Relevant bibliographies by topics / CVB3 infection

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Academic literature on the topic 'CVB3 infection'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "CVB3 infection"

1

Lasrado, Ninaad, Rajkumar Arumugam, Mahima T. Rasquinha, Meghna Sur, David Steffen, and Jay Reddy. "Mt10-CVB3 Vaccine Virus Protects against CVB4 Infection by Inducing Cross-Reactive, Antigen-Specific Immune Responses." Microorganisms 9, no. 11 (November 10, 2021): 2323. http://dx.doi.org/10.3390/microorganisms9112323.

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Group B coxsackieviruses (CVB) containing six serotypes, B1–B6, affect various organs, and multiple serotypes can induce similar diseases such as myocarditis and pancreatitis. Yet, no vaccines are currently available to prevent these infections. Translationally, the derivation of vaccines that offer protection against multiple serotypes is highly desired. In that direction, we recently reported the generation of an attenuated strain of CVB3, termed Mt10, which completely protects against both myocarditis and pancreatitis induced by the homologous wild-type CVB3 strain. Here, we report that the Mt10 vaccine can induce cross-protection against multiple CVB serotypes as demonstrated with CVB4. We note that the Mt10 vaccine could induce cross-reactive neutralizing antibodies (nABs) against both CVB1 and CVB4. In challenge studies with CVB4, the efficacy of the Mt10 vaccine was found to be 92%, as determined by histological evaluation of the heart and pancreas. Antibody responses induced in Mt10/CVB4 challenged animals indicated the persistence of cross-reactive nABs against CVB1, CVB3, and CVB4. Evaluation of antigen-specific immune responses revealed viral protein 1 (VP1)-reactive antibodies, predominantly IgG2a, IgG2b, IgG3, and IgG1. Similarly, by using major histocompatibility complex class II tetramers, we noted induction of VP1-specific CD4 T cells capable of producing multiple T cell cytokines, with interferon-γ being predominant. Finally, none of the vaccine recipients challenged with CVB4 revealed the presence of viral nucleic acid in the heart or pancreas. Taken together, our data suggest that the Mt10 vaccine can prevent infections caused by multiple CVB serotypes, paving the way for the development of monovalent CVB vaccines to prevent heart and pancreatic diseases of enteroviral origin.
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2

Mone, Kiruthiga, Ninaad Lasrado, Meghna Sur, and Jay Reddy. "Vaccines against Group B Coxsackieviruses and Their Importance." Vaccines 11, no. 2 (January 27, 2023): 274. http://dx.doi.org/10.3390/vaccines11020274.

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The group B coxsackieviruses (CVBs) exist in six serotypes (CVB1 to CVB6). Disease associations have been reported for most serotypes, and multiple serotypes can cause similar diseases. For example, CVB1, CVB3, and CVB5 are generally implicated in the causation of myocarditis, whereas CVB1 and CVB4 could accelerate the development of type 1 diabetes (T1D). Yet, no vaccines against these viruses are currently available. In this review, we have analyzed the attributes of experimentally tested vaccines and discussed their merits and demerits or limitations, as well as their impact in preventing infections, most importantly myocarditis and T1D.
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3

Gangaplara, Arunakumar, Chandirasegaran Massilamany, Ninaad Lasrado, David Steffen, and Jay Reddy. "Evidence for Anti-Viral Effects of Complete Freund’s Adjuvant in the Mouse Model of Enterovirus Infection." Vaccines 8, no. 3 (July 7, 2020): 364. http://dx.doi.org/10.3390/vaccines8030364.

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Group B coxsackieviruses (CVBs) belonging to the genus, Enterovirus and contain six serotypes that induce various diseases, whose occurrence may involve the mediation of more than one serotype. We recently identified immunogenic epitopes within coxsackieviruses B3 (CVB3) viral protein 1 that induce anti-viral T cell responses in mouse models of CVB infections. In our investigations to determine the protective responses of the viral epitopes, we unexpectedly noted that animals immunized with complete Freund’s adjuvant (CFA) alone and later challenged with CVB3 were completely protected against myocarditis. Similarly, the pancreatitis-inducing ability of CVB3 was remarkably reduced to only 10% in the CFA group as opposed to 73.3% in the control group that received no CFA. Additionally, no mortalities were noted in the CFA group, whereas 40% of control animals died during the course of 21 days post-infection with CVB3. Taken together, our data suggest that the adjuvant effects of CFA may be sufficient for protection against CVB infections. These observations may provide new insights into our understanding of the occurrence of viral infections.
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4

Fu, Yuxuan, and Sidong Xiong. "Exosomes mediate Coxsackievirus B3 transmission and expand the viral tropism." PLOS Pathogens 19, no. 1 (January 12, 2023): e1011090. http://dx.doi.org/10.1371/journal.ppat.1011090.

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Specific virus-receptor interactions are important determinants in viral host range, tropism and pathogenesis, influencing the location and initiation of primary infection as well as viral spread to other target organs/tissues in the postviremic phase. Coxsackieviruses of Group B (CVB) and its six serotypes (CVB1-6) specifically interact with two receptor proteins, coxsackievirus-adenovirus receptor (CAR) and decay-accelerating factor (DAF), and cause various lesions in most permissive tissues. However, our previous data and other studies revealed that virus receptor-negative cells or tissues can be infected with CVB type 3 (CVB3), which can also effectively replicate. To study this interesting finding, we explored the possibility that exosomes are involved in CVB3 tropism and that exosomes functionally enhance CVB3 transmission. We found that exosomes carried and delivered CVB3 virions, resulting in efficient infection in receptor-negative host cells. We also found that delivery of CVB3 virions attached to exosomes depended on the virus receptor CAR. Importantly, exosomes carrying CVB3 virions exhibited greater infection efficiency than free virions because they accessed various entry routes, overcoming restrictions to viral tropism. In vivo experiments demonstrated that inhibition of exosome coupling with virions attenuated CVB3-induced immunological system dysfunction and reduced mortality. Our study describes a new mechanism in which exosomes contribute to viral tropism, spread, and pathogenesis.
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5

Girn, Jaskamal, Mojgan Kavoosi, and Janet Chantler. "Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain." Journal of General Virology 83, no. 2 (February 1, 2002): 351–58. http://dx.doi.org/10.1099/0022-1317-83-2-351.

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Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10–50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab′)2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1–2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual.
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6

Tracy, S., K. M. Drescher, N. M. Chapman, K. S. Kim, S. D. Carson, S. Pirruccello, P. H. Lane, J. R. Romero, and J. S. Leser. "Toward Testing the Hypothesis that Group B Coxsackieviruses (CVB) Trigger Insulin-Dependent Diabetes: Inoculating Nonobese Diabetic Mice with CVB Markedly Lowers Diabetes Incidence." Journal of Virology 76, no. 23 (December 1, 2002): 12097–111. http://dx.doi.org/10.1128/jvi.76.23.12097-12111.2002.

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ABSTRACT Insulin-dependent (type 1) diabetes mellitus (T1D) onset is mediated by individual human genetics as well as undefined environmental influences such as viral infections. The group B coxsackieviruses (CVB) are commonly named as putative T1D-inducing agents. We studied CVB replication in nonobese diabetic (NOD) mice to assess how infection by diverse CVB strains affected T1D incidence in a model of human T1D. Inoculation of 4- or 8-week-old NOD mice with any of nine different CVB strains significantly reduced the incidence of T1D by 2- to 10-fold over a 10-month period relative to T1D incidences in mock-infected control mice. Greater protection was conferred by more-pathogenic CVB strains relative to less-virulent or avirulent strains. Two CVB3 strains were employed to further explore the relationship of CVB virulence phenotypes to T1D onset and incidence: a pathogenic strain (CVB3/M) and a nonvirulent strain (CVB3/GA). CVB3/M replicated to four- to fivefold-higher titers than CVB3/GA in the pancreas and induced widespread pancreatitis, whereas CVB3/GA induced no pancreatitis. Apoptotic nuclei were detected by TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay in CVB3/M-infected pancreata but not in CVB3/GA-infected pancreata. In situ hybridization detected CVB3 RNA in acinar tissue but not in pancreatic islets. Although islets demonstrated inflammatory infiltrates in CVB3-protected mice, insulin remained detectable by immunohistochemistry in these islets but not in those from diabetic mice. Enzyme-linked immunosorbent assay-based examination of murine sera for immunoglobulin G1 (IgG1) and IgG2a immunoreactivity against diabetic autoantigens insulin and HSP60 revealed no statistically significant relationship between CVB3-protected mice or diabetic mice and specific autoimmunity. However, when pooled sera from CVB3/M-protected mice were used to probe a Western blot of pancreatic proteins, numerous proteins were detected, whereas only one band was detected by sera from CVB3/GA-protected mice. No proteins were detected by sera from diabetic or normal mice. Cumulatively, these data do not support the hypothesis that CVB are causative agents of T1D. To the contrary, CVB infections provide significant protection from T1D onset in NOD mice. Possible mechanisms by which this virus-induced protection may occur are discussed.
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7

Kemball, Christopher C., Stephanie Harkins, Jason K. Whitmire, Ralph Feuer, Claudia T. Flynn, and J. Lindsay Whitton. "Coxsackievirus B3 has profoundly different inhibitory effects on the MHC class I and class II antigen presentation pathways (131.2)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 131.2. http://dx.doi.org/10.4049/jimmunol.182.supp.131.2.

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Abstract Coxsackievirus B (CVB) infections cause considerable morbidity and mortality, and strategies to treat or prevent CVB-associated disease may benefit from a clearer understanding of the host immune response to virus infection. CVB3 induces minimal endogenous naïve CD8 and CD4 T cell responses, possibly because viral antigen (Ag) presentation is extremely limited. Several CVB3 proteins are known to cooperatively downregulate MHC class I on infected cells in vitro. In this study, we used transgenic (Tg) CD4 and CD8 T cells as sensors to evaluate viral Ag presentation by the MHC class I and class II pathways in vivo. Our analysis revealed a striking difference in Tg T cell responses: CD4 Tg T cells proliferated in CVB3-infected mice whereas CD8 Tg T cells failed to divide. Moreover, virus infection generated multi-functional memory CD4 T cells, which expanded dramatically following challenge infection, and rapidly differentiated into secondary effector Th1 cells. Although naïve CD8 Tg T cells were unresponsive to CVB3, they persisted in the host and responded vigorously when stimulated by a different virus encoding their cognate Ag. These data suggest that CVB3 utilizes a powerful immune evasion strategy in vivo that differentially affects the two Ag presentation pathways, and that this difference regulates the host's capacity to mount CD4 and CD8 T cell responses. This work was supported by NIH R01 AI42314 and T32 NS41219.
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8

Gao, Guang, Jerry Wong, Jingchun Zhang, Ivy Mao, Jayant Shravah, Yan Wu, Allen Xiao, Xiaotao Li, and Honglin Luo. "Proteasome Activator REGγ Enhances Coxsackieviral Infection by Facilitating p53 Degradation." Journal of Virology 84, no. 21 (August 18, 2010): 11056–66. http://dx.doi.org/10.1128/jvi.00008-10.

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ABSTRACT 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 overexpression of REGγ promoted CVB3 replication but that knockdown of REGγ led to reduced CVB3 replication. We further demonstrated that REGγ-mediated p53 proteolysis contributes, as least in part, to the proviral function of REGγ. Although total protein levels of REGγ remained unaltered after CVB3 infection, virus infection induced a redistribution of REGγ from the nucleus to the cytoplasm, rendering an opportunity for a direct interaction of REGγ with viral proteins and/or host proteins (e.g., p53), which controls viral growth and thereby enhances viral infectivity. Further analyses suggested a potential modification of REGγ by SUMO following CVB3 infection, which was verified by both in vitro and in vivo sumoylation assays. Sumoylation of REGγ may play a role in its nuclear export during CVB3 infection. Taken together, our results present the first evidence that the host REGγ pathway is utilized and modified during CVB3 infection to promote efficient viral replication.
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9

Lasrado, Ninaad, Arunakumar Gangaplara, Rajkumar Arumugam, Chandirasegaran Massilamany, Sayli Pokal, Yuzhen Zhou, Shi-Hua Xiang, David Steffen, and Jay Reddy. "Identification of Immunogenic Epitopes That Permit the Detection of Antigen-Specific T Cell Responses in Multiple Serotypes of Group B Coxsackievirus Infections." Viruses 12, no. 3 (March 21, 2020): 347. http://dx.doi.org/10.3390/v12030347.

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Coxsackievirus group B (CVB) contains six serotypes that can affect various organs. Some of these organ-specific diseases such as myocarditis and pancreatitis can be caused by more than one serotype. Thus, development of immunological tools common to multiple serotypes is desired. This is especially critical for analyzing antigen-specific T cell responses at a single cell level. To this end, we made efforts to identify the immunogenic epitopes of CVB3 leading us to localize three T cell epitopes within the viral protein 1 (VP1) namely, VP1 681–700, VP1 721–740 and VP1 771–790. First, we confirmed their immunogenicity in the immunization settings. Second, we sought to verify the ability of VP1 epitopes to bind major histocompatibility complex (MHC) class II (IAk) molecules. Third, we created MHC class II (IAk) dextramers and tetramers and ascertained the T cell responses to be antigen-specific. Fourth, we analyzed the T cell responses in animals infected with CVB3 and noted the magnitude of antigen-specific T cell responses occurring in the order of VP1 721–740 and VP1 681–700 followed by VP1 771–790 as verified by proliferation assay and IAk tetramer staining. All epitopes induced interferon (IFN)-γ as a major cytokine. Finally, we investigated whether the VP1 tools generated for CVB3 can also be used to verify T cell responses in infections caused by other serotypes. To this end, we established the CVB4 infection model in A/J mice and found that the CVB4 infection led to the induction of IFN-γ-producing T cell responses primarily for VP1 721–740 and VP1 681–700. Thus, the VP1-specific tools, particularly IAk tetramers can be used to monitor anti-viral T cell responses in multiple CVB serotypes.
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10

Lasrado, Ninaad, Mahima T. Rasquinha, Meghna Sur, Arunakumar Gangaplara, Chandirasegaran Massilamany, Rajkumar Arumugam, David Steffen, and Jay Reddy. "A live-attenuated mutant CVB3 vaccine virus protects against multiple coxsackievirus B infections." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 64.11. http://dx.doi.org/10.4049/jimmunol.208.supp.64.11.

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Abstract Group B Coxsackieviruses (CVB) contains six serotypes, namely CVB1 through CVB6, affecting various organs. But, no vaccines are currently available to prevent these infections. We recently derived a live attenuated vaccine virus termed mutant (Mt) 10 encoding a single amino acid substitution H790A within the viral protein 1 (VP1) of the CVB3 viral canyon region. This virus could prevent myocarditis and pancreatitis caused by both homologous (CVB3) and heterologous (CVB4) serotypes in A/J mice. Mechanistically, we noted that the vaccine virus induces cross-reactive neutralizing antibodies that skewed towards mainly IgG isotypes. Similarly, by using major histocompatibility complex class II dextramers and tetramers for various VP1 epitopes, we demonstrated that the vaccine recipients develop antigen-specific T cell responses producing preferentially interferon-γ responses. Furthermore, our preliminary studies revealed that the vaccine virus could prevent the progression of diabetes-induced by CVB4 in the non-obese diabetic mice. Together, our data suggest that the Mt10 vaccine can prevent infections caused by multiple CVB serotypes, paving the way for developing monovalent CVB vaccines to prevent heart and pancreatic diseases of enteroviral origin. This work was supported by The Transformational Grant from the American Heart Association (18TPA34170206)
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Book chapters on the topic "CVB3 infection"

1

Yang, Ying-Zhen, Yan-Gang Su, Wei-Sheng Bao, Gong-Xin Liu, and Haozhu Chen. "The Effects of Taurine and Astragalus Membranaceus on Ion Currents and Their Expression in Cardiomyocytes After CVB3 Infection." In Progress in Experimental Cardiology, 379–94. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0455-9_28.

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