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Mark Sharkey

Researcher at University of Miami

Publications -  41
Citations -  3060

Mark Sharkey is an academic researcher from University of Miami. The author has contributed to research in topics: Viral replication & Medicine. The author has an hindex of 19, co-authored 31 publications receiving 2822 citations. Previous affiliations of Mark Sharkey include University of Massachusetts Amherst & University of Massachusetts Medical School.

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HIV-1 replication and immune dynamics are affected by raltegravir intensification of HAART-suppressed subjects

TL;DR: Results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation, and the ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication.
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Persistence of episomal HIV-1 infection intermediates in patients on highly active anti-retroviral therapy.

TL;DR: It is demonstrated here ongoing virus replication in a large percentage of infected individuals on highly active anti-retroviral therapy, despite sustained undetectable levels of plasma viral RNA, has important implications for the clinical management of HIV-1-infected individuals and for the development of virus eradication strategies.
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Macrophages archive HIV-1 virions for dissemination in trans.

TL;DR: It is demonstrated that virions assembling intracellularly in primary macrophages retain infectivity for extended intervals and the stable sequestration of infectious virions within cytoplasmic compartments of macrophage may represent an additional mechanism for viral persistence in HIV‐1‐infected individuals.
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Early Therapy of Vertical Human Immunodeficiency Virus Type 1 (HIV-1) Infection: Control of Viral Replication and Absence of Persistent HIV-1-Specific Immune Responses

TL;DR: Despite preservation of immune function, persistent human immunodeficiency type 1 (HIV-1)-specific immune responses were not detected in most infants, consistent with the notion that early combination antiretroviral therapy of HIV-1-infected infants allows the long-term suppression of viral replication.
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SH3-mediated Hck Tyrosine Kinase Activation and Fibroblast Transformation by the Nef Protein of HIV-1

TL;DR: It is shown that Rat-2 fibroblasts co-expressing Hck and Nef rapidly developed transformed foci, whereas control cells expressing either protein alone did not, suggesting that Hck may be activated by Nef in HIV-infected macrophages.