Pneumoviruses: the Cell Surface of Lytically and Persistently Infected Cells

Parry, J.E.; Shirodaria, P. V.; Pringle, C. R.

doi:10.1099/0022-1317-44-2-479

Cited by 39 publications

(25 citation statements)

References 1 publication

(1 reference statement)

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“…We observed infected basal cell cultures using high-resolution confocal imaging and found that they displayed viral antigen as clumps or as filaments on the apical surface. Studies using light and electron microscopy have previously shown filamentous projections on the surface of RSV-infected cells [15], and these are thought to be largely responsible for the transmission of the virus to neighbouring cells [19]. We also observed that basal cell cultures produced a greater proportion of RSV-infected cells ( fig.…”

Section: Basal Cell Cultures Infected With Rsv Increase Secretion Of supporting

confidence: 62%

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Ciliary dyskinesia is an early feature of respiratory syncytial virus infection

Smith

Kulkarni

Radhakrishnan

et al. 2013

European Respiratory Journal

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Respiratory syncytial virus is a major cause of respiratory disease. There are conflicting accounts of the response of human epithelial cells to respiratory syncytial virus and a lack of data on its effect on ciliary function. Our aim was to study the early stages of respiratory syncytial virus infection of primary human basal and ciliated cultures.Using high speed videomicroscopy, we found that ciliary beat frequency was unaffected by respiratory syncytial virus infection over 72 h; however, ciliary dyskinesia significantly increased within 24 h of infection (p,0.05). Transmission electron microscopy revealed that ultrastructural abnormalities were confined to ciliated cells, including increased cilia loss and mitochondrial damage. Confocal immunofluorescence microscopy showed that respiratory syncytial virus antigen gradually spread from the cell surface to the ciliary tip of infected cells over 3 days. Interestingly, ciliated cultures secreted fewer viruses than basal (progenitor) cell cultures and produced a chemokine response focused on recruitment of neutrophils.This study highlights differences in infection models and underscores the need to explore further the role of ciliated cells in the establishment of respiratory syncytial virus infection.Increased ciliary dyskinesia combined with ciliary loss and epithelial damage is likely to result in reduced mucociliary clearance early in the infective process. @ERSpublications Increased ciliary dyskinesia with ciliary loss and epithelial damage can result in reduced mucociliary clearance

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Section: Basal Cell Cultures Infected With Rsv Increase Secretion Of supporting

confidence: 62%

“…4c). The VFs closely resemble the structures seen by scanning electron microscopy and immunofluorescence on the surface of RSV-infected tissue culture cells [15].…”

Section: Ultrastructural Damage Following Rsv Infection Was Confined supporting

confidence: 51%

Ciliary dyskinesia is an early feature of respiratory syncytial virus infection

Smith

Kulkarni

Radhakrishnan

et al. 2013

European Respiratory Journal

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“…Previous work has shown that HRSV infection induces the formation of relatively large (length, 4 to 10 m), cell-associated filamentous particles at the plasma membrane in various cell types and that the G and F proteins target to these filaments (3,7,19,22,48,52,57). These observations appear to be in agreement with the findings that HRSV infectivity is predominantly cell associated and that the majority of infectivity is lost after passage through 0.45-m-pore-size filters (47,51).…”

Section: Fig 4 Analysis Of Gmentioning

confidence: 99%

Infectivity of a Human Respiratory Syncytial Virus Lacking the SH, G, and F Proteins Is Efficiently Mediated by the Vesicular Stomatitis Virus G Protein

Oomens

Megaw

Wertz

2003

J Virol

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To examine the requirements of the human respiratory syncytial virus (HRSV) SH (small hydrophobic), G (attachment), and F (fusion) proteins for virus infectivity and morphology, we used the prototype A2 strain of HRSV to generate a series of cDNAs from which (i) the SH open reading frame (ORF), (ii) the SH and G ORFs, or (iii) the SH, G, and F ORFs were deleted. Each deleted ORF was replaced as follows: the SH ORF was replaced with that of green fluorescent protein; the G ORF was replaced with that of G vsv , a chimeric glycoprotein consisting of the vesicular stomatitis Indiana virus (VSIV) G protein ecto-and transmembrane domains coupled to the HRSV F cytoplasmic tail; and the F ORF was replaced with that of marker protein ␤-glucuronidase. The number of genes and the intergenic junctions in the constructs were kept as found in A2 virus in order to maintain authentic levels of transcription. Infectious viruses were recovered from all three engineered cDNAs and designated RS⌬SH, RS⌬SH,G/G vsv , and RS⌬SH,G,F/G vsv , respectively. Low-pH-induced syncytium formation was observed in cells infected with viruses RS⌬SH,G/G vsv and RS⌬SH,G,F/G vsv , indicating that G vsv was expressed and functional. Neutralization of infectivity by anti-VSIV G antibodies and inhibition of entry by ammonium chloride showed that RS⌬SH,G,F/G vsv infectivity was mediated by G vsv and that an acidification step was required for entry into the host cell, similar to VSIV virions. All three engineered viruses displayed growth kinetics and virus yields similar to a wild-type A2 virus, both in Vero and HEp-2 cells. Abundant virus-induced filaments were observed at the surface of cells infected with each of the three engineered viruses or with virus A2, indicating that neither the SH and G proteins nor the F protein ecto-and transmembrane domains were required for the formation of these structures. This is the first report of the recovery of an infectious HRSV lacking a fusion protein of the Paramyxoviridae family and of manipulation of the HRSV entry pathway via incorporation of a nonparamyxoviral transmembrane glycoprotein.

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“…Both in vivo and in vitro studies of lung epithelial cells demonstrate c.p.e., fusion resulting in syncytia, and cytolysis (Parry et al, 1979;Becker et al, 1992;Merolla et al, 1992). Recent in vivo studies indicate that major histocompatibility complex (MHC) class II (HLA-DR)-expressing alveolar macrophages are also targets for RSV infection .…”

Section: Introductionmentioning

confidence: 99%

Restricted replication of respiratory syncytial virus in human alveolar macrophages

Cirino

Panuska

Villani³

et al. 1993

Journal of General Virology

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The cellular factors that regulate infection and replication of respiratory syncytial virus (RSV) in human alveolar macrophages were examined. RSV-exposed alveolar macrophages demonstrated a time-dependent expression of viral glycoproteins, maximal by 24 h postinfection resulting in infection of approx. 38 % of the cells. Essentially all (33 %) of these freshly isolated alveolar macrophages replicated RSV as shown by infectious centre assays. This RSV-permissive subpopulation of alveolar macrophages consisted primarily of major histocompatibility class II-expressing cells as determined by fluorescence-activated cell sorting. Reinfection of alveolar macrophages did not significantly alter the number of cells infected or capable of replicating RSV. However, in vitro differentiation of alveolar macrophages prior to infection resulted in a significant (P < 0-05), time-dependent decrease (approx. sevenfold) in the number of cells that replicated virus. The mechanism by which cellular differentiation restricted RSV replication is unknown. Production of defective interfering particles did not account for this decrease. Alveolar macrophages infected with RSV produce a variety of cytokines potentially contributing to this restricted viral replication. Pretreatment with several of these cytokines did not affect viral infection or replication. However, tumour necrosis factor (TNF~) significantly (P < 0"05) decreased viral replication but only by 30 to 60 %. Thus RSV replication is reduced by in vitro differentiation of alveolar macrophages and, to a lesser degree, by pretreatment with TNF.

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Pneumoviruses: the Cell Surface of Lytically and Persistently Infected Cells

Cited by 39 publications

References 1 publication

Ciliary dyskinesia is an early feature of respiratory syncytial virus infection

Ciliary dyskinesia is an early feature of respiratory syncytial virus infection

Infectivity of a Human Respiratory Syncytial Virus Lacking the SH, G, and F Proteins Is Efficiently Mediated by the Vesicular Stomatitis Virus G Protein

Restricted replication of respiratory syncytial virus in human alveolar macrophages

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