Christine M. Durand

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HIV-1 persists in a latent reservoir despite antiretroviral therapy (ART). This reservoir is the major barrier to HIV-1 eradication. Current approaches to purging the latent reservoir involve pharmacologic induction of HIV-1 transcription and subsequent killing of infected cells by cytolytic T lymphocytes (CTLs) or viral cytopathic effects. Agents that(More)
Despite antiretroviral therapy (ART), human immunodeficiency virus (HIV)-1 persists in a stable latent reservoir, primarily in resting memory CD4(+) T cells. This reservoir presents a major barrier to the cure of HIV-1 infection. To purge the reservoir, pharmacological reactivation of latent HIV-1 has been proposed and tested both in vitro and in vivo. A(More)
HIV-1 protease inhibitors (PIs) are among the most effective antiretroviral drugs. They are characterized by highly cooperative dose-response curves that are not explained by current pharmacodynamic theory. An unresolved problem affecting the clinical use of PIs is that patients who fail PI-containing regimens often have virus that lacks protease mutations,(More)
HIV-1 persists in a latent reservoir (LR) despite antiretroviral therapy (ART) 1–5. This reservoir is the major barrier to HIV-1 eradication 6,7. Current approaches to purging the LR involve pharmacologic induction of HIV-1 transcription and subsequent killing of infected cells by cytolytic T lymphocytes (CTL) or viral cytopathic effects 8–10. Agents that(More)
Human immunodeficiency virus (HIV) controllers are patients who control viral replication without antiretroviral therapy. We present the case of an HIV controller who had CD4 and CD8 coexpressed on 40% of his T cells. Although a recent study found that double-positive T cells had superior antiviral capacity in HIV-1 controllers, in this case, the(More)
  • Rezvani, Yong As, +11 authors Johns Hopkins
  • 2013
2005, the authors showed that systemic administration of STAT3 inhibitors not only inhibited tumor growth but also reduced the production of immunosuppressive cytokines while increasing production of inflammatory cytokines and chemokines, leading to augmentation of DC function and cytotoxic T-cell induction. 7 They later showed that in the same way,(More)
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