Chinese hamster ovary cells are non-permissive towards infection with coxsackievirus B3 despite functional virus-receptor interactions

Kramer, B; Huber, Michael; Kern, Christopher; Klingel, Karin; Kandolf, Reinhard; Selinka, Hans‐Christoph

doi:10.1016/s0168-1702(96)01438-4

Cited by 12 publications

(5 citation statements)

References 31 publications

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“…It is tempting to speculate that they may even remain constant because of interactions between some virus strains and the CHO cell surface. A previous report of a putative molecule on CHO cells that interacts with the cardiovirulent CVB3-N strain but does not allow for productive lytic infection provides some support for this hypothesis (Kramer et al, 1997).…”

Section: Cvb1-6 Reference Strains Wild-type Clinical Isolates and Lmentioning

confidence: 93%

The Coxsackie-Adenovirus Receptor (CAR) Is Used by Reference Strains and Clinical Isolates Representing All Six Serotypes of Coxsackievirus Group B and by Swine Vesicular Disease Virus

et al. 2000

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Group B coxsackieviruses are etiologically linked to many human diseases, and cell surface receptors are postulated to play an important role in mediating their pathogenesis. The coxsackievirus adenovirus receptor (CAR) has been shown to function as a receptor for selected strains of coxsackievirus group B (CVB) serotypes 3, 4, and 5 and is postulated to serve as a receptor for all six serotypes. In this study, we demonstrate that CAR can serve as a receptor for laboratory reference strains and clinical isolates of all six CVB serotypes. Infection of CHO cells expressing human CAR results in a 1000-fold increase in CVB progeny virus titer compared to mock transfected cells. CAR was shown to be a functional receptor for swine vesicular disease virus (SVDV), as CHO-CAR cells but not CHO mock transfected controls were susceptible to SVDV infection, produced progeny SVDV, and developed cytopathic effects. Moreover, SVDV infection could be specifically blocked by monoclonal antibody to CAR (RmcB). SVDV infection of HeLa cells was also inhibited by an anti-CD55 MAb, suggesting that this virus, like some CVB, may interact with CD55 (decay accelerating factor) in addition to CAR. Finally, pretreatment of CVB or SVDV with soluble CAR effectively blocks virus infection of HeLa cell monolayers.

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Section: Cvb1-6 Reference Strains Wild-type Clinical Isolates and Lmentioning

confidence: 93%

The Coxsackie-Adenovirus Receptor (CAR) Is Used by Reference Strains and Clinical Isolates Representing All Six Serotypes of Coxsackievirus Group B and by Swine Vesicular Disease Virus

et al. 2000

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“…Notably, 2A pro protein cleaves cytoskeletal dystrophin, and dystrophin-associated glycoproteins such as α-sarcoglycan, β-dystroglycan, and extracelluar laminin-2 [30, 59, 60]. Dystrophin is critical for connecting with the contractile protein F-actin within the cardiomyocytes [61, 62].…”

Section: Pathogenesis Of Cvb3 Infectionmentioning

confidence: 99%

Intricacies of cardiac damage in coxsackievirus B3 infection: Implications for therapy

Massilamany

Gangaplara

Reddy

2014

International Journal of Cardiology

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Heart disease is the leading cause of death in humans, and myocarditis is one predominant cause of heart failure in young adults. Patients affected with myocarditis can develop dilated cardiomyopathy (DCM), a common reason for heart transplantation, which to date is the only viable option for combatting DCM. Myocarditis/DCM patients show antibodies to coxsackievirus B (CVB)3 and cardiac antigens, suggesting a role for CVB-mediated autoimmunity in the disease pathogenesis; however, a direct causal link remains to be determined clinically. Experimentally, myocarditis can be induced in susceptible strains of mice using the human isolates of CVB3, and the disease pathogenesis of postinfectious myocarditis resembles that of human disease, making the observations made in animals relevant to humans. In this review, we discuss the complex nature of CVB3-induced myocarditis as it relates to the damage caused by both the virus and the host's response to infection. Based on recent data we obtained in the mouse model of CVB3 infection, we provide evidence to suggest that CVB3 infection accompanies the generation of cardiac myosin-specific CD4 T cells that can transfer the disease to naïve recipients. The therapeutic implications of these observations are also discussed.

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“…Different variants of encephalomyocarditis virus have been reported to use either the immunoglobulinlike molecule vascular cell adhesion molecule 1 (43) or a 70-kDa cell surface sialoglycoprotein (48) as a receptor, and hepatitis A virus (HAV) has recently been shown to use a unique membrane glycoprotein containing immunoglobulin and mucin domains (3,49). The coxsackie B viruses have been reported to use either decay-accelerating factor (11,77), a 100-kDa nucleolin-related membrane protein (33,52), or a 46-kDa membrane-bound immunoglobulin-like protein (9,24,83) ei-ther as an initial cell binding protein or in combinations that form functional receptor complexes. Interestingly, this 46-kDa protein has also been shown to be a receptor for two members of the human adenovirus family (9,83), demonstrating that viruses from different families, which do not share common structural features, can use the same receptor.…”

mentioning

confidence: 99%

Foot-and-Mouth Disease Virus Virulent for Cattle Utilizes the Integrin α _v β ₃ as Its Receptor

Neff

Sá-Carvalho

Rieder

et al. 1998

J Virol

194

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Adsorption and plaque formation of foot-and-mouth disease virus (FMDV) serotype A12 are inhibited by antibodies to the integrin αvβ3 (A. Berinstein et al., J. Virol. 69:2664–2666, 1995). A human cell line, K562, which does not normally express αvβ3 cannot replicate this serotype unless cells are transfected with cDNAs encoding this integrin (K562-αvβ3 cells). In contrast, we found that a tissue culture-propagated FMDV, type O1BFS, was able to replicate in nontransfected K562 cells, and replication was not inhibited by antibodies to the endogenously expressed integrin α5β1. A recent report indicating that cell surface heparan sulfate (HS) was required for efficient infection of type O1 (T. Jackson et al., J. Virol. 70:5282–5287, 1996) led us to examine the role of HS and αvβ3 in FMDV infection. We transfected normal CHO cells, which express HS but not αvβ3, and two HS-deficient CHO cell lines with cDNAs encoding human αvβ3, producing a panel of cells that expressed one or both receptors. In these cells, type A12 replication was dependent on expression of αvβ3, whereas type O1BFS replicated to high titer in normal CHO cells but could not replicate in HS-deficient cells even when they expressed αvβ3. We have also analyzed two genetically engineered variants of type O1Campos, vCRM4, which has greatly reduced virulence in cattle and can bind to heparin-Sepharose columns, and vCRM8, which is highly virulent in cattle and cannot bind to heparin-Sepharose. vCRM4 replicated in wild-type K562 cells and normal, nontransfected CHO (HS+αvβ3− ) cells, whereas vCRM8 replicated only in K562 and CHO cells transfected with αvβ3 cDNAs. A similar result was also obtained in assays using a vCRM4 virus with an engineered RGD→KGE mutation. These results indicate that virulent FMDV utilizes the αvβ3 integrin as a primary receptor for infection and that adaptation of type O1 virus to cell culture results in the ability of the virus to utilize HS as a receptor and a concomitant loss of virulence.

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Chinese hamster ovary cells are non-permissive towards infection with coxsackievirus B3 despite functional virus-receptor interactions

Cited by 12 publications

References 31 publications

The Coxsackie-Adenovirus Receptor (CAR) Is Used by Reference Strains and Clinical Isolates Representing All Six Serotypes of Coxsackievirus Group B and by Swine Vesicular Disease Virus

The Coxsackie-Adenovirus Receptor (CAR) Is Used by Reference Strains and Clinical Isolates Representing All Six Serotypes of Coxsackievirus Group B and by Swine Vesicular Disease Virus

Intricacies of cardiac damage in coxsackievirus B3 infection: Implications for therapy

Foot-and-Mouth Disease Virus Virulent for Cattle Utilizes the Integrin α _v β ₃ as Its Receptor

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Chinese hamster ovary cells are non-permissive towards infection with coxsackievirus B3 despite functional virus-receptor interactions

Cited by 12 publications

References 31 publications

The Coxsackie-Adenovirus Receptor (CAR) Is Used by Reference Strains and Clinical Isolates Representing All Six Serotypes of Coxsackievirus Group B and by Swine Vesicular Disease Virus

The Coxsackie-Adenovirus Receptor (CAR) Is Used by Reference Strains and Clinical Isolates Representing All Six Serotypes of Coxsackievirus Group B and by Swine Vesicular Disease Virus

Intricacies of cardiac damage in coxsackievirus B3 infection: Implications for therapy

Foot-and-Mouth Disease Virus Virulent for Cattle Utilizes the Integrin α v β 3 as Its Receptor

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Foot-and-Mouth Disease Virus Virulent for Cattle Utilizes the Integrin α _v β ₃ as Its Receptor