10.09.2018 17:00


Innate Immune Activation in HIV Infection

Hisashi Akiyama, Ph.D.

Systemic chronic immune activation and T cell dysfunction are hallmarks of HIV-1 infection.  Despite long-term viral suppression by combination antiretroviral therapy (cART), immune activation and inflammation persist in the majority of HIV-infected individuals on cART, and is associated with excess risk of mortality and morbidity. Low-levels of type I interferon (IFN-I) are thought to be a driving force for immune activation and T cell exhaustion in HIV-1 infected  individuals on cART.

Since tissue-resident myeloid cells can remain persistently infected with HIV-1 even in individuals on cART, we hypothesized that persistent infection of myeloid cells may contribute to immune activation and T cell dysfunction. Here we demonstrate that  expression and Rev–CRM1-dependent nuclear export of intron-containing HIV-1 RNA  activates host sensing mechanisms and IFN-I-dependent pro-inflammatory responses via MAVS in productively infected macrophages.

Furthermore, HIV-1 infection-induced activation of   macrophages, in turn, leads to exhaustion of co-cultured autologous T cells. This study   suggests that use of HIV RNA expression inhibitors as adjunct therapy might abrogate aberrant inflammation and restore immune function in HIV-infected individuals on cART.

Who is Hisashi Akiyama?

  • Research Assistant Professor, Department of Microbiology, Boston University School of Medicine


  • 1/2014-1/2017: Senior Research Scien., Boston University School of Medicine, Boston, MA
  • 1/2009-1/2014: Research Associate, Boston University School of Medicine, Boston, MA
  • 5/2006-12/2008: Postdoctoral Fellow, University of Heidelberg, Germany
  • 4/2004-3/2006: Postdoctoral Research Fellowship, Japanese Foundation for AIDS Prevention

For more information click here.


10.09.2018 17:00


TWINCORE Seminarraum 0.02

Anfahrt Twincore


TWINCORE, Zentrum für Experimentelle und Klinische Infektionsforschung GmbH

Feodor-Lynen-Str. 7
30625 Hannover

Tel.: 0511-220027-0
Fax: 0511-220027-186
E-Mail: twincore(at)twincore.de



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