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Platelet activation suppresses HIV-1 infection of T cells

Theodros Solomon Tsegaye1, Kerstin Gnirß12, Niels Rahe-Meyer3, Miriam Kiene1, Annika Krämer-Kühl12, Georg Behrens4, Jan Münch5 and Stefan Pöhlmann12*

Author Affiliations

1 Institute of Virology, Hannover Medical School, Hannover, Germany

2 Infection Biology Unit, German Primate Center, Göttingen, Germany

3 Department of Anesthesiology and Intensive Care Unit, Hannover Medical School, Hannover, Germany

4 Department of Clinical Immunology and Rheumatology, Hannover Medical School, Hannover, Germany

5 Institute of Molecular Virology, University Hospital Ulm, Ulm, Germany

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Retrovirology 2013, 10:48  doi:10.1186/1742-4690-10-48

Published: 1 May 2013



Platelets, anucleate cell fragments abundant in human blood, can capture HIV-1 and platelet counts have been associated with viral load and disease progression. However, the impact of platelets on HIV-1 infection of T cells is unclear.


We found that platelets suppress HIV-1 spread in co-cultured T cells in a concentration-dependent manner. Platelets containing granules inhibited HIV-1 spread in T cells more efficiently than degranulated platelets, indicating that the granule content might exert antiviral activity. Indeed, supernatants from activated and thus degranulated platelets suppressed HIV-1 infection. Infection was inhibited at the stage of host cell entry and inhibition was independent of the viral strain or coreceptor tropism. In contrast, blockade of HIV-2 and SIV entry was less efficient. The chemokine CXCL4, a major component of platelet granules, blocked HIV-1 entry and neutralization of CXCL4 in platelet supernatants largely abrogated their anti-HIV-1 activity.


Release of CXCL4 by activated platelets inhibits HIV-1 infection of adjacent T cells at the stage of virus entry. The inhibitory activity of platelet-derived CXCL4 suggests a role of platelets in the defense against infection by HIV-1 and potentially other pathogens.

HIV-1; CXCL4; Platelet; Entry