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Anders Sönnerborg

Researcher at Karolinska Institutet

Publications -  432
Citations -  21283

Anders Sönnerborg is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Viral load & Virus. The author has an hindex of 66, co-authored 407 publications receiving 19240 citations. Previous affiliations of Anders Sönnerborg include University of Missouri & University College London.

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Bilirubin—A Potential Marker of Drug Exposure in Atazanavir-Based Antiretroviral Therapy

TL;DR: A nomogram, which can be used to indicate suboptimal atazanavir exposure and non-adherence, was constructed based on model simulations, and the possible application of bilirubin as a readily available marker of atazAnavir Exposure was assessed.
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Pattern of microbial translocation in patients living with HIV-1 from Vietnam, Ethiopia and Sweden

TL;DR: This study investigates and compares the patterns of MT in patients from Vietnam, Ethiopia and Sweden to find out the role of microbial translocation in HIV patients living with HIV from low‐ and middle‐income countries.
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Increased replication capacity following evolution of PYxE insertion in Gag-p6 is associated with enhanced virulence in HIV-1 subtype C from East Africa

TL;DR: This is the first evidence of polymerase independent increased virulence and RC in HIV‐1CEA following PYxE‐insertion that is associated with suboptimal CD4+ T‐cell gain following therapy initiation.
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Nonsynonymous mutations within the human immunodeficiency virus type 1 p17 gene are clustered to sequences binding to the host human leukocyte antigen class I molecules.

TL;DR: The present data suggest that the evolution of the p17 gene is influenced by contact areas with the host HLA class I molecules.
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Role of translocated bacterial flagellin in monocyte activation among individuals with chronic HIV-1 infection.

TL;DR: The results suggest that translocated flagellin contributes to systemic immune activation in HIV-1 infection and reduces monocyte surface TLR5 expression resulting in a hyperactivated state with elevated basal cytokine production and reduced ability to respond to furtherTLR5 stimulation.