Cellular Gene Expression Survey of Vaccinia Virus Infection of Human HeLa Cells

Guerra, Susana; López-Fernández, Luis Andrés; Pascual-Montano, Alberto; Muñoz, Manuel J.; Harshman, Keith; Esteban, Mariano

doi:10.1128/jvi.77.11.6493-6506.2003

Cited by 110 publications

(150 citation statements)

References 46 publications

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“…These nonclassical class Ib molecules thus require a continuous supply of cognate peptide to maintain cell surface expression and thence mediate effective NK cell inhibition (45). One possibility to explain the specificity of MHC class I down-regulation is that vaccinia virus inhibits host protein synthesis (46,47). Thus, it could disrupt the supply of cognate peptide to HLA-E. Because HLA-E expression on the cell surface is dependent on its binding to a cognate peptide (48), a loss of supply of these peptides prevents newly synthesized HLA-E molecules from appearing on the cell surface.…”

Section: Discussionmentioning

confidence: 99%

The Inhibitory Receptor NKG2A Determines Lysis of Vaccinia Virus-Infected Autologous Targets by NK Cells

Brooks

Elliott

Parham

et al. 2006

The Journal of Immunology

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Signals transduced by inhibitory receptors that recognize self-MHC class I molecules prevent NK cells from being activated by autologous healthy target cells. In order for NK cells to be activated upon contact with an infected cell, the balance between the activating and inhibitory signals that regulate NK cell function must be altered in favor of activation. By studying liver-derived NK cells, we show that only a subpopulation of NK cells expressing high levels of the inhibitory receptor NKG2A are able to lyse autologous vaccinia-infected targets, and that this is due to selective down-regulation of HLA-E. These data demonstrate that release from an inhibitory receptor:ligand interaction is one mechanism that permits NK cell recognition of a virally infected target, and that the variegated expression of inhibitory receptors in humans generates a repertoire of NK cells with different antiviral potentials.

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Section: Discussionmentioning

confidence: 99%

The Inhibitory Receptor NKG2A Determines Lysis of Vaccinia Virus-Infected Autologous Targets by NK Cells

Brooks

Elliott

Parham

et al. 2006

The Journal of Immunology

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“…It is well established that poxviruses can interfere with cellular transcripts, leading to reductions in host proteins (35,36,40,41). Therefore, we compared the rate of Clr-b protein loss to the amount of mRNA.…”

Section: Clr-b Transcript Is Reduced During Infectionmentioning

confidence: 99%

“…Given the potential for the NKR-P1 and Clr system of receptors and ligands to be involved in the response to poxvirus infection and the ability of poxviruses to interfere with protein expression through destabilization of cellular transcripts (35)(36)(37), we tested the hypothesis that Clr-b is modulated during poxvirus infection. We found that infection of mouse cells with either VV or ECTV reduces Clr-b on the cell surface.…”

mentioning

confidence: 99%

Poxvirus Infection-Associated Downregulation of C-Type Lectin-Related-b Prevents NK Cell Inhibition by NK Receptor Protein-1B

Williams

Wilson

Davidson

et al. 2012

The Journal of Immunology

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Innate immune recognition of virus-infected cells includes NK cell detection of changes to endogenous cell-surface proteins through inhibitory receptors. One such receptor system is the NK cell receptor protein-1B (NKR-P1B) and its ligand C-type lectin-related-b (Clr-b). NKR-P1B and Clr-b are encoded within the NK cell gene complex, a locus that has been linked to strain-dependent differences in susceptibility to infection by poxviruses. In this study, we report the impact of vaccinia virus (VV) and ectromelia virus infection on expression of Clr-b and Clr-b–mediated protection from NK cells. We observed a loss of Clr-b cell-surface protein upon VV and ectromelia virus infection of murine cell lines and bone marrow-derived macrophages. The reduction of Clr-b is more rapid than MHC class I, the prototypic ligand of NK cell inhibitory receptors. Reduction of Clr-b requires active viral infection but not expression of late viral genes, and loss of mRNA appears to lag behind loss of Clr-b surface protein. Clr-b–mediated protection from NK cells is lost following VV infection. Together, these results provide the second example of Clr-b modulation during viral infection and suggest reductions of Clr-b may be involved in sensitizing poxvirus-infected cells to NK cells.

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“…The replication cycle of all poxviruses occurs exclusively within the cytoplasm of an infected cell in which the virus hijacks cellular transcriptional and translational machinery to assemble viral factories, referred to as viroplasm (7), resulting in a general shift away from cellular protein expression toward viral mRNA and protein synthesis (8,9). Importantly, the ability of poxviruses to replicate within a particular cell type is believed to typically be governed through postentry events, such as the proper recruitment of host cell machinery required for viral processes and attenuation of the innate immune response (10).…”

Section: Monkeypox Virus (Mpxv)mentioning

confidence: 99%

Characterization of Macaque Pulmonary Fluid Proteome during Monkeypox Infection

Brown

Estep

López-Ferrer

et al. 2010

Molecular & Cellular Proteomics

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Cellular Gene Expression Survey of Vaccinia Virus Infection of Human HeLa Cells

Abstract: Vaccinia virus (VV) is a cytocidal virus that causes major changes in host cell

Cited by 110 publications

References 46 publications

The Inhibitory Receptor NKG2A Determines Lysis of Vaccinia Virus-Infected Autologous Targets by NK Cells

The Inhibitory Receptor NKG2A Determines Lysis of Vaccinia Virus-Infected Autologous Targets by NK Cells

Poxvirus Infection-Associated Downregulation of C-Type Lectin-Related-b Prevents NK Cell Inhibition by NK Receptor Protein-1B

Characterization of Macaque Pulmonary Fluid Proteome during Monkeypox Infection

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