HCoV-229E Infects and Activates Monocytes

Desforges, Marc; Miletti, Tina; Gagnon, Mylène; Talbot, Pierre J.

doi:10.1007/978-0-387-33012-9_91

Cited by 4 publications

(6 citation statements)

References 14 publications

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“…This study was undertaken to determine whether cell types found in the lower respiratory tract, namely, alveolar epithelial type II cells, type I-like cells and alveolar macrophages (AMs), were susceptible to HCoV-229E infection. Previously, HCoV-229E was shown to infect bronchial epithelial cells and blood monocyte-derived macrophages (Cheung et al, 2005;Desforges et al, 2007;Wang et al, 2000), but the responses of human alveolar epithelial cells and AMs have not been defined. We also determined whether the respiratory collectins surfactant protein A (SP-A) and SP-D could inhibit HCoV-229E infection.…”

Section: Introductionmentioning

confidence: 99%

Infection of human alveolar macrophages by human coronavirus strain 229E

Funk

Wang

Ito

et al. 2012

Journal of General Virology

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Human coronavirus strain 229E (HCoV-229E) commonly causes upper respiratory tract infections. However, lower respiratory tract infections can occur in some individuals, indicating that cells in the distal lung are susceptible to HCoV-229E. This study determined the virus susceptibility of primary cultures of human alveolar epithelial cells and alveolar macrophages (AMs). Fluorescent antibody staining indicated that HCoV-229E could readily infect AMs, but no evidence was found for infection in differentiated alveolar epithelial type II cells and only a very low level of infection in type II cells transitioning to the type I-like cell phenotype. However, a human bronchial epithelial cell line (16HBE) was readily infected. The innate immune response of AMs to HCoV-229E infection was evaluated for cytokine production and interferon (IFN) gene expression. AMs secreted significant amounts of tumour necrosis factor alpha (TNF-α), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1β (MIP-1β/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-β or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-α compared with non-smokers in response to HCoV-229E infection. Surfactant protein A (SP-A) and SP-D are part of the innate immune system in the distal lung. Both surfactant proteins bound to HCoV-229E, and pre-treatment of HCoV-229E with SP-A or SP-D inhibited infection of 16HBE cells. In contrast, there was a modest reduction in infection in AMs by SP-A, but not by SP-D. In summary, AMs are an important target for HCoV-229E, and they can mount a pro-inflammatory innate immune response to infection.

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Section: Introductionmentioning

confidence: 99%

Infection of human alveolar macrophages by human coronavirus strain 229E

Funk

Wang

Ito

et al. 2012

Journal of General Virology

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“…Even though it is recognized that HCoV primarily infect airway epithelial cells and cause diseases of the respiratory tract in humans, viral material was reported in other cells and tissues. For example, HCoV-229E infection of human monocytic cell lines and of primary monocytes/macrophages was reported (Collins, 2002;Desforges et al, 2006). Infection of peritoneal macrophages (Patterson and Macnaughton, 1982) and murine dendritic cells expressing human aminopeptidase N (APN; Wentworth et al, 2005) by HCoV-229E suggests that this virus may use myeloid cells to disseminate to other tissues, where it could provoke other types of pathologies.…”

Section: Introductionmentioning

confidence: 99%

Activation of human monocytes after infection by human coronavirus 229E

et al. 2007

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Human coronaviruses (HCoV) are recognized respiratory pathogens that may be involved in other pathologies such as central nervous system (CNS) diseases. To investigate whether leukocytes could participate in respiratory pathologies and serve as vector for viral spread towards other tissues, the susceptibility of human leukocytic cell lines and peripheral blood mononuclear cells (PBMC) to HCoV-229E and HCoV-OC43 infection was investigated. Human primary monocytes/macrophages were susceptible to HCoV-229E infection, but strongly restricted HCoV-OC43 replication. Moreover, productive HCoV-229E infection of primary monocytes and of the THP-1 monocytic cell line led to their activation, as indicated by the production of pro-inflammatory mediators, including TNF-alpha, CCL5, CXCL10 and CXCL11 and MMP-9. Moreover, an in vitro chemotaxis assay showed that motility towards chemokines of THP-1 cells and primary monocytes was increased following an acute or persistent HCoV-229E infection. Taken together, these results suggest that infected monocytes could serve as a reservoir for HCoV-229E, become activated, participate in the exacerbation of pulmonary pathologies, as well as serve as potential vectors for viral dissemination to host tissues, where it could be associated with other pathologies.

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“…In this regard, killing DCs can be an efficient viral strategy to delay or prevent the establishment of adaptive immune responses. Infections by measles virus, human immunodeficiency virus, or lymphocytic choriomeningitis virus deplete DC populations in infected hosts (12,22,37). In vitro experiments have also demonstrated that filoviruses, vaccinia virus, herpes simplex virus, H5N1 influenza virus, and measles virus induce DC apoptosis or cytolysis within a few days (16,31,33,41,47).…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, in vitro experiments demonstrate that other cell types can be infected. For example, HCoV-229E was reported to infect and replicate in neural cells, hepatocytes, monocytes, and macrophages (3,11,12). The neurotropism of HCoV-229E and OC43 has also been documented in vivo, and a possible association with multiple sclerosis has been suggested (4).…”

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confidence: 99%

A Human Coronavirus Responsible for the Common Cold Massively Kills Dendritic Cells but Not Monocytes

Mesel-Lemoine

Millet

Vidalain

et al. 2012

J Virol

138

127

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Human coronaviruses are associated with upper respiratory tract infections that occasionally spread to the lungs and other organs. Although airway epithelial cells represent an important target for infection, the respiratory epithelium is also composed of an elaborate network of dendritic cells (DCs) that are essential sentinels of the immune system, sensing pathogens and presenting foreign antigens to T lymphocytes. In this report, we show that in vitro infection by human coronavirus 229E (HCoV-229E) induces massive cytopathic effects in DCs, including the formation of large syncytia and cell death within only few hours. In contrast, monocytes are much more resistant to infection and cytopathic effects despite similar expression levels of CD13, the membrane receptor for HCoV-229E. While the differentiation of monocytes into DCs in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4 requires 5 days, only 24 h are sufficient for these cytokines to sensitize monocytes to cell death and cytopathic effects when infected by HCoV-229E. Cell death induced by HCoV-229E is independent of TRAIL, FasL, tumor necrosis factor alpha, and caspase activity, indicating that viral replication is directly responsible for the observed cytopathic effects. The consequence of DC death at the early stage of HCoV-229E infection may have an impact on the early control of viral dissemination and on the establishment of long-lasting immune memory, since people can be reinfected multiple times by HCoV-229E.

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HCoV-229E Infects and Activates Monocytes

Cited by 4 publications

References 14 publications

Infection of human alveolar macrophages by human coronavirus strain 229E

Infection of human alveolar macrophages by human coronavirus strain 229E

Activation of human monocytes after infection by human coronavirus 229E

A Human Coronavirus Responsible for the Common Cold Massively Kills Dendritic Cells but Not Monocytes

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