• Nutrition Research and Practice
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• v.15 no.sup1
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• pp.1-21
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• 2021

The coronavirus disease 2019 (COVID-19) pandemic has put focus on the importance of a healthy immune system for recovery from infection and effective response to vaccination. Several nutrients have been under attention because their nutritional statuses showed associations with the incidence or severity of COVID-19 or because they affect several aspects of immune function. Nutritional status, immune function, and viral infection are closely interrelated. Undernutrition impairs immune function, which can lead to increased susceptibility to viral infection, while viral infection itself can result in changes in nutritional status. Here, we review the roles of vitamins A, C, D, and E, and zinc, iron, and selenium in immune function and viral infection and their relevance to COVID-19.

• IMMUNE NETWORK
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• v.4 no.2
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• pp.73-80
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• 2004

Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.

• Journal of Veterinary Science
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• v.24 no.4
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• pp.53.1-53.12
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• 2023

Background: Mammalian orthoreovirus type 3 (MRV3), which is responsible for gastroenteritis in many mammalian species including pigs, has been isolated from piglets with severe diarrhea. However, the use of pig-derived cells as an infection model for swine-MRV3 has rarely been studied. Objectives: This study aims to establish porcine intestinal organoids (PIOs) and examine their susceptibility as an in vitro model for intestinal MRV3 infection. Methods: PIOs were isolated and established from the jejunum of a miniature pig. Established PIOs were characterized using polymerase chain reaction (PCR) and immunofluorescence assays (IFAs) to confirm the expression of small intestine-specific genes and proteins, such as Lgr5, LYZI, Mucin-2, ChgA, and Villin. The monolayered PIOs and three-dimensional (3D) PIOs, obtained through their distribution to expose the apical surface, were infected with MRV3 for 2 h, washed with Dulbecco's phosphate-buffered saline, and observed. Viral infection was confirmed using PCR and IFA. We performed quantitative real-time reverse transcription-PCR to assess changes in viral copy numbers and gene expressions linked to intestinal epithelial genes and antiviral activity. Results: The established PIOs have molecular characteristics of intestinal organoids. Infected PIOs showed delayed proliferation with disruption of structures. In addition, infection with MRV3 altered the gene expression linked to intestinal epithelial cells and antiviral activity, and these effects were observed in both 2D and 3D models. Furthermore, viral copy numbers in the supernatant of both models increased in a time-dependent manner. Conclusions: We suggest that PIOs can be an in vitro model to study the infection mechanism of MRV3 in detail, facilitating pharmaceutical development.

• Journal of applied mathematics & informatics
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• v.29 no.5_6
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• pp.1117-1127
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• 2011

In this paper, a class of more general delayed viral infection model with lytic immune response is proposed by Song et al.[1] ([Journal of Mathematical Analysis Application 373 (2011), 345-355). We derive the basic reproduction numbers $R_0$ and $R_0^*$ 0 for the viral infection, and establish that the global dynamics are completely determined by the values of $R_0$ and $R_0^*$. If $R_0{\leq}1$, the viral-free equilibrium $E_0$ is globally asymptotically stable; if $R_0^*{\leq}1$ < $R_0$, the immune-free equilibrium $E_1$ is globally asymptotically stable; if $R_0^*$ > 1, the chronic-infection equilibrium $E_2$ is globally asymptotically stable by using the method of Lyapunov function.

• BMB Reports
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• v.45 no.4
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• pp.213-220
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• 2012

Viruses have evolved to manipulate the host cell machinery for virus propagation, in part by interfering with the host cellular signaling network. Molecular studies of individual pathways have uncovered many viral host-protein targets; however, it is difficult to predict how viral perturbations will affect the signaling network as a whole. Systems biology approaches rely on multivariate, context-dependent measurements and computational analysis to elucidate how viral infection alters host cell signaling at a network level. Here we describe recent advances in systems analyses of signaling networks in both viral and non-viral biological contexts. These approaches have the potential to uncover virus- mediated changes to host signaling networks, suggest new therapeutic strategies, and assess how cell-to-cell variability affects host responses to infection. We argue that systems approaches will both improve understanding of how individual virus-host protein interactions fit into the progression of viral pathogenesis and help to identify novel therapeutic targets.

• Journal of applied mathematics & informatics
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• v.32 no.5_6
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• pp.555-566
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• 2014

In this paper, we formulate two chemostat type models of phytoplankton and zooplankton population dynamics with instant nutrient recycling to study the role of viral infection on phytoplankton. The infection is transmitted only among phytoplankton population and it makes them more vulnerable to predation by zooplankton. It is observe that the chemostat system is very stable in the absence of viral infection but the presence of viral infection make the chemostat system sensitive with respect to the grazing rate of infected-phytoplankton by zooplankton. Further, if the grazing rate is less than certain threshold the system remain stable and exhibits Hopf-bifurcation after crossing it.

• BMB Reports
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• v.36 no.1
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• pp.138-143
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• 2003

Of many viral causes of human cancer, few are of greater global importance than the hepatitis B virus (HBV). Over 250 million people worldwide are persistently infected with HBV. A significant minority of these develop severe pathologic consequences, including chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). Earlier epidemiological evidence suggested a link between chronic HBV infection and HCC. Further, the existence of related animal viruses that induce acute and chronic infections of the liver, and eventually HCC, confirms the concept that HBV belongs to one of the few human oncogenic viruses. Although it is clear that chronic HBV infections are major risk factors, relatively little is understood about how the viral factors contribute to hepatocarcinogenesis. This review will introduce molecular aspects of the viral infection, and highlight recent findings on the viral contribution to hepatocarcinogenesis.

• Journal of fish pathology
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• v.6 no.2
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• pp.191-195
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• 1993

With the rapid progress in seed production techniques, aquaculture production of economically important species of marine fish has been accelerated in Japan. Howecer, mass mortalities due to viral infections as well as other microbial infections have often occurred during the seed production and grow-out stages. Among these diseases, four viral diseases have been known in cultured Japanese flounder (Paralichthys olivaceus) since around 1980. In this paper, viral diseases of cultured flounder in Japan are briefly reviewed, with special attention to two viral diseases. viral epidermal hyperplasia and rhabdovirus infection which are relatively important because of their frequent occurrence. Viral epidermal hyperplasia is characterized by fin opacity and associated with high mortality in larval flounder Electron microscopy of affected epidermal cells and transmission experiments with tissue filtrates demonstrated that the disease was caused by a herpesvirus but the agent has not been isolated in fish cell lines. On the other hand, rhabdovires infection occurrs in juvenile and production size fish with hemorrhage in the skeltal muscle and fins, congestion of the gonads, and ascites. A rhabdovirys was isolated in RTG-2 cells from the diseased flounder as a causative agent, which was designated hirame rhabdovirus (HRV) or Rahbdovirus olivaceus. HRV is serologically distinguishable from other known fish rhabdoviruses. Intensive researches on these viral diseases started in 1980th. but properties of the causative agents and infection mechanisms have not been fully investigated. This results in difficulty in controlling these diseases.

• Proceedings of the Microbiological Society of Korea Conference
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• 2000.10a
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• pp.66-77
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• 2000

For a variety of viruses, the primary virus infection has been shown to prevent superinfection with a homologous secondary virus; however, the mechanism of exclusion has not been clearly understood. In this work, we demonstrated that BVDV -infected MDBK cells were protected from superinfection with a homologous superinfecting BVDV, one of the positive-sense RNA pestiviruses, but not with an unrelated rhabdovirus, such as vesicular stomatitis virus. Once superinfection exclusion was established by a primary infection with BVDV, the transfected infectious BVD viral RNA genome was shown to be competent for viral translation, but not viral replication. In addition, our results also demonstrated that upon superinfection, the. viral RNA genome of viral particles was not transferred into the cytoplasm of BVDV -infected cells. Using newly developed system involving rapid generation of the MDBK cells expressing BVD viral proteins, we subsequently found that expression of the viral structural proteins was dispensable for the block occurring at the level of viral RNA replication, but required for the exclusion at the level of viral entry step. Altogether, these findings provide evidence that the superinfection exclusion of BVDV occurs not only at the level of viral replication in which the viral replicase are involved, but also at the level of viral entry with which the viral structural proteins are associated, and that a cellular factor(s) play an essential role in this process.

• Childhood Kidney Diseases
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• v.19 no.2
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• pp.118-124
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• 2015

Purpose: The symptoms and signs of urinary tract infection (UTI) in early infancy are non-specific. Prompt diagnosis of UTI is important, as untreated UTI results in renal damage. Especially, febrile UTI in young infants coexist with other serious bacterial infections. The purpose this study was to propose modified Rochester criteria to differentiate viral infection from urinary tract infection. Methods: We carried out a retrospective investigation of 168 infants less than three months old with a tympanic temperature $>38^{\circ}C$ who were admitted to Chung-Ang University Hospital between 2011 and 2014. We compared the symptoms, physical examination results, and laboratory data between viral infection and UTI groups. A modified Rochester criterion was composed of statistically significant factors. Results: A total of 76 and 92 infants with UTI and a viral infection, respectively, were included. Statistically significant differences in gender, previous admission history, neutrophil ratio, and urine WBC count were found between the two study groups. Using a cut off value of 3 points, the sensitivity and specificity of the modified Rochester criteria were 71.28% and 78.57%, respectively. Conclusion: The modified Rochester criteria may give an outline for identifying young infants with UTI.