| proapoptotic protein siva binds to the muscle protein telethonin in cardiomyocytes during coxsackieviral infection. | coxsackievirus b3 (cvb3) is known to cause a variety of human diseases including acute and chronic myocarditis as well as dilated cardiomyopathy (dcm). however, the mechanisms by which cvb3 causes diseases are not well understood. | 2009 | 18849585 |
| interaction of poly(rc)-binding protein 2 domains kh1 and kh3 with coxsackievirus rna. | recombinant hnrnp k-homology (kh) domains 1 and 3 of the poly(rc)-binding protein (pcbp) 2 were purified and assayed for interaction with coxsackievirus b3 rna in electrophoretic mobility shift assays using in vitro transcribed rnas which represent signal structures of the 5'-nontranslated region. kh domains 1 and 3 interact with the extended cloverleaf rna and domain iv rna of the internal ribosome entry site (ires). kh1 but not kh3 interacts with subdomain iv/c rna, whereas kh3 interacts with ... | 2008 | 18929541 |
| inhibition of rna virus infections with peptide-conjugated morpholino oligomers. | rna virus infections cause immense human disease burdens globally, and few effective antiviral drugs are available for their treatment. peptide-conjugated phosphorodiamidate morpholino oligomers (ppmo) are nuclease resistant and water-soluble single-stranded-dna-analogues that can enter cells readily and act as steric-blocking antisense agents through stable duplex formation with complementary rna. recently there have been a number of publications documenting sequence-specific and dose-dependent ... | 2008 | 18991679 |
| polybrominated diphenyl ether exposure suppresses cytokines important in the defence to coxsackievirus b3 infection in mice. | environmental pollutants can adversely affect the immune system. the host defence during infection depends on cytokine signalling and proper function of immune cells. however, no studies have addressed how polybrominated diphenyl ethers (pbdes) affect cytokine responses. we investigated the combined effects in balb/c mice of human coxsackievirus b3 (cvb3) infection and exposure to pbdes (bde-99 or bromkal mixture) on 21 serum cytokines. the mice were infected (i.p.) on day 0, orally treated with ... | 2009 | 19022362 |
| coxsackievirus b3 vaccines: use as an expression vector for prevention of myocarditis. | coxsackievirus b3 (cvb3), a member of the picornaviridae family, is considered to be one of the most important infectious agents to cause virus-induced myocarditis. despite improvements in studying virus pathology, structure and molecular biology, as well as the diagnosis of this disease, there is still no virus-specific drug or vaccine in clinical use. during the last 20 years many investigations have been performed to develop classic and modern immunization techniques against cvb3-induced hear ... | 2008 | 19053211 |
| [effects of pravastatin on myocardial connexin 43, ifn-gamma and il-10 expressions in a murine model of viral myocarditis induced by coxsackievirus b3]. | to observe the effects of pravastatin on myocardial connexin 43 (cx43), ifn-gamma and il-10 expressions in a murine model of viral myocarditis (vmc) induced by coxsackievirus b3. | 2008 | 19099934 |
| [intracellular clearance of coxsakievirus b3 infection by short interfering rna and its mechanism study]. | to evaluate the possibility of short interfering rna (sirna) inhibiting coxsackievirus b3 (cvb3) infection in vitro, and discover the mechanism initially. | 2008 | 19105337 |
| pathogenesis of myocarditis and dilated cardiomyopathy. | myocarditis is a disease with a variable clinical presentation, ranging from asymptomatic to a fatal outcome. among the recognized causes of myocarditis are mutations in multiple genes; infection by bacterial, rickettsial, mycotic, protozoan, and viral agents; and exposure to drugs, toxins, and alcohol. some subtypes of myocarditis, such as giant cell myocarditis or eosinophilic necrotizing myocarditis, are suspected to be caused by an autoimmune inflammation. several lines of evidence support t ... | 2008 | 19117533 |
| gonadectomy of male balb/c mice increases tim-3(+) alternatively activated m2 macrophages, tim-3(+) t cells, th2 cells and treg in the heart during acute coxsackievirus-induced myocarditis. | the incidence of cardiovascular disease, including inflammatory heart diseases like myocarditis, is increased in men. similarly, male balb/c mice infected with coxsackievirus b3 (cvb3) develop more severe acute inflammation in the heart compared to females. to better understand the effect of male sex hormones on cardiac inflammation, we gonadectomized (gdx) male balb/c mice and examined acute cvb3-induced myocarditis compared to sham controls. viral replication in the heart was not significantly ... | 2009 | 19126426 |
| [effect of cell proliferation and opn expression in rat myocardial fibroblasts infected with coxsackievirus b3]. | | 2008 | 19134257 |
| the effects of nk4 on viral myocarditis mice. | nk4 may be a promising agent to inhibit tumor invasion and metastasis. to observe the effects of nk4 on the cardiovascular system with pathological injury and to discuss the mechanism, we established an experimental model of viral myocarditis (vcm) by coxsackievirus b3 infection in balb/c mice on day 0 and administered nk4 twice daily to the vcm and control mice from day 20 to day 45. we then evaluated the cardiac function by means of ultrasonic inspection. hepatocyte growth factor, tnf (tumor n ... | 2009 | 19150247 |
| attenuation of coxsackievirus b3 by vp2 mutation and its application as a vaccine against virus-induced myocarditis and pancreatitis. | coxsackievirus b3 (cvb3) is a common agent of viral myocarditis, a major cause of sudden cardiac death, and ultimately dilated cardiomyopathy. however, there is no vaccine in clinical use. in this study, we identified the conserved amino acid sequences in the c-terminal region of the vp2 of the coxsackievirus b group and some echoviruses. the mutant virus, yyff, with phenylalanines substituted for two tyrosines in these conserved sequences was highly attenuated in vivo and could induce a high ne ... | 2009 | 19168108 |
| cxcl10 inhibits viral replication through recruitment of natural killer cells in coxsackievirus b3-induced myocarditis. | coxsackievirus (cv)b3 is the primary cause of viral myocarditis. we previously observed cxc chemokine ligand 10 (cxcl10) upregulation in the myocardium early in infection. however, the impact of cxcl10 in cvb3-induced myocarditis is unknown. using isolated primary mouse cardiomyocytes we demonstrated for the first time that cardiomyocytes can express cxcl10 on interferon-gamma stimulation. to explore the role of cxcl10 in cvb3-induced myocarditis, both cxcl10 transgenic and knockout mice were us ... | 2009 | 19168435 |
| impact of myocardial inflammation on cytosolic and mitochondrial creatine kinase activity and expression. | the disturbance of myocardial energy metabolism has been discussed as contributing to the progression of heart failure. little however is known about the cardiac mitochondrial/cytosolic energy transfer in murine and human inflammatory heart disease. we examined the myocardial creatine kinase (ck) system, which connects mitochondrial atp-producing and cytosolic atp-consuming processes and is thus of central importance to the cellular energy homeostasis. the time course of expression and enzymatic ... | 2009 | 19190956 |
| glycerol-3-phosphate acyltransferase 1 is essential for the immune response to infection with coxsackievirus b3 in mice. | livers and hearts from mice deficient in glycerol-3-phosphate acyltransferase 1 (gpat1; gpat1(-/-)) have a decreased content of glycerolipid intermediates and triacylglycerol, an altered composition of liver phospholipids, and elevated markers of oxidative stress. compared with control c57bl/6 mice, infection of gpat1(-/-) mice with coxsackievirus b3 (cvb3) resulted in higher mortality, an approximately 50% increase in heart pathology, a significant increase in liver viral titers, and a 100-fold ... | 2009 | 19193813 |
| bosentan enhances viral load via endothelin-1 receptor type-a-mediated p38 mitogen-activated protein kinase activation while improving cardiac function during coxsackievirus-induced myocarditis. | reduced cardiac output is one of the consequences of myocarditis. bosentan, an endothelin-1 receptor (et1r) antagonist, could be useful to reduce cardiac afterload, preserving cardiac output. in this study, we investigated the potential therapeutic use of bosentan in an animal model of viral myocarditis. using a mouse model of coxsackievirus b3 (cvb3)-induced myocarditis, we demonstrated preserved ejection fraction (ef) and fractional shortening (fs) by treatment with bosentan (68+/-5.8% ef and ... | 2009 | 19213955 |
| the evidence of coxsackievirus b3 induced myocarditis as the cause of death in a sichuan snub-nosed monkey (rhinopithecus roxellana). | a 5-year-old female sichuan snub-nosed monkey died at the zoological garden from infection with coxsackievirus b3. | 2009 | 19220685 |
| enhanced resistance to coxsackievirus b3-induced myocarditis by intranasal co-immunization of lymphotactin gene encapsulated in chitosan particle. | coxsackievirus b3 (cvb3) is a gastrointestinal virus causing myocarditis in human and mice. an ideal vaccine for cvb3-myocarditis requires both humoral and cellular immunity at systemic and mucosal compartments. we described here an enhancing strategy for chitosan-pvp1 vaccine by co-immunizing with lymphotactin (ltn) gene, a t cell-attractive-chemokine, encapsulated in chitosan particle to provide more protection against cvb3. mice were intranasally co-immunized with 4 doses of chitosan-dna vacc ... | 2009 | 19233446 |
| mutations in the nonstructural protein 3a confer resistance to the novel enterovirus replication inhibitor ttp-8307. | a novel compound, ttp-8307, was identified as a potent inhibitor of the replication of several rhino- and enteroviruses. ttp-8307 inhibits viral rna synthesis in a dose-dependent manner, without affecting polyprotein synthesis and/or processing. drug-resistant variants of coxsackievirus b3 were all shown to carry at least one amino acid mutation in the nonstructural protein 3a. in particular, three mutations located in a nonstructured region preceding the hydrophobic domain (v45a, i54f, and h57y ... | 2009 | 19237651 |
| coxsackievirus b3 infection induced viral myocarditis by regulating the expression pattern of chemokines in cardiac myocytes. | viral myocarditis is a common cardiovascular disease, which has greatly threatened human health. however, up to now, the pathogenesis of viral myocarditis has been unclear, which leads to the lack of its effective treatments. to investigate the role of chemokines in pathogenesis of viral myocarditis, mrna expression for a panel of 19 chemokines detected by rt-pcr in myocardial tissue of balb/c mice that were inoculated intraperitoneally with coxsackievirus b3. moreover primary cultured cardiac m ... | 2009 | 19279353 |
| rotavirus and coxsackievirus infection activated different profiles of toll-like receptors and chemokines in intestinal epithelial cells. | to understand the inflammatory-immune response in intestinal epithelial cells after infection of rotavirus and coxsackievirus b3. | 2009 | 19296205 |
| arsenic trioxide affects the trace element balance in tissues in infected and healthy mice differently. | acquired infections are common in cancer patients. as2o3 treatment and infections affect the body's trace element balance. however, it is unknown whether concomitant infections cause adverse element interactions that endanger the safety and therapeutic effect of as2o3. | 2009 | 19331136 |
| cardiac deletion of the coxsackievirus-adenovirus receptor abolishes coxsackievirus b3 infection and prevents myocarditis in vivo. | we investigated the role of the coxsackievirus-adenovirus receptor (car) in viral myocarditis. | 2009 | 19341864 |
| systemic analysis of a novel coxsackievirus gene delivery system in a mouse model. | in order to systemically investigate the possibility of using coxsackievirus b3 (cvb3) to deliver foreign genes in vivo, a recombinant strain of cvb3 encoding the renilla gene (cvb3- renilla) was constructed. the recombinant cvb3 resulted in extensive and transient expression of the renilla protein within mouse organs, especially the pancreas. the level of expression was generally dependent upon the viral titer present. moreover, the cvb3-renilla strain was completely attenuated. interestingly, ... | 2009 | 19349757 |
| [effect of resveratrol on myocardial fibrosis in mice with chronic viral myocarditis]. | some research has shown that resveratrol can ameliorate myocardial injury and improve cardiac function in mice with acute viral myocarditis (vmc), and can inhibit cardiac fibroblast proliferation and myofibroblast differentiation in vitro. this study was designed to investigate whether resveratrol has similar effects in the mouse model of chronic vmc. | 2009 | 19374815 |
| [effect of ifn-lambda2 on apoptotic protein in the myocardium in mice with viral myocarditis]. | inf-lambda has anti-viral and anti-tumor activities. its application in viral myocarditis (vmc) has not been reported. this study investigated the role of inf-lambda in acute vmc in mice. | 2009 | 19374816 |
| packaging limits and stability of hiv-1 sequences in a coxsackievirus b vector. | enteroviruses elicit protective mucosal immune responses that could be harnessed as part of a strategy to prevent sexual transmission of the human immunodeficiency virus-1 (hiv-1). we report the construction of replication-competent recombinant vectors of coxsackievirus b3 (cvb3) that express one or more portions of the hiv-1 gag protein. vectors containing the capsid domain of gag were initially genetically unstable with protein expression lost after brief passage in tissue culture. codon modif ... | 2009 | 19389440 |
| development of troponin autoantibodies in experimental coxsackievirus b3 myocarditis. | autoantibodies against various endogenous proteins are found in myocarditis. troponin autoantibodies are detected in patients with chronic dilated cardiomyopathy, but their presence in myocarditis remains unknown. we set out to study the presence of troponin autoantibodies in experimental viral myocarditis. | 2009 | 19397694 |
| sequential changes in serum cytokines reflect viral rna kinetics in target organs of a coxsackievirus b infection in mice. | the pattern of cytokine responses related to viral replication during the course of the common human coxsackievirus b3 (cvb3) infection is not known. | 2009 | 19430896 |
| altered interactions between stem-loop iv within the 5' noncoding region of coxsackievirus rna and poly(rc) binding protein 2: effects on ires-mediated translation and viral infectivity. | coxsackievirus b3 (cvb3) is a causative agent of viral myocarditis, meningitis, pancreatitis, and encephalitis. much of what is known about the coxsackievirus intracellular replication cycle is based on the information already known from a well-studied and closely related virus, poliovirus. like that of poliovirus, the 5' noncoding region (5' ncr) of cvb3 genomic rna contains secondary structures that function in both viral rna replication and cap-independent translation initiation. for poliovir ... | 2009 | 19446305 |
| inhibition of coxsackievirus b3 and related enteroviruses by antiviral short interfering rna pools produced using phi6 rna-dependent rna polymerase. | coxsackievirus b3 (cbv3) is a member of the human enterovirus b species and a common human pathogen. even though much is known about the enteroviral life cycle, no specific drugs are available to treat enterovirus infections. rna interference (rnai) has evolved to be an important tool for antiviral experimental therapies and gene function studies. we describe here a novel approach for rnai against cbvs by using a short interfering (sirna) pool covering 3.5 kb of cbv3 genomic sequence. the rna-de ... | 2009 | 19553393 |
| viral persistence and chronic immunopathology in the adult central nervous system following coxsackievirus infection during the neonatal period. | coxsackieviruses are significant human pathogens, and the neonatal central nervous system (cns) is a major target for infection. despite the extreme susceptibility of newborn infants to coxsackievirus infection and viral tropism for the cns, few studies have been aimed at determining the long-term consequences of infection on the developing cns. we previously described a neonatal mouse model of coxsackievirus b3 (cvb3) infection and determined that proliferating stem cells in the cns were prefer ... | 2009 | 19570873 |
| protein degradation systems in viral myocarditis leading to dilated cardiomyopathy. | the primary intracellular protein degradation systems, including the ubiquitin-proteasome and the lysosome pathways, have been emerging as central regulators of viral infectivity, inflammation, and viral pathogenicity. viral myocarditis is an inflammatory disease of the myocardium caused by virus infection in the heart. the disease progression of viral myocarditis occurs in three distinct stages: acute viral infection, immune cell infiltration, and cardiac remodelling. growing evidence suggests ... | 2010 | 19578074 |
| effect of interleukin-15 on the course of myocarditis in coxsackievirus b3-infected balb/c mice. | cytokines have an important role in both the initiation and perpetuation of viral myocarditis. because a causative therapy of myocarditis is not yet well established and immunomodulation is a promising approach, the influence of interleukin (il)-15, a proinflammatory cytokine, on the course of experimental myocarditis in coxsackievirus b3 (cvb3)-infected mice was examined. | 2009 | 19584981 |
| lack of il-6 during coxsackievirus infection heightens the early immune response resulting in increased severity of chronic autoimmune myocarditis. | chronic myocarditis is often initiated by viral infection, the most common of which is coxsackievirus infection. the precise mechanism by which viral infection leads to chronic autoimmune pathology is poorly understood, however it is clear that the early immune response plays a critical role. previous results have shown that the inflammatory cytokine interleukin (il)-6 is integral to the development of experimental-induced autoimmune myocarditis. however, the function of il-6 during viral-mediat ... | 2009 | 19587788 |
| differential interferon responses enhance viral epitope generation by myocardial immunoproteasomes in murine enterovirus myocarditis. | murine models of coxsackievirus b3 (cvb3)-induced myocarditis mimic the divergent human disease course of cardiotropic viral infection, with host-specific outcomes ranging from complete recovery in resistant mice to chronic disease in susceptible hosts. to identify susceptibility factors that modulate the course of viral myocarditis, we show that type-i interferon (ifn) responses are considerably impaired in acute cvb3-induced myocarditis in susceptible mice, which have been linked to immunoprot ... | 2009 | 19590042 |
| combination of soluble coxsackievirus-adenovirus receptor and anti-coxsackievirus sirnas exerts synergistic antiviral activity against coxsackievirus b3. | coxsackievirus b3 (cvb-3) is a major causative agent of chronic heart muscle infections. the present study describes a cell culture system with an ongoing virus infection to evaluate two novel inhibitory strategies, either individually or combined: (1) rna interference (rnai) to degrade cytoplasmatic cvb-3 rna and (2) a vector-delivered soluble variant of the coxsackievirus-adenovirus receptor fused to a human immunoglobulin (scar-fc), which inhibits cellular uptake of cvb-3. both approaches wer ... | 2009 | 19591879 |
| depletion of gammadelta+ t cells increases cd4+ foxp3 (t regulatory) cell response in coxsackievirus b3-induced myocarditis. | coxsackievirus b3 (cvb3) causes severe myocarditis in balb/c mice which depends upon cd4(+) t helper type 1 [th1; i.e. interferon-gamma(+) (ifn-gamma(+))] and gammadelta(+) cells. depleting gammadelta(+) cells using anti-gammadelta antibody suppresses myocarditis and cd4(+) ifn-gamma(+) cell numbers in the spleen and heart of infected mice while increasing cd4(+) foxp3(+) cells. mice deficient in gammadelta(+) cells have increased numbers of naïve (cd44(lo) cd62l(hi)) and fewer effector (cd44(hi ... | 2009 | 19604307 |
| differential macrophage polarization in male and female balb/c mice infected with coxsackievirus b3 defines susceptibility to viral myocarditis. | myocardial infiltrating macrophages play an important role in the pathogenesis of viral myocarditis in male balb/c mice following coxsackievirus b3 (cvb3) infection. interestingly, comparable macrophage numbers were observed in the myocardium of female mice during acute myocarditis. | 2009 | 19608981 |
| targeted delivery of anti-coxsackievirus sirnas using ligand-conjugated packaging rnas. | coxsackievirus b3 (cvb3) is a common pathogen of myocarditis. we previously synthesized a sirna targeting the cvb3 protease 2a (sirna/2a) gene and achieved reduction of cvb3 replication by 92% in vitro. however, like other drugs under development, cvb3 sirna faces a major challenge of targeted delivery. in this study, we investigated a novel approach to deliver cvb3 sirnas to a specific cell population (e.g. hela cells containing folate receptor) using receptor ligand (folate)-linked packaging r ... | 2009 | 19616030 |
| bypass suppression of small-plaque phenotypes by a mutation in poliovirus 2a that enhances apoptosis. | the rate of protein secretion in host cells is inhibited during infection with several different picornaviruses, with consequences likely to have significant effects on viral growth, spread, and pathogenesis. this sin(+) (secretion inhibition) phenotype has been documented for poliovirus, foot-and-mouth disease virus, and coxsackievirus b3 and can lead to reduced cell surface expression of major histocompatibility complex class i and tumor necrosis factor receptor as well as reduced extracellula ... | 2009 | 19625405 |
| amyocarditic coxsackievirus b3 causes myocarditis in immunocompromised mice. | in the present study, we investigated the role of the immune status of the host in the pathogenesis and development of coxsackievirus b3 myocarditis. we compared the disease expression in myocarditic coxsackievirus b3 (cb3m)-infected balb/c wild-type mice and severe combined immunodeficient (scid) mice and in amyocarditic coxsackievirus b3 (cb3o)-infected balb/c wild-type mice untreated or treated with immunosuppressive agents and scid mice. there were no differences in viral growth in vitro bet ... | 2003 | 19641653 |
| from gene expression profiles to biological validation in enteroviral heart disease. | in humans, coxsackievirus b3 is the primary etiological agent of viral myocarditis, an inflammatory disease process involving the heart muscle. specific therapy is currently unavailable. viral myocarditis is a complex, multiphasic infectious-inflammatory-reparative process. to address the temporal dimensionality of myocarditis, array- and nonarray-based molecular techniques, and histological and functional assays were used to help define enteroviral pathogenesis and its relation to heart failure ... | 2003 | 19641703 |
| coxsackievirus b3 infection promotes generation of myeloid dendritic cells from bone marrow and accumulation in the myocardium. | myocarditis is associated with increased number of cd4+ t cells in the myocardium after coxsackievirus b3 (cvb3) infection. previous studies show that cd11c+ myeloid dendritic cells (mdc) loaded with myosin could induce myocarditis. this study aims to investigate the generation and accumulation of mdc in cvb3-induced myocarditis. the presence of mdc in myocardium was detected by immunohistochemisty. bone marrow-derived mdc were generated from uninfected and cvb3-infected mice. the percentage of ... | 2009 | 19664723 |
| monoclonal antibodies to vp1 recognize a broad range of enteroviruses. | enteroviruses (evs) are common seasonal viruses that are associated with a variety of diseases. high-quality monoclonal antibodies (mabs) are needed to improve the accuracy of ev diagnosis in clinical laboratories. in the present study, the full-length vp1 genes of poliovirus 1 (polio 1) and coxsackievirus b3 (cox b3) were cloned, and the encoded proteins were expressed and used as antigens in an attempt to raise broad-spectrum mabs to evs. two pan-ev mabs were isolated: one raised against polio ... | 2009 | 19710278 |
| functional role of the 5' terminal cloverleaf in coxsackievirus rna replication. | using cell-free reactions, we investigated the role of the 5' cloverleaf (5'cl) and associated c-rich sequence in coxsackievirus b3 rna replication. we showed that the binding of poly(c) binding protein (pcbp) to the c-rich sequence was the primary determinant of rna stability. in addition, inhibition of negative-strand synthesis was only observed when pcbp binding to both stem-loop 'b' and the c-rich sequence was inhibited. taken together, these findings suggest that pcbp binding to the c-rich ... | 2009 | 19732932 |
| gbf1, a guanine nucleotide exchange factor for arf, is crucial for coxsackievirus b3 rna replication. | the replication of enteroviruses is sensitive to brefeldin a (bfa), an inhibitor of endoplasmic reticulum-to-golgi network transport that blocks activation of guanine exchange factors (gefs) of the arf gtpases. mammalian cells contain three bfa-sensitive arf gefs: gbf1, big1, and big2. here, we show that coxsackievirus b3 (cvb3) rna replication is insensitive to bfa in mdck cells, which contain a bfa-resistant gbf1 due to mutation m832l. further evidence for a critical role of gbf1 stems from th ... | 2009 | 19740986 |
| effects of levosimendan in experimental acute coxsackievirus myocarditis. | acute heart failure is a potentially fatal manifestation of viral myocarditis. development of myocardial damage in myocarditis involves cardiomyocyte apoptosis. levosimendan is a novel calcium sensitizing inotropic agent with anti-apoptotic properties. we studied the feasibility of inotropic treatment with levosimendan and its effects on apoptosis in experimental acute heart failure caused by coxsackievirus myocarditis. | 2009 | 19772522 |
| immunomodulation by atorvastatin upregulates expression of gap junction proteins in coxsackievirus b3 (cvb3)-induced myocarditis. | to investigate the effect of atorvastatin on myocardial expression of gap junction proteins, connexins (cxs), during coxsackievirus b3 (cvb3)-induced myocarditis. | 2010 | 19774449 |
| myocarditis: infection versus autoimmunity. | myocarditis, which is the inflammation of the heart muscle, remains a vexing therapeutic problem. many cases are associated with viral infection, and appropriate treatment may depend upon whether the disease is primarily infectious, immune-mediated, or both. | 2009 | 19826933 |
| coxsackievirus b3 inhibits antigen presentation in vivo, exerting a profound and selective effect on the mhc class i pathway. | many viruses encode proteins whose major function is to evade or disable the host t cell response. nevertheless, most viruses are readily detected by host t cells, and induce relatively strong t cell responses. herein, we employ transgenic cd4(+) and cd8(+) t cells as sensors to evaluate in vitro and in vivo antigen presentation by coxsackievirus b3 (cvb3), and we show that this virus almost completely inhibits antigen presentation via the mhc class i pathway, thereby evading cd8(+) t cell immun ... | 2009 | 19834548 |
| [role of interleukin 17 in viral myocarditis and dilated cardiomyopathy]. | to explore the role of interleukin-17 (il-17) in the evolution of viral myocarditis (vmc) into dilated cardiomyopathy (dcm). | 2009 | 19861249 |
| blocking the cd40-cd40l interaction by cd40-ig reduces disease progress in murine myocarditis induced by cvb3. | cd40 and cd40l, as costimulatory molecules, are reported to play a critical role for cytokine production and antigen-specific t-cell activation in acute viral myocarditis (vmc). the purpose of this study was to probe the therapeutic effect of cd40-ig in coxsackievirus b3 (cvb3)-induced myocarditis. | 2010 | 19914091 |
| the heart-protective mechanism of qishaowuwei formula on murine viral myocarditis induced by cvb3. | the heart-protective effect and mechanism of qishaowuwei formula (qsw), a traditional chinese medicine formula composed of radix astragali, radix paeoniae rubra and fructus schisandrae was investigated on murine model of viral myocarditis (vmc) induced by coxsackievirus b3 (cvb3). | 2010 | 19932162 |
| neutralization of il-17 inhibits the production of anti-ant autoantibodies in cvb3-induced acute viral myocarditis. | anti-adenine nucleotide translocator (ant) autoantibodies are related to the development of coxsackievirus b3 (cvb3)-triggered acute viral myocarditis (avmc). recently, studies suggested that il-17 especially produced by a novel cd4(+) th-cell subset th17 cells contributed to the production of pathogenic autoantibodies in some autoimmune diseases. however, the pathogenic role of il-17 in avmc remains largely unknown. in this study, we investigated whether il-17 was associated with the disease pr ... | 2010 | 19932195 |
| prevention of cardiac dysfunction in acute coxsackievirus b3 cardiomyopathy by inducible expression of a soluble coxsackievirus-adenovirus receptor. | group b coxsackieviruses (cvbs) are the prototypical agents of acute myocarditis and chronic dilated cardiomyopathy, but an effective targeted therapy is still not available. here, we analyze the therapeutic potential of a soluble (s) virus receptor molecule against cvb3 myocarditis using a gene therapy approach. | 2009 | 19933937 |
| systematic analysis of attenuated coxsackievirus expressing a foreign gene as a viral vaccine vector. | recombinant viruses expressing foreign antigens may provide a convenient vaccine vector capable of inducing preventative immunity. in this study, we explored the capacity of highly attenuated coxsackievirus b3 (cvb3) to act as a recombinant vector to deliver foreign genes into experimental animals for the purpose of vaccination. the infectious cdna of highly attenuated cvb3, yyff, which has been reported previously (vaccine 27:1974), was used to construct a recombinant yyff cdna (yyff-hcv) by in ... | 2010 | 19941986 |
| pro-apoptotic activity of mbnip-21 depends on its bnip-2 and cdc42gap homology (bch) domain and is enhanced by coxsackievirus b3 infection. | our previous study reported that mouse bnip-21 (mbnip-21) induces apoptosis through a mitochondria-dependent pathway. to map the functional domains of mbnip-21, we performed mutational analyses and demonstrated that the bnip-2 and cdc42gap homology (bch) domain is required for apoptosis induction by mbnip-21 targeting the mitochondria and inducing cytochrome c release. this pro-apoptotic activity was enhanced by coxsackievirus infection. however, deletion of the bcl-2 homology 3 (bh3)-like domai ... | 2010 | 19951366 |
| [structure and function of the genome of coxsackievirus b3]. | | 2009 | 19954118 |
| generation of in silico predicted coxsackievirus b3-derived mhc class i epitopes by proteasomes. | proteasomes are known to be the main suppliers of mhc class i (mhc-i) ligands. in an attempt to identify coxsackievirus b3 (cvb3)-mhc-i epitopes, a combined approach of in silico mhc-i/transporters associated with antigen processing (tap)-binding and proteasomal cleavage prediction was applied. accordingly, 13 potential epitopes originating from the structural and non-structural protein region of cvb3 were selected for further in vitro processing analysis by proteasomes. mass spectrometry demons ... | 2010 | 19997756 |
| application of small interfering rnas modified by unlocked nucleic acid (una) to inhibit the heart-pathogenic coxsackievirus b3. | this study describes the first application of unlocked nucleic acid (una)-modified small interfering rnas (sirnas) directed against a medically relevant target, the coxsackievirus b3. we systematically analyzed the impact of different sirna modification patterns and observed good compatibility of the introduction of una with the maintenance of high antiviral activity. additionally, the polarity of an sirna was successfully reversed by modulating the relative stability of the termini with locked ... | 2010 | 20005874 |
| left ventricular enlargement in coxsackievirus-b3 induced chronic myocarditis--ongoing inflammation and an imbalance of the matrix degrading system. | enteroviruses, especially coxsackie b3 virus (cvb-3), cause acute viral myocarditis, but the detailed mechanisms leading to chronic left ventricular dysfunction and dilatation remain elusive. myocardial tissues of cvb-3 infected and sham infected male swr/j mice were analyzed after hemodynamic evaluation on days 4, 7, and 28 p.i. by rt-pcr, gelatin zymography, elisa, immunohistochemistry, sirius red staining, and luxol fast blue staining. in the early phase after infection an abnormal diastolic ... | 2010 | 20035743 |
| polypyrimidine tract-binding protein interacts with coxsackievirus b3 rna and influences its translation. | we have investigated the possible role of trans-acting factors interacting with the untranslated regions (utrs) of coxsackievirus b3 (cvb3) rna. we show here that polypyrimidine tract-binding protein (ptb) binds specifically to both 5' and 3' utrs, but with different affinity. we have demonstrated that ptb is a bona fide internal ribosome entry site (ires) trans-acting factor (itaf) for cvb3 rna by characterizing the effect of partial silencing of ptb ex vivo in hela cells. furthermore, ires act ... | 2010 | 20071487 |
| phagocytosis of enterovirus-infected pancreatic beta-cells triggers innate immune responses in human dendritic cells. | type 1 diabetes is a chronic endocrine disorder in which enteroviruses, such as coxsackie b viruses and echoviruses, are possible environmental factors that can trigger or accelerate disease. the development or acceleration of type 1 diabetes depends on the balance between autoreactive effector t-cells and regulatory t-cells. this balance is particularly influenced by dendritic cells (dcs). the goal of this study was to investigate the interaction between enterovirus-infected human pancreatic is ... | 2010 | 20071599 |
| characterization of attenuated coxsackievirus b3 strains and prospects of their application as live-attenuated vaccines. | coxsackievirus strain cvb3 is widespread in the human population and causes myocarditis or pancreatitis. however, despite its clinical impact, there is no commercially available and clinically applicable prophylactic vaccine. this study examines the characteristics of attenuated cvb3 strains developed so far and their application as live-attenuated cvb3 vaccines, and discusses problems to be overcome in the development of live-attenuated vaccines. | 2010 | 20088713 |
| tumor necrosis factor-alpha promotes myocarditis in female mice infected with coxsackievirus b3 through upregulation of cd1d on hematopoietic cells. | coxsackievirus b3 (cvb3) induces cardiac inflammation (myocarditis) in male but not female c57bl/6 mice. protection of females correlates with reduced expression of tnf-alpha and il-1beta at both the mrna and protein levels in the heart. treatment of females with 300 ng/mouse of recombinant tnf-alpha on days +1 and +3 relative to infection restores myocarditis susceptibility to levels approximating those of infected male mice, showing that tnf-alpha deficiency is central to disease resistance. f ... | 2010 | 20121405 |
| melanoma differentiation-associated protein-5 (mda-5) limits early viral replication but is not essential for the induction of type 1 interferons after coxsackievirus infection. | coxsackievirus infections are associated with severe diseases such as myocarditis, meningitis and pancreatitis. to study the contribution of the intracellular viral sensor melanoma differentiation-associated protein-5 (mda-5) in the host immune response to coxsackievirus b3 (cvb3) we infected c57bl/6 and 129/svj mice lacking mda-5. mice deficient in mda-5 showed a dramatically increased susceptibility to cvb3 infection. the loss of mda-5 allowed the virus to replicate faster, resulting in increa ... | 2010 | 20206372 |
| viral myocarditis induced by coxsackievirus b3 in a.by/snj mice: analysis of changes in the myocardial proteome. | enteroviral myocarditis displays highly diverse clinical phenotypes ranging from mild dyspnoea or chest pain to cardiogenic shock and death. despite detailed studies of the virus life cycle in vitro and in vivo, the molecular interplay between host and virus in disease progression is largely unresolved. murine models of coxsackievirus b3 (cvb3)-induced myocarditis well mimic the human disease patterns and can thus be explored to study mechanisms leading from acute to chronic myocarditis. here, w ... | 2010 | 20213679 |
| myeloid differentiation factor-88 contributes to tlr9-mediated modulation of acute coxsackievirus b3-induced myocarditis in vivo. | toll-like receptor 9 (tlr9) is a member of the innate immune system and has been shown to influence myocardial function, but its role in myocarditis is hitherto unknown. we therefore investigated whether or not tlr9 plays a role in this disease in coxsackievirus b3 (cvb3)-induced myocarditis in mice. left ventricular (lv) function, cardiac immune cell infiltration, virus mrna, and components of the tlr9 downstream pathway were investigated in tlr9-deficient [knockout (ko)] and wild-type (wt) mic ... | 2010 | 20228254 |
| [immune effects of four coxsackievirus b3 vp1 dna fusion vaccines in mice]. | to compare the immunogenicity and protective effects on cvb3 infected mice of four dna fusion vaccines coupling coxsackievirus b3 (cvb3) vp1 with macrophage-derived chemokine (mdc), c3d3, shiga toxin b subuit (stxb) and mouse beta-defensin-2 (mbd2), respectively. | 2010 | 20230664 |
| antiviral effect of bosentan and valsartan during coxsackievirus b3 infection of human endothelial cells. | in viral myocarditis, adeno- and enteroviruses have most commonly been implicated as causes of infection. both viruses require the human coxsackie-adenovirus receptor (car) to infect the myocardium. due to its crucial role for viral entry, car-downregulation may lead to novel approaches for treatment for viral myocarditis. in this study, we report on pharmaceutical drug influences on car levels in human umbilical vein endothelial cells (huvec) and cervical carcinoma cells (hela) detected by immu ... | 2010 | 20392896 |
| molecular epidemiology of coxsackievirus b3. | molecular epidemiological characteristics are needed to understand the impact of coxsackievirus b3 (cv-b3) infection, since no cv-b3 genotyping literature is available. twenty-nine cv-b3 taiwan strains obtained from 1992 to 2005 were analyzed. a phylogenetic tree was constructed based on the 290 nucleotide sequence of the vp1 gene of taiwan isolates and in 91 other cv-b3 genbank sequences. five genotypes (gi-gv) were depicted. the gi, gii, and giii were dominant in america and europe, whereas gi ... | 2010 | 20398802 |
| osteopontin: a biomarker to predict the outcome of inflammatory heart disease. | inflammatory processes of the heart are often induced by viruses. although most acute virus-induced myocarditis quickly resolves, some patients develop chronic myocarditis resulting in a considerable disruption of the myocardial matrix network, finally leading to cardiac dysfunction. the death of cardiomyocytes due to virus replication is followed by the attraction of macrophages and t cells to the sites of cardiac damage. ongoing inflammation is usually suppressed by interleukin-10 and transfor ... | 2010 | 20414835 |
| [etiology of hand, foot and mouth disease in guangzhou in 2008]. | to understand the etiology of hand, foot and mouth disease (hfmd) in guangzhou area in 2008. | 2010 | 20426938 |
| carvedilol treatment ameliorates acute coxsackievirus b3-induced myocarditis associated with oxidative stress reduction. | oxidative stress has been implicated in the pathogenesis of acute myocarditis. the imbalance between the occurrence of reactive oxygen species and the cellular antioxidant defense mechanism plays a key role in myocardial injury of viral myocarditis. carvedilol, a nonselective beta-adrenoceptor antagonist with additional alpha1-adrenergic blocking and antioxidant properties, has been shown to be cardioprotective in experimental myocarditis. however, the expression of 4-hydroxy-2-nonenal (4-hne), ... | 2010 | 20457150 |
| influence of cinnamaldehyde on viral myocarditis in mice. | this study was designed to examine the effects of cinnamaldehyde on coxsackievirus b3 (cvb3)-induced viral myocarditis (vmc) and underlying signaling, with a focus on the toll-like receptor (tlr)4-nuclear factor (nf)-kappab pathway. | 2010 | 20460981 |
| a role for toll-like receptor 3 variants in host susceptibility to enteroviral myocarditis and dilated cardiomyopathy. | the innate antiviral response is mediated, at least in part, by toll-like receptors (tlrs). tlr3 signaling is activated in response to viral infection, and the absence of tlr3 in mice significantly increases mortality after infection with enteroviruses that cause myocarditis and/or dilated cardiomyopathy. we screened tlr3 in patients diagnosed with enteroviral myocarditis/cardiomyopathy and identified a rare variant in one patient as well as a significantly increased occurrence of a common polym ... | 2010 | 20472559 |
| differential effects of the putative gbf1 inhibitors golgicide a and ag1478 on enterovirus replication. | the genus enterovirus, belonging to the family picornaviridae, includes well-known pathogens, such as poliovirus, coxsackievirus, and rhinovirus. brefeldin a (bfa) impedes replication of several enteroviruses through inhibition of golgi-specific bfa resistance factor 1 (gbf1), a regulator of secretory pathway integrity and transport. gbf1 mediates the gtp exchange of arf1, which in activated form recruits coatomer protein complex i (cop-i) to golgi vesicles, a process important in transport betw ... | 2010 | 20504936 |
| regulatory t cells protect mice against coxsackievirus-induced myocarditis through the transforming growth factor beta-coxsackie-adenovirus receptor pathway. | coxsackievirus b3 infection is an excellent model of human myocarditis and dilated cardiomyopathy. cardiac injury is caused either by a direct cytopathic effect of the virus or through immune-mediated mechanisms. regulatory t cells (tregs) play an important role in the negative modulation of host immune responses and set the threshold of autoimmune activation. this study was designed to test the protective effects of tregs and to determine the underlying mechanisms. | 2010 | 20530002 |
| coxsackievirus b3 infection activates the unfolded protein response and induces apoptosis through downregulation of p58ipk and activation of chop and srebp1. | cardiomyocyte apoptosis is a hallmark of coxsackievirus b3 (cvb3)-induced myocarditis. we used cardiomyocytes and hela cells to explore the cellular response to cvb3 infection, with a focus on pathways leading to apoptosis. cvb3 infection triggered endoplasmic reticulum (er) stress and differentially regulated the three arms of the unfolded protein response (upr) initiated by the proximal er stress sensors atf6a (activating transcription factor 6a), ire1-xbp1 (x box binding protein 1), and perk ... | 2010 | 20554776 |
| a novel population of myeloid cells responding to coxsackievirus infection assists in the dissemination of virus within the neonatal cns. | enterovirus infection in newborn infants is a significant cause of aseptic meningitis and encephalitis. using a neonatal mouse model, we previously determined that coxsackievirus b3 (cvb3) preferentially targets proliferating neural stem cells located in the subventricular zone within 24 h after infection. at later time points, immature neuroblasts, and eventually mature neurons, were infected as determined by expression of high levels of viral protein. here, we show that blood-derived mac3(+) m ... | 2010 | 20573913 |
| design, synthesis, and biological evaluation of novel coxsackievirus b3 inhibitors. | the synthesis and sar study of a novel class of coxsackievirus b3 (cvb3) inhibitors are reported. these compounds could be considered as the 6-chloropurines substituted at position 9 with variously substituted bicyclic scaffolds (bicyclo[2.2.1]heptane/ene-norbornane or norbornene). the synthesis and biological evaluation of 31 target compounds are described. several of the analogues inhibited cvb3 in the low micromolar range (0.66-2mum). minimal or no cytotoxicity was observed. | 2010 | 20576576 |
| development of an rna extraction protocol for detection of waterborne viruses by reverse transcriptase quantitative pcr (rt-qpcr). | rna extraction from environmental samples yields frequently an rna preparation containing inhibitors of molecular reactions. commercial rna extraction kits commonly permit extraction of only 0.1-0.2 ml sample volume. an rna extraction buffer (rnax buffer) was formulated for the extraction of viral rna from 4.0 ml using a silica column based protocol. to evaluate the rnax buffer based protocol, we used hepatitis a virus (hav) and coxsackievirus b3 (cvb3) to monitor the rna extraction efficiency f ... | 2010 | 20600332 |
| [effect of qihong capsule on hela cells infected by coxsackievirus b3 in vitro]. | to investigate the effects of qihong capsule (qh) on hela cells infected by coxsackievirus b3 (cvb3) in vitro and its potential antiviral mechanism. | 2010 | 20602882 |
| arsenic trioxide influences viral replication in target organs of coxsackievirus b3-infected mice. | new antiviral agents are urgently needed. based on in vitro studies, arsenic trioxide (as₂o₃) seems to affect viral replication, although this has been studied only marginally in vivo. in this study the replication of coxsackievirus b3 (cvb3) was studied in balb/c mice administered 1 mg as₂o₃/kg bw once daily during 7 days of infection and in vero cells exposed for 3 or 5 days to 0.4, 2 or 4 μm as₂o₃. viral rna was measured by reverse transcription pcr (rt-pcr) (in vitro and in vivo) and arsenic ... | 2010 | 20638482 |
| [biological characters of a coxsackievirus b3 variant strain isolated from a hand-foot-mouth disease patient with severe clinical symptoms]. | to analyze the genetic and biological characters of a new isolate of coxsackievirus b3 (coxb3), i.e. fy-19 strain, and investigate its mechanistic role in causing different clinical symptoms of hand-foot-mouth disease (hfmd). | 2010 | 20646436 |
| [relationship between variation of coxsackievirus b3 vp1 sequence from cerebrospinal fluid of children and severity of damage to central nervous system]. | to investigate the possible relationship between variation of coxsackievirus b3 (coxb3) vp1 sequence from cerebrospinal fluid of children with severe and mild central nervous system (cns) infection and damage to cns in children from shandong province. | 2010 | 20654015 |
| antibody-dependent enhancement of coxsackievirus b3 infection of primary cd19+ b lymphocytes. | 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 ... | 2010 | 20712481 |
| [molecular characterization of coxsackievirus b3 isolated from an outbreak of aseptic meningitis in shandong province, china]. | to identify the pathogen caused an outbreak of aseptic meningitis in tancheng county of shandong province in 2008, and to analyze the molecular characterization of vp1 gene of the coxsackievirus b3(cvb3) isolates. | 2009 | 20718355 |
| proteasome activator reggamma enhances coxsackieviral infection by facilitating p53 degradation. | coxsackievirus b3 (cvb3) is a small rna virus associated with diseases such as myocarditis, meningitis, and pancreatitis. we have previously demonstrated that proteasome inhibition reduces cvb3 replication and attenuates virus-induced myocarditis. however, the underlying mechanisms by which the ubiquitin/proteasome system regulates cvb replication remain unclear. in this study, we investigated the role of regγ, a member of the 11s proteasome activator, in cvb3 replication. we showed that overexp ... | 2010 | 20719955 |
| α-galactosylceramide protects mice from lethal coxsackievirus b3 infection and subsequent myocarditis. | myocarditis is an inflammation of the myocardium which often follows virus infections. coxsackievirus b3 (cvb3), as a marker of the enterovirus group, is one of the most important infectious agents of virus-induced myocarditis. using a cvb3-induced myocarditis model, we show that injection α-galactosylceramide (α-galcer), a ligand for invariant natural killer (nk) t (ink t) cells, can protect the mice from viral myocarditis. after the systemic administration of α-galcer in cvb3 infected mice, vi ... | 2010 | 20726989 |
| th17 cells contribute to viral replication in coxsackievirus b3-induced acute viral myocarditis. | acute viral myocarditis (avmc) is characterized by virus-triggered myocardial inflammation, and coxsackievirus b3 (cvb3) is the primary pathogen. we previously proved that th17 cells, besides having proinflammatory effects, were involved in avmc by enhancing humoral response. however, the relationship between th17 cells and cvb3 replication remains unknown. in this experiment, we infected balb/c mice with cvb3 for establishing avmc models and then found that, with the increase of viral replicati ... | 2010 | 20802148 |
| pairwise network mechanisms in the host signaling response to coxsackievirus b3 infection. | signal transduction networks can be perturbed biochemically, genetically, and pharmacologically to unravel their functions. but at the systems level, it is not clear how such perturbations are best implemented to extract molecular mechanisms that underlie network function. here, we combined pairwise perturbations with multiparameter phosphorylation measurements to reveal causal mechanisms within the signaling network response of cardiomyocytes to coxsackievirus b3 (cvb3) infection. using all pos ... | 2010 | 20833815 |
| coxsackievirus infection induces autophagy-like vesicles and megaphagosomes in pancreatic acinar cells in vivo. | autophagy can play an important part in protecting host cells during virus infection, and several viruses have developed strategies by which to evade or even exploit this homeostatic pathway. tissue culture studies have shown that poliovirus, an enterovirus, modulates autophagy. herein, we report on in vivo studies that evaluate the effects on autophagy of coxsackievirus b3 (cvb3). we show that in pancreatic acinar cells, cvb3 induces the formation of abundant small autophagy-like vesicles and p ... | 2010 | 20861268 |
| interaction of decay-accelerating factor with echovirus 7. | echovirus 7 (ev7) belongs to the enterovirus genus within the family picornaviridae. many picornaviruses use igg-like receptors that bind in the viral canyon and are required to initiate viral uncoating during infection. however, in addition, some of the enteroviruses use an alternative or additional receptor that binds outside the canyon. decay-accelerating factor (daf) has been identified as a cellular receptor for ev7. the crystal structure of ev7 has been determined to 3.1-å resolution and u ... | 2010 | 20881044 |
| synthesis and evaluation of pyrazolone compounds as sars-coronavirus 3c-like protease inhibitors. | a series of pyrazolone compounds as possible sars-cov 3cl protease inhibitors were designed, synthesized, and evaluated by in vitro protease assay using fluorogenic substrate peptide in which several showed potent inhibition against the 3cl protease. interestingly, one of the inhibitors was also active against 3c protease from coxsackievirus b3. these inhibitors could be potentially developed into anti-coronaviral and anti-picornaviral agents. | 2010 | 20947359 |
| autoimmunity in coxsackievirus b3 induced myocarditis: role of estrogen in suppressing autoimmunity. | picornaviruses are small, non-enveloped, single stranded, positive sense rna viruses which cause multiple diseases including myocarditis/dilated cardiomyopathy, type 1 diabetes, encephalitis, myositis, orchitis and hepatitis. although picornaviruses directly kill cells, tissue injury primarily results from autoimmunity to self antigens. viruses induce autoimmunity by: aborting deletion of self-reactive t cells during t cell ontogeny; reversing anergy of peripheral autoimmune t cells; eliminating ... | 2010 | 20963181 |
| cardioprotective effect of no-metoprolol in murine coxsackievirus b3-induced myocarditis. | the effect of no-metoprolol, that is, 3-nitrooxypivaloyl metoprolol-amide, a novel no-releasing derivative of the β1-blocking drug metoprolol was investigated in a.ca/snj mice infected with coxsackievirus b3 (cvb3) and compared to metoprolol and placebo. daily treatment of mice with the respective drug started immediately (experiment a) or 3 days after virus infection (experiment b) and was continued until day 13 post-infection (p.i.). two doses of no-metoprolol were administered. body mass diff ... | 2010 | 20981792 |
| a fluorescence resonance energy transfer-based fluorometer assay for screening anti-coxsackievirus b3 compounds. | in view of the need to develop a simple and rapid method to screen for antiviral therapeutic agents, a fluorescence resonance energy transfer (fret)-based reporter system consisting of engineered mammalian cells expressing a cyan fluorescent protein-yellow fluorescent protein (cfp-yfp) pair linked by a short peptide containing the cleavage site of viral protease 2a (2a(pro)) was developed. by detecting the 2a(pro) produced early during the virus infection cycle, the cfp-yfp pair effectively iden ... | 2010 | 21029747 |
| synthesis and antiviral activities of synthetic glutarimide derivatives. | a series of novel glutarimide compounds were synthesized and their antiviral activities were evaluated. the compounds displaying the strongest antiviral activities included 5, 6f, 7e and 9 against coxsackievirus b3 (cox b3), 10 and 6f against influenza virus a (influenza a) and 7a against herpes simplex virus 2 (hsv-2). however, most of the synthetic glutarimides showed comparatively much weaker activity against influenza a, cox b3 and hsv-2 than the natural glutarimide compounds tested. based o ... | 2010 | 21048333 |