Human parvovirus B19 experimental infection in human fibroblasts and endothelial cells cultures

Zakrzewska, K.; Cortivo, Roberta; Tonello, C; Panfilo, Susi; Abatangelo, Giovanni; Giuggioli, Dilia; Ferri, Clodoveo; Corcioli, Fabiana; Azzi, Alberta

doi:10.1016/j.virusres.2005.05.003

Cited by 32 publications

(24 citation statements)

References 31 publications

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“…P antigen was detected not only on EPCs, but also on a variety of other cell types, including primary endothelial cells from umbilical cord blood (HU-VEC) (26). In line with these data, experimental infection of HU-VEC with detection of NS1 mRNA and small amounts of VP mRNAs has been reported (27). Whereas P antigen is required for primary B19V attachment to its target cells, it is not sufficient to trigger the internalization step (26).…”

mentioning

confidence: 59%

“…Despite enhanced uptake of B19V in the presence of antibodies, the B19V infection of endothelial cells remained abortive, with only low levels of the NS1 mRNA and no detectable VP2 transcripts or DNA replication. It has been shown previously that endothelial cells are susceptible to B19V infection in vitro, with detection of low levels of NS1 and VP1 transcripts, but no evidence for a productive infection, such as an increase in B19V DNA amounts or detectable levels of VP1 or VP2 capsid proteins, was found (27). In vivo, B19V infection of endothelial cells has been demonstrated in myocardium (20) and skin (66), but again without any hints of a productive infection.…”

Section: Discussionmentioning

confidence: 87%

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Antibody-Mediated Enhancement of Parvovirus B19 Uptake into Endothelial Cells Mediated by a Receptor for Complement Factor C1q

Kietzell

Pozzuto

Heilbronn

et al. 2014

J Virol

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Despite its strong host tropism for erythroid progenitor cells, human parvovirus B19 (B19V) can also infect a variety of additional cell types. Acute and chronic inflammatory cardiomyopathies have been associated with a high prevalence of B19V DNA in endothelial cells of the myocardium. To elucidate the mechanisms of B19V uptake into endothelium, we first analyzed the surface expression of the well-characterized primary B19V receptor P antigen and the putative coreceptors ␣ 5 ␤ 1 integrins and Ku80 antigen on primary and permanent endothelial cells. The receptor expression pattern and also the primary attachment levels were similar to those in the UT7/Epo-S1 cell line regarded as functional for B19V entry, but internalization of the virus was strongly reduced. As an alternative B19V uptake mechanism in endothelial cells, we demonstrated antibody-dependent enhancement (ADE), with up to a 4,000-fold increase in B19V uptake in the presence of B19V-specific human antibodies. ADE was mediated almost exclusively at the level of virus internalization, with efficient B19V translocation to the nucleus. In contrast to monocytes, where ADE of B19V has been described previously, enhancement does not rely on interaction of the virus-antibody complexes with Fc receptors (FcRs), but rather, involves an alternative mechanism mediated by the heat-sensitive complement factor C1q and its receptor, CD93. Our results suggest that ADE represents the predominant mechanism of endothelial B19V infection, and it is tempting to speculate that it may play a role in the pathogenicity of cardiac B19V infection. IMPORTANCEBoth efficient entry and productive infection of human parvovirus B19 (B19V) seem to be limited to erythroid progenitor cells. However, in vivo, the viral DNA can also be detected in additional cell types, such as endothelial cells of the myocardium, where its presence has been associated with acute and chronic inflammatory cardiomyopathies. In this study, we demonstrated that uptake of B19V into endothelial cells most probably does not rely on the classical receptor-mediated route via the primary B19V receptor P antigen and coreceptors, such as ␣ 5 ␤ 1 integrins, but rather on antibody-dependent mechanisms. Since the strong antibody-dependent enhancement (ADE) of B19V entry requires the CD93 surface protein, it very likely involves bridging of the B19V-antibody complexes to this receptor by the complement factor C1q, leading to enhanced endocytosis of the virus.

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mentioning

confidence: 59%

Section: Discussionmentioning

confidence: 87%

Antibody-Mediated Enhancement of Parvovirus B19 Uptake into Endothelial Cells Mediated by a Receptor for Complement Factor C1q

Kietzell

Pozzuto

Heilbronn

et al. 2014

J Virol

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“…Primary cultures of human fibroblasts (HF) and human umbilical vein endothelial cells (HUVEC) exposed to B19V can be infected, but only low levels of NS and VP mRNAs might be detected in the absence of any significant increase of B19V DNA levels. Then, HF and HUVEC are normally not permissive for B19V replication, but it is possible that stimulation with different growth factors or cytokines could be required for a B19V productive infection to occur [149]. In an experimental system using a human endothelial cell line, HMEC-1, B19V infection, or NS overexpression produced a significant upregulation in the phosphorylation of STAT3, accompanied by dimerization, nuclear translocation, and DNA binding of pSTAT3, without increased STAT1 activation.…”

Section: Nonpermissive Systemsmentioning

confidence: 99%

Parvovirus B19 Achievements and Challenges

Gallinella

2013

ISRN Virology

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Parvovirus B19 is a widespread human pathogenic virus, member of the Erythrovirus genus in the Parvoviridae family. Infection can be associated with an ample range of pathologies and clinical manifestations, whose characteristics and outcomes depend on the interplay between the pathogenetic potential of the virus, its adaptation to different cellular environments, and the physiological and immune status of the infected individuals. The scope of this review is the advances in knowledge on the biological characteristics of the virus and of virus-host relationships; in particular, the interactions of the virus with different cellular environments in terms of tropism and ability to achieve a productive replicative cycle, or, on the contrary, to establish persistence; the consequences of infection in terms of interference with the cell physiology; the process of recognition of the virus by the innate or adaptive immune system, hence the role of the immune system in controlling the infection or in the development of clinical manifestations. Linked to these issues is the continuous effort to develop better diagnostic algorithms and methods and the need for development of prophylactic and therapeutic options for B19V infections.

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“…4 In vitro infection of endothelial cells, however, did not show evidence of a productive infection. 17 In vivo, endothelial cell infection has been previously documented in myocardium 18 and skin 19 even though a productive infection was not demonstrated; in the circumstances reported above the endothelium damage was believed to play a crucial role in determining irreversible myocardial damage and in sustaining the progression of scleroderma disease, respectively. In the present case, a productive infection of endothelial cells has been documented for the first time in the context of placental villi by the coincident detection of B19V nucleic acids and both non-structural and capsid proteins.…”

Section: Discussionmentioning

confidence: 95%