Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coxsackievirus B4 (CVB4) can cause a broad range of diseases such as aseptic meningitis, meningoencephalitis, myocarditis, hepatitis, pancreatitis, gastroenteritis, necrotizing enterocolitis, pneumonia and sudden death in the neonates. CVB4 has also been implicated as a possible etiological agent for type 1 insulin dependent diabetes mellitus (IDDM). In this study, the possibility of RNA interference (RNAi) as a potential therapeutic approach to treat CVB4 infection was explored. The results showed that the Rhabdomyosarcoma (RD) cells treated with 19-mer siRNAs displayed high specificity against CVB4 replication without displaying any sign of target effects. The siRNA targeting the 3C(pro) region of CVB4 genome was also established to be the most effective in inhibition of CVB4 replication in RD cell line in a dosage dependent manner, indicating its potential to be developed as an antiviral strategy against CVB4.
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PMID:Development of potential antiviral strategy against coxsackievirus B4. 2021 33

Coxsackievirus B3 (CVB3) is associated with several different acute and chronic forms of human disease, including myocarditis, aseptic meningitis, and pancreatitis. Moreover, CVB3 also infects immune cells like CD19+ B lymphocytes, but the viral uptake mechanism into these cells is not well understood. Therefore, primary murine and human CD19+ B cells were isolated by magnetic-activated cell separation technology and analyzed for virus receptor expression, antibody-dependent enhancement of viral infection, and different cellular surface proteins, that might be involved in mechanisms of viral uptake. Western blot analysis of these cells revealed no significant expression of the coxsackievirus-adenovirus receptor CAR. But incubation of CVB3 with serum dilutions, which exhibited binding but not neutralizing characteristics, increased viral uptake and replication significantly in a dose-dependent manner. Viral entry was reduced when Fc portions of immunoglobulins were blocked by protein A treatment. Moreover, the classical complement system rather than Fc-gamma-receptor-mediated mechanisms could be involved in viral uptake. Taken together, these data suggest an antibody-dependent enhancement of CVB3 infection of primary murine and human CD19+ B cells.
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PMID:Antibody-dependent enhancement of coxsackievirus B3 infection of primary CD19+ B lymphocytes. 2071 77

Coxsackievirus B3 (CVB3) is an enterovirus in the family Picornaviridae that is significant to human health, being associated with myocarditis, aseptic meningitis, and pancreatitis, among other conditions. In addition to humans, Sichuan snub-nosed monkeys can be infected and killed by CVB3. Here, we report the first complete genome sequence of a novel coxsackievirus B3 strain, SSM-CVB3, which was isolated from a deceased Sichuan snub-nosed monkey with severe myocarditis. Our findings may aid in understanding the evolutionary characteristics and molecular pathogenesis of this virus.
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PMID:Complete genome sequence of a coxsackievirus B3 isolated from a Sichuan snub-nosed monkey. 2311 60

Coxsackievirus B3 (CVB3), a member of the picornavirus family and enterovirus genus, causes viral myocarditis, aseptic meningitis, and pancreatitis in humans. We genetically engineered a unique molecular marker, "fluorescent timer" protein, within our infectious CVB3 clone and isolated a high-titer recombinant viral stock (Timer-CVB3) following transfection in HeLa cells. "Fluorescent timer" protein undergoes slow conversion of fluorescence from green to red over time, and Timer-CVB3 can be utilized to track virus infection and dissemination in real time. Upon infection with Timer-CVB3, HeLa cells, neural progenitor and stem cells (NPSCs), and C2C12 myoblast cells slowly changed fluorescence from green to red over 72 hours as determined by fluorescence microscopy or flow cytometric analysis. The conversion of "fluorescent timer" protein in HeLa cells infected with Timer-CVB3 could be interrupted by fixation, suggesting that the fluorophore was stabilized by formaldehyde cross-linking reactions. Induction of a type I interferon response or ribavirin treatment reduced the progression of cell-to-cell virus spread in HeLa cells or NPSCs infected with Timer-CVB3. Time lapse photography of partially differentiated NPSCs infected with Timer-CVB3 revealed substantial intracellular membrane remodeling and the assembly of discrete virus replication organelles which changed fluorescence color in an asynchronous fashion within the cell. "Fluorescent timer" protein colocalized closely with viral 3A protein within virus replication organelles. Intriguingly, infection of partially differentiated NPSCs or C2C12 myoblast cells induced the release of abundant extracellular microvesicles (EMVs) containing matured "fluorescent timer" protein and infectious virus representing a novel route of virus dissemination. CVB3 virions were readily observed within purified EMVs by transmission electron microscopy, and infectious virus was identified within low-density isopycnic iodixanol gradient fractions consistent with membrane association. The preferential detection of the lipidated form of LC3 protein (LC3 II) in released EMVs harboring infectious virus suggests that the autophagy pathway plays a crucial role in microvesicle shedding and virus release, similar to a process previously described as autophagosome-mediated exit without lysis (AWOL) observed during poliovirus replication. Through the use of this novel recombinant virus which provides more dynamic information from static fluorescent images, we hope to gain a better understanding of CVB3 tropism, intracellular membrane reorganization, and virus-associated microvesicle dissemination within the host.
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PMID:Coxsackievirus B exits the host cell in shed microvesicles displaying autophagosomal markers. 2472 73

Mumps is a systemic viral illness, preventable by vaccination, that typically affects children and is characterized by unilateral or bilateral swelling of the parotid glands. Uncommon complications such as orchitis, oophoritis, deafness, pancreatitis, aseptic meningitis, and encephalitis occur more often in adults. Recent outbreaks of the disease appear to be caused by a failure to maintain herd immunity in certain populations, particularly in affluent white communities. This article reviews the clinical manifestations, diagnosis, and potential complications in patients with mumps.
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PMID:Mumps: Resurgence of a once-dormant disease. 2964 91

Coxsakievirus (CV) B4, CVB5, and CVA9 belong to the species Enterovirus B. These viruses can cause viral encephalitis, aseptic meningitis, pancreatitis, flaccid paralysis, dilated myocarditis, and hand, foot, and mouth disease (HFMD). In order to analyze the evolution of CVB4, CVB5, and CVA9, we analyzed all of the available genome sequences of Enterovirus B (EVB) isolates and found that there were 12 putative recombination events that produced CVB4, 13 putative recombination events that produced CVB5, and 10 putative recombination events that produced CVA9. These recombination events involved 17 EVB serotypes as major or minor parents. The most active Echovirus (EchoV) appears to have been involved in 20 of the 35 recombination events, acting as one of the parental viruses of circulating CVB4, CVB5, and CVA9 strains. Our study indicates that EchoV plays a major role in recombination in the CVB group, and Echov_E30 is the most active in CVB4, whereas Echov_E3 and Echov_E25 are the most active in CVA9.
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PMID:Echovirus plays a major role in natural recombination in the coxsackievirus B group. 3060 Mar 51


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