6 results on '"Victoria P. Strouvelle"'
Search Results
2. Alteration of physical activity during COVID-19 pandemic lockdown in young adults
- Author
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Tanja Graupe, Eileen Deuster, Victoria P. Strouvelle, Jenny Schlichtiger, Steffen Massberg, Stefan Brunner, Martin R. Fischer, Bruno C. Huber, and Julius Steffen
- Subjects
Adult ,Male ,Risk ,Gerontology ,2019-20 coronavirus outbreak ,Adolescent ,Coronavirus disease 2019 (COVID-19) ,Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ,Pneumonia, Viral ,Physical activity ,lcsh:Medicine ,Public Policy ,General Biochemistry, Genetics and Molecular Biology ,Young Adult ,Pandemic ,Humans ,Medicine ,Young adult ,Letter to the Editor ,Exercise ,Pandemics ,Internet ,business.industry ,lcsh:R ,COVID-19 ,General Medicine ,Sedentary behavior ,Cross-Sectional Studies ,Social Isolation ,Multicenter study ,Communicable Disease Control ,Female ,Sedentary Behavior ,Coronavirus Infections ,business - Published
- 2020
3. EBV renders B cells susceptible to HIV-1 in humanized mice
- Author
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Bithi Chatterjee, Erika Schlaepfer, Michael Spohn, Victoria P Strouvelle, Roberto F. Speck, Thomas Menter, Kwai Fung Hui, Donal McHugh, Christian Münz, Markus G. Manz, Yik Lim Kok, Kathrin Neumann, Renier Myburgh, Alexandra Trkola, Mohaned Shilaih, Adam Grundhoff, Riccarda Capaul, Werner Kempf, Isaak Quast, Obinna Chijioke, Christine Engelmann, Stephan Dirnhofer, Nicole Caduff, Simon Bredl, Julia Rühl, Adriano Aguzzi, Karin J. Metzner, Andrea Zbinden, Silvia Sorce, Alan Ks Chiang, Janice Kp Lam, Jan D. Lünemann, Anita Murer, and Christian W. Keller
- Subjects
0301 basic medicine ,Male ,Epstein-Barr Virus Infections ,Herpesvirus 4, Human ,Receptors, CXCR4 ,Health, Toxicology and Mutagenesis ,viruses ,T-Lymphocytes ,CD34 ,HIV Infections ,Plant Science ,Biology ,Biochemistry, Genetics and Molecular Biology (miscellaneous) ,CXCR4 ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Immune system ,Mice, Inbred NOD ,HIV Seropositivity ,medicine ,Animals ,Humans ,Research Articles ,B-Lymphocytes ,Ecology ,Coinfection ,virus diseases ,medicine.disease ,Hematopoietic Stem Cells ,Virology ,In vitro ,Transplantation ,Disease Models, Animal ,030104 developmental biology ,030220 oncology & carcinogenesis ,Humanized mouse ,CD4 Antigens ,HIV-1 ,Disease Susceptibility ,CD8 ,Research Article - Abstract
A proportion of EBV+ B cells are infectible by CXCR4-tropic HIV-1 in vitro and in vivo, and these HIV-infected B cells can transmit infection to previously virus-naïve humanized mice., HIV and EBV are human pathogens that cause a considerable burden to worldwide health. In combination, these viruses are linked to AIDS-associated lymphomas. We found that EBV, which transforms B cells, renders them susceptible to HIV-1 infection in a CXCR4 and CD4-dependent manner in vitro and that CXCR4-tropic HIV-1 integrates into the genome of these B cells with the same molecular profile as in autologous CD4+ T cells. In addition, we established a humanized mouse model to investigate the in vivo interactions of EBV and HIV-1 upon coinfection. The respective mice that reconstitute human immune system components upon transplantation with CD34+ human hematopoietic progenitor cells could recapitulate aspects of EBV and HIV immunobiology observed in dual-infected patients. Upon coinfection of humanized mice, EBV/HIV dual-infected B cells could be detected, but were susceptible to CD8+ T-cell–mediated immune control.
- Published
- 2020
4. No Effect of Pegylated Interferon-α on Total HIV-1 DNA Load in HIV-1/HCV Coinfected Patients
- Author
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Dominique L Braun, Marcel Stöckle, Andri Rauch, Huldrych F. Günthard, Matthias Hoffmann, Zurich Primary Hiv Infection Study, Victoria P Strouvelle, Karin J. Metzner, Roger D. Kouyos, Valentina Vongrad, Katharine E A Darling, Yik Lim Kok, and Alexandra U. Scherrer
- Subjects
Adult ,Male ,0301 basic medicine ,Hepatitis C virus ,Human immunodeficiency virus (HIV) ,HIV Infections ,610 Medicine & health ,Pegylated interferon α ,Hepacivirus ,medicine.disease_cause ,Antiviral Agents ,Peripheral blood mononuclear cell ,03 medical and health sciences ,chemistry.chemical_compound ,medicine ,Humans ,Immunology and Allergy ,Hiv 1 dna ,Retrospective Studies ,Coinfection ,business.industry ,Immunotherapeutic agent ,Interferon-alpha ,virus diseases ,Hepatitis C ,Hepatitis C, Chronic ,Middle Aged ,Viral Load ,medicine.disease ,Virology ,030104 developmental biology ,Infectious Diseases ,chemistry ,DNA, Viral ,HIV-1 ,Leukocytes, Mononuclear ,Female ,business ,DNA - Abstract
Pegylated interferon-alpha (pIFN-α) is suggested to lower human immunodeficiency virus type-1 (HIV-1) DNA load in antiretroviral therapy (ART)-treated patients. We studied kinetics of HIV-1 DNA levels in 40 HIV-1/hepatitis C virus (HCV) coinfected patients, treated with pIFN-α for HCV and categorized into 3 groups according to start of ART: chronic HIV-1 infection (n = 22), acute HIV-1 infection (n = 8), no-ART (n = 10). Total HIV-1 DNA levels in 247 peripheral blood mononuclear cell samples were stable before, during, and after pIFN-α treatment in all groups. Our results question the benefit of pIFN-α as an immunotherapeutic agent for reducing the HIV-1 reservoir.
- Published
- 2018
5. In Vivo and in Vitro Proteome Analysis of Human Immunodeficiency Virus (HIV)-1-infected, Human CD4+ T Cells*
- Author
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Karin J. Metzner, Rainer Weber, Victoria P Strouvelle, Valentina Vongrad, Johannes Nemeth, Ruedi Aebersold, Patrick G. A. Pedrioli, Ben C. Collins, Huldrych F. Günthard, University of Zurich, and Günthard, Huldrych F
- Subjects
0301 basic medicine ,1303 Biochemistry ,610 Medicine & health ,Biology ,Proteomics ,Biochemistry ,Analytical Chemistry ,10234 Clinic for Infectious Diseases ,03 medical and health sciences ,Immune system ,SDG 3 - Good Health and Well-being ,In vivo ,1312 Molecular Biology ,Molecular Biology ,1602 Analytical Chemistry ,Acquired immune system ,Virology ,In vitro ,3. Good health ,Cell biology ,Special Issue: Proteomics and Infectious Disease ,030104 developmental biology ,Viral replication ,Proteome ,Signal transduction - Abstract
Host-directed therapies against HIV-1 are thought to be critical for long term containment of the HIV-1 pandemic but remain elusive. Because HIV-1 infects and manipulates important effectors of both the innate and adaptive immune system, identifying modulations of the host cell systems in humans during HIV-1 infection may be crucial for the development of immune based therapies. Here, we quantified the changes of the proteome in human CD4+ T cells upon HIV-1 infection, both in vitro and in vivo. A SWATH-MS approach was used to measure the proteome of human primary CD4+ T cells infected with HIV-1 in vitro as well as CD4+ T cells from HIV-1-infected patients with paired samples on and off antiretroviral treatment. In the in vitro experiment, the proteome of CD4+ T cells was quantified over a time course following HIV-1 infection. 1,725 host cell proteins and 4 HIV-1 proteins were quantified, with 145 proteins changing significantly during the time course. Changes in the proteome peaked 24 h after infection, concomitantly with significant HIV-1 protein production. In the in vivo branch of the study, CD4+ T cells from viremic patients and those with no detectable viral load after treatment were sorted, and the proteomes were quantified. We consistently detected 895 proteins, 172 of which were considered to be significantly different between the viremic patients and patients undergoing successful treatment. The proteome of the in vitro-infected CD4+ T cells was modulated on multiple functional levels, including TLR-4 signaling and the type 1 interferon signaling pathway. Perturbations in the type 1 interferon signaling pathway were recapitulated in CD4+ T cells from patients. The study shows that proteome maps generated by SWATH-MS indicate a range of functionally significant changes in the proteome of HIV-infected human CD4+ T cells. Exploring these perturbations in more detail may help identify new targets for immune based interventions.
- Published
- 2017
6. Host and Viral Determinants of Mx2 Antiretroviral Activity
- Author
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Melissa Kane, Daniel Blanco-Melo, Suzannah J. Rihn, Sam J. Wilson, Hannah F. Preugschas, Paul D. Bieniasz, Joseph Hughes, Victoria P. Strouvelle, Brian J. Willett, Chris Boutell, Idoia Busnadiego, and Trinity Zang
- Subjects
Myxovirus Resistance Proteins ,Effector ,DNA Mutational Analysis ,Immunology ,Mutant ,HIV Core Protein p24 ,Mutagenesis (molecular biology technique) ,Biology ,Microbiology ,Virology ,Reverse transcriptase ,Virus ,Virus-Cell Interactions ,Evolution, Molecular ,chemistry.chemical_compound ,chemistry ,Capsid ,Mutagenesis ,Insect Science ,HIV-1 ,Animals ,Humans ,Gene ,DNA - Abstract
Myxovirus resistance 2 (Mx2/MxB) has recently been uncovered as an effector of the anti-HIV-1 activity of type I interferons (IFNs) that inhibits HIV-1 at an early stage postinfection, after reverse transcription but prior to proviral integration into host DNA. The mechanistic details of Mx2 antiviral activity are not yet understood, but a few substitutions in the HIV-1 capsid have been shown to confer resistance to Mx2. Through a combination of in vitro evolution and unbiased mutagenesis, we further map the determinants of sensitivity to Mx2 and reveal that multiple capsid (CA) surfaces define sensitivity to Mx2. Intriguingly, we reveal an unanticipated sensitivity determinant within the C-terminal domain of capsid. We also report that Mx2s derived from multiple primate species share the capacity to potently inhibit HIV-1, whereas selected nonprimate orthologs have no such activity. Like TRIM5α, another CA targeting antiretroviral protein, primate Mx2s exhibit species-dependent variation in antiviral specificity against at least one extant virus and multiple HIV-1 capsid mutants. Using a combination of chimeric Mx2 proteins and evolution-guided approaches, we reveal that a single residue close to the N terminus that has evolved under positive selection can determine antiviral specificity. Thus, the variable N-terminal region can define the spectrum of viruses inhibited by Mx2. IMPORTANCE Type I interferons (IFNs) inhibit the replication of most mammalian viruses. IFN stimulation upregulates hundreds of different IFN-stimulated genes (ISGs), but it is often unclear which ISGs are responsible for inhibition of a given virus. Recently, Mx2 was identified as an ISG that contributes to the inhibition of HIV-1 replication by type I IFN. Thus, Mx2 might inhibit HIV-1 replication in patients, and this inhibitory action might have therapeutic potential. The mechanistic details of how Mx2 inhibits HIV-1 are currently unclear, but the HIV-1 capsid protein is the likely viral target. Here, we determine the regions of capsid that specify sensitivity to Mx2. We demonstrate that Mx2 from multiple primates can inhibit HIV-1, whereas Mx2 from other mammals (dogs and sheep) cannot. We also show that primate variants of Mx2 differ in the spectrum of lentiviruses they inhibit and that a single residue in Mx2 can determine this antiviral specificity.
- Published
- 2014
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