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  1. Article ; Online: Association of human papillomavirus type 31 variants with risk of cervical intraepithelial neoplasia grades 2-3.

    Xi, Long Fu / Schiffman, Mark / Koutsky, Laura A / Hulbert, Ayaka / Lee, Shu-Kuang / Defilippis, Victor / Shen, Zhenping / Kiviat, Nancy B

    International journal of cancer

    2012  Volume 131, Issue 10, Page(s) 2300–2307

    Abstract: Although the lineages of human papillomavirus type 31 (HPV31) variants are recognized, their clinical relevance is unknown. The purpose of our study was to examine risk of cervical intraepithelial neoplasia Grades 2-3 (CIN2/3) by HPV31 variants. Study ... ...

    Abstract Although the lineages of human papillomavirus type 31 (HPV31) variants are recognized, their clinical relevance is unknown. The purpose of our study was to examine risk of cervical intraepithelial neoplasia Grades 2-3 (CIN2/3) by HPV31 variants. Study subjects were women who participated in the atypical squamous cells of undetermined significance and low-grade squamous intraepithelial lesion Triage Study and who had HPV31 infections detected at one or more visits. They were followed semi-annually over 2 years for detection of HPV DNA and cervical lesion. HPV31 isolates were characterized by DNA sequencing and assigned into 1 of 3 variant lineages. CIN2/3 was histologically confirmed in 127 (27.0%) of the 470 HPV31-positive women, 83 diagnosed at the first HPV31-positive visit and 44 thereafter. The odds ratio for the association of 2-year cumulative risk of CIN2/3 was 1.7 (95% CI: 1.0-2.9) for infections with A variants and 2.2 (95% CI: 1.2-3.9) for infections with B variants as compared to those with C variants. Among women without CIN2/3 at the first HPV31-positive visit, the risk of subsequent CIN2/3 was 2.2-fold greater for those with A variants (95% CI: 1.0-4.8) and 2.0-fold greater for those with B variants (95% CI: 0.9-4.9) as compared to those with C variants. Similar associations were observed when CIN3 was used as the endpoint. The findings from our study help to tag HPV31 variants that differ in risk of CIN2/3 and to explain in part why some HPV31 infections regress spontaneously and others lead to disease progression.
    MeSH term(s) Adolescent ; Adult ; Cervical Intraepithelial Neoplasia/mortality ; Cervical Intraepithelial Neoplasia/pathology ; Cervical Intraepithelial Neoplasia/virology ; Female ; Human papillomavirus 31/classification ; Human papillomavirus 31/genetics ; Humans ; Kaplan-Meier Estimate ; Neoplasm Grading ; Papillomavirus Infections ; Risk ; Uterine Cervical Neoplasms/mortality ; Uterine Cervical Neoplasms/pathology ; Uterine Cervical Neoplasms/virology ; Vaginal Smears ; Young Adult
    Language English
    Publishing date 2012-11-15
    Publishing country United States
    Document type Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.27520
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Chikungunya virus induces IPS-1-dependent innate immune activation and protein kinase R-independent translational shutoff.

    White, Laura K / Sali, Tina / Alvarado, David / Gatti, Evelina / Pierre, Philippe / Streblow, Daniel / Defilippis, Victor R

    Journal of virology

    2010  Volume 85, Issue 1, Page(s) 606–620

    Abstract: Chikungunya virus (CHIKV) is an arthritogenic mosquito-transmitted alphavirus that is undergoing reemergence in areas around the Indian Ocean. Despite the current and potential danger posed by this virus, we know surprisingly little about the induction ... ...

    Abstract Chikungunya virus (CHIKV) is an arthritogenic mosquito-transmitted alphavirus that is undergoing reemergence in areas around the Indian Ocean. Despite the current and potential danger posed by this virus, we know surprisingly little about the induction and evasion of CHIKV-associated antiviral immune responses. With this in mind we investigated innate immune reactions to CHIKV in human fibroblasts, a demonstrable in vivo target of virus replication and spread. We show that CHIKV infection leads to activation of the transcription factor interferon regulatory factor 3 (IRF3) and subsequent transcription of IRF3-dependent antiviral genes, including beta interferon (IFN-β). IRF3 activation occurs by way of a virus-induced innate immune signaling pathway that includes the adaptor molecule interferon promoter stimulator 1 (IPS-1). Despite strong transcriptional upregulation of these genes, however, translation of the corresponding proteins is not observed. We further demonstrate that translation of cellular (but not viral) genes is blocked during infection and that although CHIKV is found to trigger inactivation of the translational molecule eukaryotic initiation factor subunit 2α by way of the double-stranded RNA sensor protein kinase R, this response is not required for the block to protein synthesis. Furthermore, overall diminution of cellular RNA synthesis is also observed in the presence of CHIKV and transcription of IRF3-dependent antiviral genes appears specifically blocked late in infection. We hypothesize that the observed absence of IFN-β and antiviral proteins during infection results from an evasion mechanism exhibited by CHIKV that is dependent on widespread shutoff of cellular protein synthesis and a targeted block to late synthesis of antiviral mRNA transcripts.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line ; Cells, Cultured ; Chikungunya virus/immunology ; Chikungunya virus/pathogenicity ; Cricetinae ; Fibroblasts/immunology ; Fibroblasts/virology ; Gene Expression Regulation ; Humans ; Immune Evasion/immunology ; Immunity, Innate/immunology ; Interferon-beta ; Protein Biosynthesis/immunology ; Proteins/genetics ; Proteins/metabolism ; eIF-2 Kinase/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; MAVS protein, human ; Proteins ; Interferon-beta (77238-31-4) ; eIF-2 Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2010-10-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00767-10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Chikungunya virus infection results in higher and persistent viral replication in aged rhesus macaques due to defects in anti-viral immunity.

    Messaoudi, Ilhem / Vomaske, Jennifer / Totonchy, Thomas / Kreklywich, Craig N / Haberthur, Kristen / Springgay, Laura / Brien, James D / Diamond, Michael S / Defilippis, Victor R / Streblow, Daniel N

    PLoS neglected tropical diseases

    2013  Volume 7, Issue 7, Page(s) e2343

    Abstract: Chikungunya virus (CHIKV) is a re-emerging mosquito-borne Alphavirus that causes a clinical disease involving fever, myalgia, nausea and rash. The distinguishing feature of CHIKV infection is the severe debilitating poly-arthralgia that may persist for ... ...

    Abstract Chikungunya virus (CHIKV) is a re-emerging mosquito-borne Alphavirus that causes a clinical disease involving fever, myalgia, nausea and rash. The distinguishing feature of CHIKV infection is the severe debilitating poly-arthralgia that may persist for several months after viral clearance. Since its re-emergence in 2004, CHIKV has spread from the Indian Ocean region to new locations including metropolitan Europe, Japan, and even the United States. The risk of importing CHIKV to new areas of the world is increasing due to high levels of viremia in infected individuals as well as the recent adaptation of the virus to the mosquito species Aedes albopictus. CHIKV re-emergence is also associated with new clinical complications including severe morbidity and, for the first time, mortality. In this study, we characterized disease progression and host immune responses in adult and aged Rhesus macaques infected with either the recent CHIKV outbreak strain La Reunion (LR) or the West African strain 37997. Our results indicate that following intravenous infection and regardless of the virus used, Rhesus macaques become viremic between days 1-5 post infection. While adult animals are able to control viral infection, aged animals show persistent virus in the spleen. Virus-specific T cell responses in the aged animals were reduced compared to adult animals and the B cell responses were also delayed and reduced in aged animals. Interestingly, regardless of age, T cell and antibody responses were more robust in animals infected with LR compared to 37997 CHIKV strain. Taken together these data suggest that the reduced immune responses in the aged animals promotes long-term virus persistence in CHIKV-LR infected Rhesus monkeys.
    MeSH term(s) Age Factors ; Alphavirus Infections/immunology ; Alphavirus Infections/virology ; Animals ; B-Lymphocytes/immunology ; Blood/virology ; Chikungunya Fever ; Chikungunya virus/immunology ; Chikungunya virus/physiology ; Disease Models, Animal ; Female ; Macaca mulatta/virology ; Male ; Spleen/virology ; T-Lymphocytes/immunology ; Viral Load ; Virus Replication
    Language English
    Publishing date 2013-07-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2429704-5
    ISSN 1935-2735 ; 1935-2727
    ISSN (online) 1935-2735
    ISSN 1935-2727
    DOI 10.1371/journal.pntd.0002343
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Rat cytomegalovirus gene expression in cardiac allograft recipients is tissue specific and does not parallel the profiles detected in vitro.

    Streblow, Daniel N / van Cleef, Koen W R / Kreklywich, Craig N / Meyer, Christine / Smith, Patricia / Defilippis, Victor / Grey, Finn / Früh, Klaus / Searles, Robert / Bruggeman, Cathrien / Vink, Cornelis / Nelson, Jay A / Orloff, Susan L

    Journal of virology

    2007  Volume 81, Issue 8, Page(s) 3816–3826

    Abstract: Rat cytomegalovirus (RCMV) is a beta-herpesvirus with a 230-kbp genome containing over 167 open reading frames (ORFs). RCMV gene expression is tightly regulated in cultured cells, occurring in three distinct kinetic classes (immediate early, early, and ... ...

    Abstract Rat cytomegalovirus (RCMV) is a beta-herpesvirus with a 230-kbp genome containing over 167 open reading frames (ORFs). RCMV gene expression is tightly regulated in cultured cells, occurring in three distinct kinetic classes (immediate early, early, and late). However, the extent of viral-gene expression in vivo and its relationship to the in vitro expression are unknown. In this study, we used RCMV-specific DNA microarrays to investigate the viral transcriptional profiles in cultured, RCMV-infected endothelial cells, fibroblasts, and aortic smooth muscle cells and to compare these profiles to those found in tissues from RCMV-infected rat heart transplant recipients. In cultured cells, RCMV expresses approximately 95% of the known viral ORFs with few differences between cell types. By contrast, in vivo viral-gene expression in tissues from rat heart allograft recipients is highly restricted. In the tissues studied, a total of 80 viral genes expressing levels twice above background (5,000 to 10,000 copies per mug total RNA) were detected. In each tissue type, there were a number of genes expressed exclusively in that tissue. Although viral mRNA and genomic DNA levels were lower in the spleen than in submandibular glands, the number of individual viral genes expressed was higher in the spleen (60 versus 41). This finding suggests that the number of viral genes expressed is specific to a given tissue and is not dependent upon the viral load or viral mRNA levels. Our results demonstrate that the profiles, as well as the amplitude, of viral-gene expression are tissue specific and are dramatically different from those in infected cultured cells, indicating that RCMV gene expression in vitro does not reflect viral-gene expression in vivo.
    MeSH term(s) Animals ; Aorta/virology ; Cells, Cultured ; DNA, Viral/analysis ; Endothelial Cells/virology ; Fibroblasts/virology ; Gene Expression ; Gene Expression Profiling ; Heart Transplantation ; Herpesviridae Infections/virology ; Muromegalovirus/genetics ; Muromegalovirus/growth & development ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/virology ; Myocytes, Smooth Muscle/virology ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; RNA, Messenger/biosynthesis ; RNA, Viral/biosynthesis ; Rats ; Rats, Inbred F344 ; Spleen/virology ; Submandibular Gland/virology ; Transplantation, Homologous
    Chemical Substances DNA, Viral ; RNA, Messenger ; RNA, Viral
    Language English
    Publishing date 2007-04
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.02425-06
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: Show issues Location:
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  5. Article: West Nile virus infection activates the unfolded protein response, leading to CHOP induction and apoptosis.

    Medigeshi, Guruprasad R / Lancaster, Alissa M / Hirsch, Alec J / Briese, Thomas / Lipkin, W Ian / Defilippis, Victor / Früh, Klaus / Mason, Peter W / Nikolich-Zugich, Janko / Nelson, Jay A

    Journal of virology

    2007  Volume 81, Issue 20, Page(s) 10849–10860

    Abstract: West Nile virus (WNV)-mediated neuronal death is a hallmark of WNV meningitis and encephalitis. However, the mechanisms of WNV-induced neuronal damage are not well understood. We investigated WNV neuropathogenesis by using human neuroblastoma cells and ... ...

    Abstract West Nile virus (WNV)-mediated neuronal death is a hallmark of WNV meningitis and encephalitis. However, the mechanisms of WNV-induced neuronal damage are not well understood. We investigated WNV neuropathogenesis by using human neuroblastoma cells and primary rat hippocampal neurons. We observed that WNV activates multiple unfolded protein response (UPR) pathways, leading to transcriptional and translational induction of UPR target genes. We evaluated the role of the three major UPR pathways, namely, inositol-requiring enzyme 1-dependent splicing of X box binding protein 1 (XBP1) mRNA, activation of activating transcription factor 6 (ATF6), and protein kinase R-like endoplasmic reticulum (ER) kinase-dependent eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation, in WNV-infected cells. We show that XBP1 is nonessential or can be replaced by other UPR pathways in WNV replication. ATF6 was rapidly degraded by proteasomes, consistent with induction of ER stress by WNV. We further observed a transient phosphorylation of eIF2alpha and induction of the proapoptotic cyclic AMP response element-binding transcription factor homologous protein (CHOP). WNV-infected cells exhibited a number of apoptotic phenotypes, such as (i) induction of growth arrest and DNA damage-inducible gene 34, (ii) activation of caspase-3, and (iii) cleavage of poly(ADP-ribose) polymerase. The expression of WNV nonstructural proteins alone was sufficient to induce CHOP expression. Importantly, WNV grew to significantly higher viral titers in chop(-)(/)(-) mouse embryonic fibroblasts (MEFs) than in wild-type MEFs, suggesting that CHOP-dependent premature cell death represents a host defense mechanism to limit viral replication that might also be responsible for the widespread neuronal loss observed in WNV-infected neuronal tissue.
    MeSH term(s) Activating Transcription Factor 6/metabolism ; Animals ; Apoptosis ; Cell Line ; DNA-Binding Proteins/genetics ; Eukaryotic Initiation Factor-2/metabolism ; Gene Expression Regulation ; Humans ; Mice ; Neurons/pathology ; Neurons/virology ; Nuclear Proteins/genetics ; Rats ; Regulatory Factor X Transcription Factors ; Signal Transduction ; Transcription Factor CHOP/genetics ; Transcription Factors ; Virus Replication ; West Nile Fever/etiology ; West Nile Fever/metabolism ; West Nile Fever/pathology ; West Nile virus/pathogenicity ; X-Box Binding Protein 1
    Chemical Substances ATF6 protein, human ; Activating Transcription Factor 6 ; DDIT3 protein, human ; DNA-Binding Proteins ; Eukaryotic Initiation Factor-2 ; Nuclear Proteins ; Regulatory Factor X Transcription Factors ; Transcription Factors ; X-Box Binding Protein 1 ; XBP1 protein, human ; Xbp1 protein, mouse ; Xbp1 protein, rat ; Transcription Factor CHOP (147336-12-7)
    Language English
    Publishing date 2007-08-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.01151-07
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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