of VHSV, a recombinant VHSV expressing vesicular stomatitis virus (VSV) glycoprotein instead of VHSV IVa glycoprotein (rVHSV-VSV-G) was generated by reverse genetics and inoculated into several fish cell lines, then, cytopathic effect (CPE) and viral growth caused by rVHSV-VSV-G infection were compared with those caused by rVHSV-wild that was previously generated and has the same genomic sequence with wild-type VHSV except a few nucleotides. The plaque numbers of rVHSV-VSV-G were significantly higher in EPC, BF-2 and GF cells than those of rVHSV-wild. However, in HINAE cells (originated from olive flounder), rVHSV-VSV-G titer was significantly lower than rVHSV-wild titer, and both recombinant VHSVs were not grown well in CHSE-214 cells. Although statistical significances were detected in the titers between rVHSV-wild and rVHSV-VSV-G in several cell lines, the cell line-preference order of rVHSV-VSV-G was not different from that of rVHSV-wild. These results suggest that the replacement of VHSV glycoprotein may not completely change host cell preference, and other regions of VHSV might also involve in the determination of host cell preference.

• Molecules and Cells
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• v.37 no.7
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• pp.518-525
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• 2014

Gammaherpesvirus (${\gamma}HV$) infection of the central nervous system (CNS) has been implicated in diverse neurological diseases, and murine ${\gamma}HV$-68 (MHV-68) is known to persist in the brain after cerebral infection. The underlying molecular mechanisms of persistency of virus in the brain are poorly understood. Here, we characterized a unique pattern of MHV-68 persistent infection in neuroblastoma cells. On infection with MHV-68, both murine and human neuroblastoma cells expressed viral lytic proteins and produced virions. However, the infected cells survived productive infection and could be cultured for multiple passages without affecting their cellular growth. Latent infection as well as productive replication was established in these prolonged cultures, and lytic replication was further increased by treatment with lytic inducers. Our results provide a novel system to study persistent infection of ${\gamma}HVs$ in vitro following de novo infection and suggest application of MHV-68 as a potential gene transfer vector to the brain.

• Biomolecules & Therapeutics
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• v.26 no.3
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• pp.290-297
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• 2018

We aimed to understand the molecular changes in host cells that accompany infection by the seasonal influenza A H1N1 virus because the initial response rapidly changes owing to the fact that the virus has a robust initial propagation phase. Human epithelial alveolar A549 cells were infected and total RNA was extracted at 30 min, 1 h, 2 h, 4 h, 8 h, 24 h, and 48 h post infection (h.p.i.). The differentially expressed host genes were clustered into two distinct sets of genes as the infection progressed over time. The patterns of expression were significantly different at the early stages of infection. One of the responses showed roles similar to those associated with the enrichment gene sets to known 'gp120 pathway in HIV.' This gene set contains genes known to play roles in preventing the progress of apoptosis, which infected cells undergo as a response to viral infection. The other gene set showed enrichment of 'Drug Metabolism Enzymes (DMEs).' The identification of two distinct gene sets indicates that the virus regulates the cell's mechanisms to create a favorable environment for its stable replication and protection of gene metabolites within 8 h.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.6 no.1
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• pp.108-115
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• 2006

The inherent biology of neural stem cells (NSCs) endows them with capabilities that not only circumvent many of the limitations of other gene transfer vehicles, but that enable a variety of novel therapeutic strategies heretofore regarded as beyond the purview of neural transplantation, Most neurodegenerative diseases are characterized not by discrete, focal abnormalities but rather by extensive, multifocal, or even global neuropathology. Such widely disseminated lesions have not conventionally been regarded as amenable to neural transplantation. However, the ability of NSCs to engraft diffusely and become integral members of structures throughout the host CNS while also expressing therapeutic molecules may permit these cells to address that challenge. Intriguingly, while NSCs can be readily engineered to express specified foreign genes, other intrinsic factors appear to emanate spontaneously from NSCs and, in the context of reciprocal donor-host signaling, seem to be capable of neuroprotective and/or neuroregenerative functions. Stem cells additionally have the appealing ability to "home in" on pathology, even over great distances. Such observations help to advance the idea that NSCs - as a prototype for stem cells from other solid organs - might aid in reconstructing the molecular and cellular milieu of maid eve loped or damaged organs.

• Biomedical Science Letters
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• v.28 no.4
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• pp.211-222
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• 2022

After more than two years of efforts to end the corona pandemic, a gradual recovery is starting in countries with high vaccination rates. Easing public health policies for a full-fledged post-corona era, such as lifting the mandatory use of outdoor mask and quarantine measures in entry have been considered in Korea. However, the continuous emergence of new variants of SARS-CoV-2 and limitations in vaccine efficacy still remain challenging. Fortunately, T cells and memory T cells, which are key components of adaptive immunity appear to contribute substantially in COVID-19 control. SARS-CoV-2 specific CD4⁺/CD8⁺ T cells are induced by natural infection or vaccination, and rapid induction and activation of T cells is mainly associated with viral clearance and attenuated clinical severity. In addition, T cell responses induced by recognition of a wide range of epitopes were minimally affected and conserved against the highly infectious subsets of omicron variants. Polyfunctional SARS-CoV-2 specific T cell memory including stem cell-like memory T cells were also developed in COVID-19 convalescent patients, suggesting long lasting protective T cell immunity. Thus, a robust T-cell immune response appears to serve as a reliable and long-term component of host protection in the context of reduced efficacy of humoral immunity and persistent mutations and/or immune escape.

• IMMUNE NETWORK
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• v.19 no.1
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• pp.6.1-6.14
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• 2019

Plasmacytoid dendritic cells (pDCs) are a unique subset of cells with different functional characteristics compared to classical dendritic cells. The pDCs are critical for the production of type I IFN in response to microbial and self-nucleic acids. They have an important role for host defense against viral pathogen infections. In addition, pDCs have been well studied as a critical player for breaking tolerance to self-nucleic acids that induce autoimmune disorders such as systemic lupus erythematosus. However, pDCs have an immunoregulatory role in inducing the immune tolerance by generating Tregs and various regulatory mechanisms in mucosal tissues. Here, we summarize the recent studies of pDCs that focused on the functional characteristics of gut pDCs, including interactions with other immune cells in the gut. Furthermore, the dynamic role of gut pDCs will be investigated with respect to disease status including gut infection, inflammatory bowel disease, and cancers.

• Journal of Microbiology and Biotechnology
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• v.27 no.3
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• pp.610-615
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• 2017

When Shigella infect host cells, various effecter molecules are delivered into the cytoplasm of the host cell through the type III secretion system (TTSS) to facilitate their invasion process and control the host immune responses. Among these effectors, the S. flexneri effector OspF dephosphorylates mitogen-activated protein kinases and translocates itself to the nucleus, thus preventing histone H3 modification to regulate expression of proinflammatory cytokines. Despite the critical role of OspF, the mechanism by which it localizes in the nucleus has remained to be elucidated. In the present study, we identified a potential small ubiquitin-related modifier (SUMO) modification site within OspF and we demonstrated that Shigella TTSS effector OspF is conjugated with SUMO in the host cell and this modification mediates the nuclear translocation of OspF. Our results show a bacterial virulence factor can exploit host post-translational machinery to execute its intracellular trafficking.

• Animal cells and systems
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• v.3 no.3
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• pp.243-246
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• 1999

A type of symbiosis was previously described from nature in which the gametophytes of Laminariales were endophytic in filamentous red algae. Here we reconstruct this symbiosis for the first time in laboratory culture using zoospores of the kelp, Undaria pinnatifida, and the red alga, Aglaothamnion oosumiense. Zoospores of U. pinnatifida readily attached to A. oosumiense. In 48 h these spores germinated and the initial germ tube penetrated into the host cell wall leaving only an empty zoospore wall outside the host. Within ten days, four to five-celled endophytic gametophytes were present. Zoospores of Laminaria religiosa which were also inoculated into cultures of A. oosumiense rarely attached to the red alga and never became endophytic. Within ten days the free-living gametophytes of L. religiosa on cover slips became fertile and produced young sporophytes. These observations demonstrate the ability of U. pinnatifida to become endophytic, and show differences in host specificity among kelp species.

• Molecules and Cells
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• v.26 no.5
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• pp.415-426
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• 2008

The interactions between the host and microbial pathogen largely dictate the onset, progression, and outcome of infectious diseases. Pathogens subvert host components to promote their pathogenesis and, among these, cell surface heparan sulfate proteoglycans are exploited by many pathogens for their initial attachment and subsequent cellular entry. The ability to interact with heparan sulfate proteoglycans is widespread among viruses, bacteria, and parasites. Certain pathogens also use heparan sulfate proteoglycans to evade host defense mechanisms. These findings suggest that heparan sulfate proteoglycans are critical in microbial pathogenesis, and that heparan sulfate proteoglycan-pathogen interactions are potential targets for novel prophylactic and therapeutic approaches.

• IMMUNE NETWORK
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• v.3 no.4
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• pp.261-267
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• 2003

The periodontal diseases are infections caused by bacteria in oral biofilm, a gelatinous mat commonly called dental plaque, which is a complex microbial community that forms and adhere to tooth surfaces. Host immune-pathogen interaction in periodontal disease appears to be a complex process, which is regulated not only by the acquired immunity to deal with ever-growing and -invading microorganisms in periodontal pockets, but also by genetic and/or environmental factors. However, our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system in fighting the virulent periodontal pathogens and in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response, in particular, $CD4^+$ T-cells plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction.