• Journal of Periodontal and Implant Science
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• v.43 no.1
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• pp.3-11
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• 2013

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.163-167
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• 2013

The dynamics of the virus-host interface in the response to respiratory virus infection is not well-understood; however, it is at this juncture that host immunity to infection evolves. Respiratory viruses have been shown to modulate the host response to gain a replication advantage through a variety of mechanisms. Viruses are parasites and must co-opt host genes for replication, and must interface with host cellular machinery to achieve an optimal balance between viral and cellular gene expression. Host cells have numerous strategies to resist infection, replication and virus spread, and only recently are we beginning to understand the network and pathways affected. The following is a short review article covering some of the studies associated with the Tripp laboratory that have addressed how respiratory syncytial virus (RSV) operates at the virus-host interface to affects immune outcome and disease pathogenesis.

• Journal of Microbiology and Biotechnology
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• v.29 no.8
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• pp.1184-1192
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• 2019

The influenza A virus is a highly infectious respiratory pathogen that sickens many people with respiratory disease annually. To prevent outbreaks of this viral infection, an understanding of the characteristics of virus-host interaction and development of an anti-viral agent is urgently needed. The influenza A virus can infect mammalian species including humans, pigs, horses and seals. Furthermore, this virus can switch hosts and form a novel lineage. This so-called zoonotic infection provides an opportunity for virus adaptation to the new host and leads to pandemics. Most influenza A viruses express proteins that antagonize the antiviral defense of the host cell. The non-structural protein 1 (NS1) of the influenza A virus is the most important viral regulatory factor controlling cellular processes to modulate host cell gene expression and double-stranded RNA (dsRNA)-mediated antiviral response. This review focuses on the influenza A virus NS1 protein and outlines current issues including the life cycle of the influenza A virus, structural characterization of the influenza A virus NS1, interaction between NS1 and host immune response factor, and design of inhibitors resistant to the influenza A virus.

• 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.

• Journal of Microbiology and Biotechnology
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• v.31 no.2
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• pp.226-232
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• 2021

Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging phlebovirus of the Phenuiviridae family that has been circulating in the following Asian countries: Vietnam, Myanmar, Taiwan, China, Japan, and South Korea. Despite the increasing infection rates and relatively high mortality rate, there is limited information available regarding SFTSV pathogenesis. In addition, there are currently no vaccines or effective antiviral treatments available. Previous reports have shown that SFTSV suppresses the host immune response and its nonstructural proteins (NSs) function as an antagonist of type I interferon (IFN), whose induction is an essential part of the host defense system against viral infections. Given that SFTSV NSs suppress the innate immune response by inhibiting type I IFN, we investigated the mechanism utilized by SFTSV NSs to evade IFNmediated response. Our co-immunoprecipitation data suggest the interactions between NSs and retinoic acid inducible gene-I (RIG-I) or TANK binding kinase 1 (TBK1). Furthermore, confocal analysis indicates the ability of NSs to sequester RIG-I and related downstream molecules in the cytoplasmic structures called inclusion bodies (IBs). NSs are also capable of inhibiting TBK1-interferon regulatory factor 3 (IRF3) interaction, and therefore prevent the phosphorylation and nuclear translocation of IRF3 for the induction of type I IFN. The ability of SFTSV NSs to interact with and sequester TBK1 and IRF3 in IBs demonstrate an effective yet unique method utilized by SFTSV to evade and suppress host immunity.

• The Plant Pathology Journal
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• v.26 no.3
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• pp.209-215
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• 2010

Plant pathogenic oomycetes, such as Phytophthora spp., are the causal agent of the most devastating plant diseases. During infection, these pathogens accomplish parasitic colonization of plants by modulating host defenses through an array of disease effector proteins. These effectors are classified in two classes based on their target sites in the host plant. Apoplastic effectors are secreted into the plant extracellular space, and cytoplasmic effectors are translocated inside the plant cell, through the haustoria that enter inside living host cell. Recent characterization of some oomycete Avr genes showed that they encode effector protein with general modular structure including N-terminal conserved RXLR-DEER motif. More detailed evidences suggest that these AVR effectors are secreted by the pathogenic oomycetes and then translocated into the host plant cell during infection. Recent findings indicated that one of the P. infestans effector, Avrblb2, specifically induces hypersensitive response (HR) in the presence of Solanum bulbocastanum late blight resistance genes Rpi-blb2. On the other hand, another secreted RXLR protein PexRD8 originated from P. infestans suppressed the HCD triggered by the elicitin INF1. In this review, we described recent progress in characterized RXLR effectors in Phytophthora spp. and their dual functions as modulators of host plant immunity.

• 한국균학회소식:학술대회논문집
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• 2014.10a
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• pp.48-48
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• 2014

Arbuscular Mycorrhizal Fungi(AMF) is widespread symbiont forming mutualistic relationship with plant root in terrestrial forest in ecosystem. They provide improved absorption of nutrient and water, and enhance the resistance against plant pathogen or polluted soil, therefore AM fungi are important for survival and maintaining of individual or community of plant. For last decade, many studies about the functional variation of AM fungi on host plant growth response were showed that different geographic isolates, even same species, have different effect on host plant. However, little was known about functional variation of AM fungal isolates originated single population, which provide important insight about intraspecific diversity of AMF and their role in forest ecosystem. In this study, four AM fungal isolates of Rhizophagus clarus were cultured in vitro using transformed carrot (Daucus carota) root and they showed the difference between isolates in ontogenic characteristics such as spore density and hyphal length. The plant growth response by mycorrhizas were measured also. After 20 weeks from inoculation of these isolates to host plants, dry weight, Root:Shoot ratio, colonization rates and N, P concentration of host plant showed host plant was affected differently by AM fungal isolates. This results suggest that AM fungi have high diversity in their functionality in intraspecific level, even in same population.

• The Plant Pathology Journal
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• v.38 no.5
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• pp.432-448
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• 2022

Planthopper infestation in rice causes direct and indirect damage through feeding and viral transmission. Host microbes and small RNAs (sRNAs) play essential roles in regulating biological processes, such as metabolism, development, immunity, and stress responses in eukaryotic organisms, including plants and insects. Recently, advanced metagenomic approaches have facilitated investigations on microbial diversity and its function in insects and plants, highlighting the significance of microbiota in sustaining host life and regulating their interactions with the environment. Recent research has also suggested significant roles for sRNA-regulated genes during rice-planthopper interactions. The response and behavior of the rice plant to planthopper feeding are determined by changes in the host transcriptome, which might be regulated by sRNAs. In addition, the roles of microbial symbionts and sRNAs in the host response to viral infection are complex and involve defense-related changes in the host transcriptomic profile. This review reviews the structure and potential functions of microbes and sRNAs in rice and the associated planthopper species. In addition, the involvement of the microbiota and sRNAs in the rice-planthopper-virus interactions during planthopper infestation and viral infection are discussed.

• 한국생태학회:학술대회논문집
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• 2002.08a
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• pp.83-91
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• 2002

The Red Queen hypothesis for the advantage of sex predicts that pathogens will evolve by increasing fitness with frequent encounters with specific host genotypes. In this study, BMV population size, measured as an indicator of fitness, was investigated during repeated passages through the same, or different host genotypes of the crop host, Hordeum vulgare (barley). Overall, mean BMV concentration within individual hosts was significantly higher in genetically homogeneous compared to heterogeneous host passage lines. In addition, BMV populations, passaged through a specific host variety, showed higher growth in that host variety compared to BMV passaged through varying varieties. These results supports the Red Queen hypothesis. However, the decrease in viral populations during passages contradicts the Red Queen. Nevertheless, the results found here show that even under simplified conditions, pathogens do not evolve in simple, predictable ways. Constraints on pathogen evolution may lead to counterintuitive results.

• The Korean Journal of Ecology
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• v.25 no.4
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• pp.217-225
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• 2002

The Red Queen hypothesis for the advantage of sex predicts that pathogens will evolve by increasing fitness with frequent encounters with specific host genotypes. In this study, BMV population size, measured as an indicator of fitness, was investigated during repeated passages through the same, or different host genotypes of the crop host, Hordeum vulgare (barley). Overall, mean BMV concentration within individual hosts was significantly higher in genetically homogeneous compared to heterogeneous host passage lines. In addition, BMV populations, passaged through a specific host variety, showed higher growth in that host variety compared to BMV passaged through varying varieties. These results supports the Red Queen hypothesis. However, the decrease in viral populations during passages contradicts the Red Queen. Nevertheless, the results found here show that even under simplified conditions, pathogens do not evolve in simple, predictable ways. Constraints on pathogen evolution may lead to counterintuitive results.