Neutrophil Uptake of Vaccinia Virus in Vitro

West, Burton C.; Eschete, Mary L.; Cox, Margaret E.; King, John W.

doi:10.1093/infdis/156.4.597

Cited by 20 publications

(11 citation statements)

References 21 publications

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“…In particular, depletion of alveolar macrophages increases Gr1(+) granulocytes and ER-MP20(+) cells, the latter of which are progenitors of granulocytes and monocytes. Prior studies performed predominantly in vitro show that monocytes/macrophages and potentially neutrophils have direct roles in controlling replication of vaccinia virus (Jones, 1982;Karupiah and Harris, 1995;West et al, 1987). However, our data show that the enhanced inflammatory response is associated with more severe disease, indicating that enhanced recruitment of these cells is detrimental to the host.…”

Section: Discussioncontrasting

confidence: 48%

Murine alveolar macrophages limit replication of vaccinia virus

et al. 2007

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Because of concerns about zoonotic transmission of monkeypox to humans and the bioterrorism threat posed by orthopoxviruses, there is renewed interest in probing cellular and molecular mechanisms of host defense to these pathogens. In particular, it is essential to understand viral-host interactions in the respiratory tract, which is the route of infection for smallpox and a likely route of transmission for monkeypox. In this study, we analyze functions of alveolar macrophages in poxvirus infection, using a recombinant vaccinia virus expressing firefly luciferase to quantify infection in mice and cell culture. Depletion of alveolar macrophages with liposomal clodronate worsens the overall severity of infection in mice, including greater replication and systemic dissemination of vaccinia as determined by bioluminescence imaging. Absence of alveolar macrophages increases total numbers of granulocytes and granulocytes/monocyte progenitor cells in the lungs during vaccinia infection, indicating that protective effects of alveolar macrophages may be mediated in part by reducing the host inflammation. Alveolar macrophages also limit vaccinia infection in respiratory epithelium, as shown by a co-culture model of cell lines derived from alveolar macrophages and lung epithelium. Collectively, these data demonstrate that alveolar macrophages are key determinants of host defense against local and systemic infection with poxviruses.

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Section: Discussioncontrasting

confidence: 48%

Murine alveolar macrophages limit replication of vaccinia virus

et al. 2007

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“…It is clear that inflammatory cells, once present in a lesion, have a number of properties which may potentially limit virus spread: (i) oxygen-dependent antimicrobial products, (ii) oxygen-independent antimicrobial products, (iii) phagocytosis mediated by Fc and complement C3b receptors followed by virucidal action, and (iv) secretion of interferons and lymphokines which attract additional cell populations. Neutrophils and macrophages can apparently destroy antibody-coated poxviruses following phagocytosis, but can also allow limited virus replication (30,41,137,246,404,432,506). In the absence of virus destruction, the phagocytic cell could actively enhance the dissemination of the virus, as proposed by Florman and Enders (170).…”

Section: Inflammatory Cellsmentioning

confidence: 97%

Poxvirus pathogenesis.

Buller

Palumbo

1991

Microbiological Reviews

293

163

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Marchal (285) and Downie (126) bodies, respectively. Because of the ambiguity associated with describing structures solely on the basis of their reaction with various histochemical stains, Kato et al. (253) carefully examined the virusspecific cytoplasmic structures of a large number of poxvirus species and, using a criterion based on morphologic observations, histochemical staining, and immunochemical reactivity, suggested that the acidophilic and basophilic inclusion bodies be referred to as A-and B-type inclusion bodies, respectively. Under the auspices of a Poxvirus Subcommittee created at the Sixth International Congress for Microbiology in 1953, Fenner and Burnet (161) wrote a review which summarized the characteristics of the poxvirus group. This article remains the basis for the subsequent classification of poxviruses. The poxvirus family is divided into two subfamilies: Entomopoxvirinae (poxviruses of the insects) and Chordopoxvirinae (poxviruses of the vertebrates); the latter group of viruses is the focus of this review (Table 1). The vertebrate poxviruses share a group-specific NP antigen (511) and are able, in a reciprocal fashion, to participate in nongenetic reactivation (160, 168). This is a process whereby an infectious poxvirus is able to reactivate a second, heatinactivated poxvirus, as indicated by the production of progeny virus. Poxviruses were further classified into genera by comparing cross-protection in animal studies, crossneutralization of infectivity in tissue culture, and crosshybridization of genomic DNA from virions. This latter criterion is now the method of choice for preliminary classification of poxvirus isolates. In general, members of the same genera have similar morphology and biological properties. Virion Morphology Poxviruses are the largest of all animal viruses and can be visualized by light microscopy, although the details of the

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“…Vaccinia virus (VACV) induces activation and functional priming of neutrophils (6), which phagocytize and inactivate VACV by an antibody-dependent mechanism (7,8). Systemic myxoma virus infection induces neutrophil recruitment to the liver microvasculature, where adherent neutrophils form large aggregates with platelets, releasing neutrophil extracellular traps that help to prevent infection of adjacent cells (9).…”

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confidence: 99%

Chemokine (C-C Motif) Receptor 1 Is Required for Efficient Recruitment of Neutrophils during Respiratory Infection with Modified Vaccinia Virus Ankara

Price

Luckow

Torres-Domínguez

et al. 2014

J Virol

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Modified vaccinia virus Ankara (MVA) serves as a versatile platform in vaccine development. This highly attenuated orthopoxvirus, which cannot replicate in mammalian cells, triggers strong innate immune responses, including cell migration. Previously, we have shown that induction of chemokine (C-C motif) ligand 2 (CCL2) by MVA is necessary for the recruitment of monocytes and T cells, but not neutrophils, to the lung. Here, we identified neutrophil-attracting chemokines produced by MVA-infected primary murine lung fibroblasts and murine bone marrow-derived macrophages. We demonstrate that MVA, but not vaccinia virus (VACV) strain WR, induces chemokine expression, which is independent of Toll-like receptor 2 (TLR2) signaling. Additionally, we show that both chemokine (C-C motif) receptor 1 (CCR1) and chemokine (C-X-C motif) receptor 2 (CXCR2) are involved in MVA-induced neutrophil chemotaxis in vitro. Finally, intranasal infection of Ccr1 ؊/؊ mice with MVA, as well as application of the CCR1 antagonist J-113863, revealed a role for CCR1 in leukocyte recruitment, including neutrophils, into the lung.

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Neutrophil Uptake of Vaccinia Virus in Vitro

Cited by 20 publications

References 21 publications

Murine alveolar macrophages limit replication of vaccinia virus

Murine alveolar macrophages limit replication of vaccinia virus

Poxvirus pathogenesis.

Chemokine (C-C Motif) Receptor 1 Is Required for Efficient Recruitment of Neutrophils during Respiratory Infection with Modified Vaccinia Virus Ankara

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