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  • 1
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    Online Resource
    Multicenter evaluation of PCR methods fordetecting CMV DNA in blood donors
    Wiley ; 2001
    In:  Transfusion Vol. 41, No. 10 ( 2001-10), p. 1249-1257
    Details
    In: Transfusion, Wiley, Vol. 41, No. 10 ( 2001-10), p. 1249-1257
    Type of Medium: Online Resource
    ISSN: 0041-1132 , 1537-2995
    URL: Article
    DOI: 10.1046/j.1537-2995.2001.41101249.x
    Language: English
    Publisher: Wiley
    Publication Date: 2001
    detail.hit.zdb_id: 2018415-3
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  • 2
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    Human Cytomegalovirus Latency-Associated Protein pORF94 Is Dispensable for Productive and Latent Infection
    American Society for Microbiology ; 2000
    In:  Journal of Virology Vol. 74, No. 19 ( 2000-10), p. 9333-9337
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 74, No. 19 ( 2000-10), p. 9333-9337
    Abstract: Human cytomegalovirus latency in bone marrow-derived myeloid progenitors is characterized by the presence of latency-associated transcripts encoded in the ie1/ie2 region of the viral genome. To assess the role of ORF94 (UL126a), a conserved open reading frame on these transcripts, a recombinant virus (RC2710) unable to express this gene was constructed. This virus replicated at wild-type levels and expressed productive as well as latency-associated ie1/ie2 region transcripts. During latency in granulocyte-macrophage progenitors, RC2710 DNA was detected at levels indistinguishable from wild-type virus, latent-phase transcription was present, and RC2710 reactivated when latently infected cells were cocultured with permissive fibroblasts. These data suggest pORF94 is not required for either productive or latent infection as assayed in cultured cells despite being the only known nuclear latency-associated protein.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.74.19.9333-9337.2000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2000
    detail.hit.zdb_id: 1495529-5
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  • 3
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    A Novel Viral Transcript with Homology to Human Interleukin-10 Is Expressed during Latent Human Cytomegalovirus Infection
    American Society for Microbiology ; 2004
    In:  Journal of Virology Vol. 78, No. 3 ( 2004-02), p. 1440-1447
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 78, No. 3 ( 2004-02), p. 1440-1447
    Abstract: Human cytomegalovirus (CMV) establishes latent infections in hematopoietic cells such as granulocyte-macrophage progenitors (GM-Ps). During latency the virus is sequestered in a nonreplicating state, although limited transcriptional activity has been previously reported. In this study we sought to further examine viral gene expression during the latent phase of infection. Using an experimental model of latency, primary human GM-Ps were latently infected with CMV strain Toledo and extracted RNA subjected to reverse transcription-PCR by using CMV gene-specific primers. Using this approach, we detected transcription from the UL111.5A region of the viral genome. This transcription was also detected in GM-Ps latently infected with AD169 and Towne strains, indicating that expression was CMV strain independent. Significantly, we detected UL111.5A-region transcripts in mononuclear cells from healthy bone marrow and mobilized peripheral blood allograft donors, demonstrating expression during natural latent infection. Mapping experiments with RNA extracted from latently infected GM-Ps revealed the expression of a novel UL111.5A region transcript with a splicing pattern that differed from that reported during productive infection of permissive cells. This UL111.5A region transcript expressed during latent infection is predicted to encode a 139-amino-acid protein with homology to the potent immunosuppressor interleukin-10 (IL-10) and to the viral IL-10 homolog that is expressed during productive CMV infection. Expression of a latency-associated cmvIL-10 may confer upon the virus an ability to avoid immune recognition and clearance during the latent phase of infection.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.78.3.1440-1447.2004
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2004
    detail.hit.zdb_id: 1495529-5
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  • 4
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    Impact of Human Cytomegalovirus Latent Infection on Myeloid Progenitor Cell Gene Expression
    American Society for Microbiology ; 2004
    In:  Journal of Virology Vol. 78, No. 8 ( 2004-04-15), p. 4054-4062
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 78, No. 8 ( 2004-04-15), p. 4054-4062
    Abstract: Herpesviruses establish lifelong latent infections in their hosts. Human cytomegalovirus (CMV) targets a population of bone marrow-derived myeloid lineage progenitor cells that serve as a reservoir for reactivation; however, the mechanisms by which latent CMV infection is maintained are unknown. To gain insights into mechanisms of maintenance and reactivation, we employed microarrays of ∼26,900 sequence-verified human cDNAs to assess global changes in cellular gene expression during experimental CMV latent infection of granulocyte-macrophage progenitors (GM-Ps). This analysis revealed at least 29 host cell genes whose expression was increased and six whose expression was decreased during CMV latency. These changes in transcript levels appeared to be authentic, judging on the basis of further analysis of a subset by semiquantitative reverse transcription-PCR. This study provides a comprehensive snapshot of changes in host cell gene expression that result from latent infection and suggest that CMV regulates genes that encode proteins involved in immunity and host defense, cell growth, signaling, and transcriptional regulation. The host genes whose expression we found altered are likely to contribute to an environment that sustains latent infection.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.78.8.4054-4062.2004
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2004
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  • 5
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    Modulation of Major Histocompatibility Class II Protein Expression by Varicella-Zoster Virus
    American Society for Microbiology ; 2000
    In:  Journal of Virology Vol. 74, No. 4 ( 2000-02-15), p. 1900-1907
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 74, No. 4 ( 2000-02-15), p. 1900-1907
    Abstract: We sought to investigate the effects of varicella-zoster virus (VZV) infection on gamma interferon (IFN-γ)-stimulated expression of cell surface major histocompatibility complex (MHC) class II molecules on human fibroblasts. IFN-γ treatment induced cell surface MHC class II expression on 60 to 86% of uninfected cells, compared to 20 to 30% of cells which had been infected with VZV prior to the addition of IFN-γ. In contrast, cells that were treated with IFN-γ before VZV infection had profiles of MHC class II expression similar to those of uninfected cell populations. Neither IFN-γ treatment nor VZV infection affected the expression of transferrin receptor (CD71). In situ and Northern blot hybridization of MHC II (MHC class II DR-α) RNA expression in response to IFN-γ stimulation revealed that MHC class II DR-α mRNA accumulated in uninfected cells but not in cells infected with VZV. When skin biopsies of varicella lesions were analyzed by in situ hybridization, MHC class II transcripts were detected in areas around lesions but not in cells that were infected with VZV. VZV infection inhibited the expression of Stat 1α and Jak2 proteins but had little effect on Jak1. Analysis of regulatory events in the IFN-γ signaling pathway showed that VZV infection inhibited transcription of interferon regulatory factor 1 and the MHC class II transactivator. This is the first report that VZV encodes an immunomodulatory function which directly interferes with the IFN-γ signal transduction via the Jak/Stat pathway and enables the virus to inhibit IFN-γ induction of cell surface MHC class II expression. This inhibition of MHC class II expression on VZV-infected cells in vivo may transiently protect cells from CD4 + T-cell immune surveillance, facilitating local virus replication and transmission during the first few days of cutaneous lesion formation.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.74.4.1900-1907.2000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2000
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  • 6
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    Varicella-Zoster Virus Retains Major Histocompatibility Complex Class I Proteins in the Golgi Compartment of Infected Cells
    American Society for Microbiology ; 2001
    In:  Journal of Virology Vol. 75, No. 10 ( 2001-05-15), p. 4878-4888
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 75, No. 10 ( 2001-05-15), p. 4878-4888
    Abstract: We sought to examine the effects of varicella-zoster virus (VZV) infection on the expression of major histocompatibility complex class I (MHC I) molecules by human fibroblasts and T lymphocytes. By flow cytometry, VZV infection reduced the cell surface expression of MHC I molecules on fibroblasts significantly, yet the expression of transferrin receptor was not affected. Importantly, when human fetal thymus/liver implants in SCID-hu mice were inoculated with VZV, cell surface MHC I expression was downregulated specifically on VZV-infected human CD3 + T lymphocytes, a prominent target that sustains VZV viremia. The stage in the MHC I assembly process that was disrupted by VZV in fibroblasts was examined in pulse-chase and immunoprecipitation experiments in the presence of endoglycosidase H. MHC I complexes continued to be assembled in VZV-infected cells and were not retained in the endoplasmic reticulum. In contrast, immunofluorescence and confocal microscopy showed that VZV infection resulted in an accumulation of MHC I molecules which colocalized to the Golgi compartment. Inhibition of late viral gene expression by treatment of infected fibroblasts with phosphonoacetic acid did not influence the modulation of MHC I expression, nor did transfection of cells with plasmids expressing immediate early viral proteins. However, cells transfected with a plasmid carrying the early gene ORF66 did result in a significant downregulation of MHC I expression, suggesting that this gene encodes a protein with an immunomodulatory function. Thus, VZV downregulates MHC I expression by impairing the transport of MHC I molecules from the Golgi compartment to the cell surface; this effect may enable the virus to evade CD8 + T-cell immune recognition during VZV pathogenesis, including the critical phase of T-lymphocyte-associated viremia.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.75.10.4878-4888.2001
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
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  • 7
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    Latent cytomegalovirus down-regulates major histocompatibility complex class II expression on myeloid progenitors
    American Society of Hematology ; 2002
    In:  Blood Vol. 100, No. 8 ( 2002-10-15), p. 2867-2873
    Details
    In: Blood, American Society of Hematology, Vol. 100, No. 8 ( 2002-10-15), p. 2867-2873
    Abstract: Following primary infection, human cytomegalovirus (CMV) establishes a lifelong latent infection in bone marrow–derived myeloid lineage cells. Although downmodulation of major histocompatibility complex (MHC) class I and class II protein levels occurs during active viral replication, little is known about the modulation of these proteins during latent infection. When analyzed by flow cytometry, latently infected adherent cells collected from granulocyte macrophage progenitor (GM-P) cultures exhibited a striking reduction in MHC class II antigen present on the cell surface starting very early after exposure to virus that continued for more than 2 weeks. In comparison, cell surface levels of the monocyte cell surface marker CD14 remained unaltered in these cells. A recombinant virus (RV798) lacking the virus genes US2-US11 retained the ability to downmodulate MHC class II levels during latent infection. Immunoblot and immunofluorescent antibody staining analyses showed that the reduction in MHC class II surface levels during latency was associated with a block in protein trafficking. HLA-DR was retained within cytoplasmic vesicles that also contained HLA-DM. Thus, downmodulation remained independent of all previously characterized MHC class I and class II immunomodulatory viral gene products and involved a mechanism not previously ascribed to any viral function. These data show that latent infection is accompanied by reduced cell surface expression of MHC class II proteins, a strategy that would afford the virus escape from immunosurveillance and increase the chances for lifelong latent infection.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V100.8.2867
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2002
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 8
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    Varicella-Zoster Virus Infection of Human Dendritic Cells and Transmission to T Cells: Implications for Virus Dissemination in the Host
    American Society for Microbiology ; 2001
    In:  Journal of Virology Vol. 75, No. 13 ( 2001-07), p. 6183-6192
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 75, No. 13 ( 2001-07), p. 6183-6192
    Abstract: During primary varicella-zoster virus (VZV) infection, it is presumed that virus is transmitted from mucosal sites to regional lymph nodes, where T cells become infected. The cell type responsible for VZV transport from the mucosa to the lymph nodes has not been defined. In this study, we assessed the susceptibility of human monocyte-derived dendritic cells to infection with VZV. Dendritic cells were inoculated with the VZV strain Schenke and assessed by flow cytometry for VZV and dendritic cell (CD1a) antigen expression. In five replicate experiments, 34.4% ± 6.6% (mean ± SEM) of CD1a + cells were also VZV antigen positive. Dendritic cells were also shown to be susceptible to VZV infection by the detection of immediate-early (IE62), early (ORF29), and late (gC) gene products in CD1a + dendritic cells. Infectious virus was recovered from infected dendritic cells, and cell-to-cell contact was required for transmission of virus to permissive fibroblasts. VZV-infected dendritic cells showed no significant decrease in cell viability or evidence of apoptosis and did not exhibit altered cell surface levels of major histocompatibility complex (MHC) class I, MHC class II, CD86, CD40, or CD1a. Significantly, when autologous T lymphocytes were incubated with VZV-infected dendritic cells, VZV antigens were readily detected in CD3 + T lymphocytes and infectious virus was recovered from these cells. These data provide the first evidence that dendritic cells are permissive to VZV and that dendritic cell infection can lead to transmission of virus to T lymphocytes. These findings have implications for our understanding of how virus may be disseminated during primary VZV infection.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.75.13.6183-6192.2001
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
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  • 9
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    Varicella-Zoster Virus Productively Infects Mature Dendritic Cells and Alters Their Immune Function
    American Society for Microbiology ; 2003
    In:  Journal of Virology Vol. 77, No. 8 ( 2003-04-15), p. 4950-4959
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 77, No. 8 ( 2003-04-15), p. 4950-4959
    Abstract: Mature dendritic cells (DCs) are potent antigen-presenting cells essential for initiating successful antiviral immune responses and would therefore serve as an ideal target for viruses seeking to evade or delay the immune response by disrupting their function. We have previously reported that VZV productively infects immature DCs (A. Abendroth, G. Morrow, A. L. Cunningham, and B. Slobedman, J. Virol. 75:6183-6192, 2001), and in the present study we assessed the ability of VZV to infect mature DCs. Mature DCs were generated from immature monocyte-derived DCs by lipopolysaccharide treatment before being exposed to VZV-infected fibroblasts. On day 4 postexposure, flow cytometry analysis revealed that 15 to 45% of mature DCs were VZV antigen positive, and immunofluorescent staining together with infectious-center assays demonstrated that these cells were fully permissive for the complete VZV replicative cycle. VZV infection of mature DCs resulted in a selective downregulation of cell surface expression of the functionally important immune molecules major histocompatibility complex (MHC) class I, CD80, CD83, and CD86 but did not alter MHC class II expression. Immunofluorescent staining showed that the downregulation of cell surface CD83 was concomitant with a retention of CD83 in cytoplasmic vesicles. Importantly, VZV infection of mature DCs significantly reduced their ability to stimulate the proliferation of allogeneic T lymphocytes. These data demonstrate that mature DCs are permissive for VZV and that infection of these cells reduces their ability to function properly. Thus, VZV has evolved yet another immune evasion strategy that would likely impair immunosurveillance and enhance the chances for lifelong persistence in the human population.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.77.8.4950-4959.2003
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2003
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