Platelet activation suppresses HIV-1 infection of T cells
- Equal contributors
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
Retrovirology 2013, 10:48 doi:10.1186/1742-4690-10-48Published: 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.