High number of CD56bright NK-cells and persistently low CD4+ T-cells in a hemophiliac HIV/HCV co-infected patient without opportunistic infections
1 Inserm U1016, Institut Cochin, Département d’Hématologie et d’Immunologie, Paris, France
2 Université Paris Descartes Sorbonne Paris Cité, CNRS (UMR8104), Paris, France
3 Service d’Hématologie et d’Immunologie, Hôpital Ambroise Paré, Boulogne-Billancourt, France
4 UFR des Sciences et de la Santé Paris Ile-de-France Ouest, Université de Versailles St Quentin en Yvelines, St Quentin en Yvelines, France
5 Laboratoire d’Hématologie, Hôtel-Dieu-CHU, Nantes, France
6 Service de Médecine Interne, Hôpital Ambroise Paré, Boulogne-Billancourt, France
7 Unité de Régulation des Infections Rétrovirales, Institut Pasteur, Paris, France
8 Institute of Pathology, Centre Hospitalier Universitaire Vaudois, Faculty of Biology and Medecine, University of Lausanne, Lausanne, Switzerland
Virology Journal 2013, 10:33 doi:10.1186/1743-422X-10-33Published: 26 January 2013
Both the human immunodeficiency virus (HIV) and hepatitis C virus (HCV), either alone or as coinfections, persist in their hosts by destroying and/or escaping immune defenses, with high morbidity as consequence. In some cases, however, a balance between infection and immunity is reached, leading to prolonged asymptomatic periods. We report a case of such an indolent co-infection, which could be explained by the development of a peculiar subset of Natural Killer (NK) cells.
Persistently high peripheral levels of CD56+ NK cells were observed in a peculiar hemophiliac HIV/HCV co-infected patient with low CD4 counts, almost undetectable HIV viral load and no opportunistic infections. Thorough analysis of NK-subsets allowed to identify a marked increase in the CD56bright/dim cell ratio and low numbers of CD16+/CD56- cells. These cells have high levels of natural cytotoxicity receptors but low NCR2 and CD69, and lack both CD57 and CD25 expression. The degranulation potential of NK-cells which correlates with target cytolysis was atypically mainly performed by CD56bright NK-cells, whereas no production of interferon γ (IFN-γ) was observed following NK activation by K562 cells.
These data suggest that the expansion and lytic capacity of the CD56bright NK subset may be involved in the protection of this « rare » HIV/HCV co-infected hemophiliac A patient from opportunistic infections and virus-related cancers despite very low CD4+ cell counts.