• Clinical and Experimental Vaccine Research
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• v.12 no.2
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• pp.176-178
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• 2023

We report the case of a toddler, with a history of mild atopic dermatitis (AD) since early infancy, presented to the Giannina Gaslini, a pediatric polyclinic hospital, 14 days after measles-mumps-rubella (MMR) vaccination, for the occurrence of a disseminated vesico-pustular rash, accompanied by general malaise, fever, restlessness, and anorexia. Eczema herpeticum (EH) was diagnosed clinically and confirmed by laboratory examinations. The exact pathogenesis of EH in AD is still debated and possibly involves an inter-play between altered cell-mediated and humoral immunity, failure to up-regulate antiviral proteins, and exposure of viral binding sites through the dermatitis and an epidermal barrier failure. We hypothesize that in this particular case, MMR vaccination might have played an additional important role in the alteration of innate immune response, facilitating the manifestation of herpes simplex virus type 1 in the form of EH.

• IMMUNE NETWORK
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• v.15 no.4
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• pp.191-198
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• 2015

Hepatitis B virus (HBV) is responsible for approximately 350 million chronic infections worldwide and is a leading cause of broad-spectrum liver diseases such as hepatitis, cirrhosis and liver cancer. Although it has been well established that adaptive immunity plays a critical role in viral clearance, the pathogenetic mechanisms that cause liver damage during acute and chronic HBV infection remain largely known. This review describes our current knowledge of the immune-mediated pathogenesis of HBV infection and the role of immune cells in the liver injury during hepatitis B.

• 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.

• Clinical and Experimental Pediatrics
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• v.55 no.11
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• pp.445-448
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• 2012

Kikuchi-Fujimoto disease (KFD) is a benign self-limiting disease characterized by fever and lymphadenitis. The etiology and pathogenesis of KFD is unclear. However, two hypotheses have been suggested: a viral infection hypothesis and an autoimmune hypothesis. Several KFD patients with various types of autoimmune diseases have been reported, and these reports support the hypothesis for autoimmune pathogenesis of KFD. Here, we report the case of a 17-year-old female patient diagnosed with KFD and autoimmune thyroiditis. This case serves as additional evidence that the etiology of KFD is autoimmune origin.

• Journal of applied mathematics & informatics
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• v.32 no.3_4
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• pp.475-489
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• 2014

In this paper, a mathematical model for HIV infection with saturating infection rate and time delay is established. By some analytical skills, we study the global asymptotical stability of the viral free equilibrium of the model, and obtain the sufficient conditions for the local asymptotical stability of the other two infection equilibria. Finally, some related numerical simulations are also presented to verify our results.

• BMB Reports
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• v.29 no.2
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• pp.180-182
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• 1996

One of the essential functions of virus surface proteins is the recognition of specific receptors on target cell membranes, and cellular receptors play an important role in viral pathogenesis. But the earliest steps of hepatitis B virus (HBV) infection, such as hepatocyte receptor interaction with the virus, are poorly understood. Previous work has suggested an important role of the preS1 region of HBV envelope protein in mediating viral binding to hepatocytes. Although hepatitis B virus (HBV) infection appears to be initiated by specific binding of virions to cell membrane structures via one or potentially several viral surface proteins, data showing the identification or isolation of the HBV receptor (s) are not yet available. The receptor-like proteins on the plasma membrane surface of HepG2 cells that bind to PreS1 were separated and identified using affinity chromatography, and the amino-terminal amino acid sequences of the receptor-like proteins were determined.

• IMMUNE NETWORK
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• v.22 no.4
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• pp.32.1-32.20
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• 2022

Sjögren syndrome (SS) is a chronic autoimmune disorder that primarily targets the salivary and lacrimal glands. The pathology of these exocrine glands is characterized by periductal focal lymphocytic infiltrates, and both T cell-mediated tissue injury and autoantibodies that interfere with the secretion process underlie glandular hypofunction. In addition to these adaptive mechanisms, multiple innate immune pathways are dysregulated, particularly in the salivary gland epithelium. Our understanding of the pathogenetic mechanisms of SS has substantially improved during the past decade. In contrast to viral infection, bacterial infection has never been considered in the pathogenesis of SS. In this review, oral dysbiosis associated with SS and evidence for bacterial infection of the salivary glands in SS were reviewed. In addition, the potential contributions of bacterial infection to innate activation of ductal epithelial cells, plasmacytoid dendritic cells, and B cells and to the breach of tolerance via bystander activation of autoreactive T cells and molecular mimicry were discussed. The added roles of bacteria may extend our understanding of the pathogenetic mechanisms and therapeutic approaches for this autoimmune exocrinopathy.

• Natural Product Sciences
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• v.17 no.3
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• pp.165-174
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• 2011

Naturally occurring small molecules from plants, microorganisms, and animals allow the design of drugs that can be beneficial in virtually all kinds of human diseases. Liver diseases with diverse etiologies such as viral infection, chemical intoxication, and metabolic fat accumulation are one of the leading causes of human mortality. Unfortunately, however, there are few effective drugs available capable of stopping or reversing the progress of liver disease. Here, we discuss the current advances in developing hepatoprotective natural products for several arrays of liver disease pathogenesis.

• The Journal of Korean Medicine
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• v.20 no.4
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• pp.98-105
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• 2000

Miller Fisher syndrome is characterized by acute external ophthalmoplegia, ataxia and areflexia in the abscence of significant motor or sensory deficit in the limbs and usually results in a complete recovery. Most cases have anteceding events like upper respiratory infection or other viral infections. Its accurate anatomic lesion sites and pathogenesis is still unknown. Recently we experienced a 47 year-old man who had a sudden onset of complete total ophthalmoplegia, ataxia, diplopia and whose condition was improved through Oriental medical treatment.

• The Journal of the Korean Society for Microbiology
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• v.22 no.1
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• pp.1-8
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• 1987

Hantaan virus(HV) 76-118 strain was inoculated into suckling ICR mice by intra-nasal route with an inoculum of $10LD_{50}$. Mortality was 65% at the 3rd week after inoculation, but declined to 35% at the 4th week. Infectivity was determined by the measuring immuno-fluorescent antibody in sera. The peak of infectivity was 80% at the 4'th week after inoculation. Viremia was reached peak level of $1.7{\times}10^4\;PFU/ml$ by day 10. Immunofluorescent antibody and neutralizing antibody appeared by 2 weeks and 15-17 days respectively, but achieved similar titer by 35 days. By using a monoclonal antibody to HV 76-118, viral antigens were initially detected in inguinal and axillary lymph node by 2 days. Viral antigens in bone marrow and lung were delayed much more than in those of lymph node. These were similar with those of intra-peritoneal and intra-muscular route. Immune complex against IgG, IgM and C3 appeared by 16 days, 14 days, and 18 days respectively. The pattern of immunofluorescence in the basement membrane of glomeruli was diffuse membranous. Spotted pattern was also observed in the tissue stained with anti-mouse C3 antibody. By 20 days, control tissue was also shown immune complex in the glomeruli.