Alexandra Borch
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Alexandra Borch has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Albert D. M. E. Osterhaus
Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands
1 shared publication - Christina Martina Stürzel
Institute of Molecular Virology, Ulm University Medical Centre, Meyerhofstraße 1, 89081 Ulm, Germany
1 shared publication - Daniela Krnavek
Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany
1 shared publication - Frank Kirchhoff
Institute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany
1 shared publication - Hangxing Yu
Institute of Molecular Virology, Ulm University Medical Center, Ulm 89081, Germany
1 shared publication - Julia Krämer
Institute of Molecular Virology, Ulm University Medical Center, Ulm 89081, Germany
1 shared publication
Latest Publications
- Open Access
- 5 March 2013
- Published by Springer Nature in Retrovirology
- Vol. 10 (1) , 27
The efficiency of Vpx-mediated SAMHD1 antagonism does not correlate with the potency of viral control in HIV-2-infected individuals
Background: The presence of avpxgene distinguishes HIV-2 from HIV-1, the main causative agent of AIDS. Vpx degrades the restriction factor SAMHD1 to boost HIV-2 infection of macrophages and dendritic cells and it has been suggested that the activation of antiviral innate immune responses after Vpx-dependent infection of myeloid cells may explain why most HIV-2-infected individuals efficiently control viral replication and become long-term survivors. However, the role of Vpx-mediated SAMHD1 antagonism in the virological and clinical outcome of HIV-2 infection remained to be investigated.Results: Here, we analyzed the anti-SAMHD1 activity ofvpxalleles derived from seven viremic and four long-term aviremic HIV-2-infected individuals. We found that effective Vpx-mediated SAMHD1 degradation and enhancement of myeloid cell infection was preserved in most HIV-2-infected individuals including all seven that failed to control the virus and developed AIDS. The only exception werevpxalleles from an aviremic individual that predicted a M68K change in a highly conserved nuclear localization signal which disrupted the ability of Vpx to counteract SAMHD1. We also found that HIV-2 is less effective than HIV-1 in inducing innate immune activation in dendritic cells.Conclusions: Effective immune control of viral replication in HIV-2-infected individuals is not associated with increased Vpx-mediated degradation of SAMHD1.
- 5 March 2013
- Published by Springer Nature in Retrovirology
- Vol. 10 (1) , 27
Open AccessThe efficiency of Vpx-mediated SAMHD1 antagonism does not correlate with the potency of viral control in HIV-2-infected individuals
Background: The presence of avpxgene distinguishes HIV-2 from HIV-1, the main causative agent of AIDS. Vpx degrades the restriction factor SAMHD1 to boost HIV-2 infection of macrophages and dendritic cells and it has been suggested that the activation of antiviral innate immune responses after Vpx-dependent infection of myeloid cells may explain why most HIV-2-infected individuals efficiently control viral replication and become long-term survivors. However, the role of Vpx-mediated SAMHD1 antagonism in the virological and clinical outcome of HIV-2 infection remained to be investigated.Results: Here, we analyzed the anti-SAMHD1 activity ofvpxalleles derived from seven viremic and four long-term aviremic HIV-2-infected individuals. We found that effective Vpx-mediated SAMHD1 degradation and enhancement of myeloid cell infection was preserved in most HIV-2-infected individuals including all seven that failed to control the virus and developed AIDS. The only exception werevpxalleles from an aviremic individual that predicted a M68K change in a highly conserved nuclear localization signal which disrupted the ability of Vpx to counteract SAMHD1. We also found that HIV-2 is less effective than HIV-1 in inducing innate immune activation in dendritic cells.Conclusions: Effective immune control of viral replication in HIV-2-infected individuals is not associated with increased Vpx-mediated degradation of SAMHD1.