1Department of Internal Medicine II 2Department of Internal Medicine I 3INSERM U943 4Université Paris 6 Pierre et Marie Curie UMR S 943, F-75013, Paris 5Department of Pathology, Hôpital Antoine Béclère, AP-HP, Clamart 6Université Paris-Sud, UFR Médecine, Le Kremlin-Bicêtre, F-94275 7Hematology and Immunology department 8Inserm U-1012, Le Kremlin-Bicêtre, F-94275 9Department of Hematology, Hôpital La Conception, Marseille 10Department of Infectious Diseases, AP-HP, le Kremlin-Bicêtre, F-94275 11Department of Hematology, Groupe Hospitalier Pitié-Salpétrière, AP-HP, F-75013 12Department of Hematology, Centre Hospitalier Sud-Francilien, Corbeil-Essonne 13Department of Infectious Diseases, CHU, Vandoeuvre Les Nancy 14Department of Hematology and 15Department of Infectious Diseases, CHU, Nantes 16Department of Pathology 17Department of Hematology, APHP, Hôpital Necker-Enfants Malades, Paris F-75015 18CNRS UMR 8126, IGR, Villejuif F-94800.
Hepatitis C virus (HCV) infection is frequent among HIV infected patients. We describe the characteristics of 6 HIV-HCV coinfected patients with B-cell non-Hodgkin lymphoma (NHL) included in a prospective cohort study of HIV related lymphomas. Five of the six cases had features of marginal zone/lymphoplasmacytic NHL versus one out of 33 HIV only infected patients. Remarkably, anti-HCV treatment led to a hematological response in a patient with splenic marginal zone lymphoma. This supports the role of chronic antigenic stimulation by HCV on lymphomagenesis and further evaluation of HCV antiviral therapy in coinfected patients with NHL.
[Show abstract][Hide abstract] ABSTRACT: Previous studies suggest that active selection limits the number of HIV-1 variants acquired by a newly infected individual from the diverse variants circulating in the transmitting partner. We compared HIV-1 envelopes from 9 newly infected subjects and their linked transmitting partner to explore potential mechanisms for selection.
Recipient virus envelopes had significant genotypic differences compared to those present in the transmitting partner. Recombinant viruses incorporating pools of recipient and transmitter envelopes showed no significant difference in their sensitivity to receptor and fusion inhibitors, suggesting they had relatively similar entry capacity in the presence of low CD4 and CCR5 levels. Aggregate results in primary cells from up to 4 different blood or skin donors showed that viruses with envelopes from the transmitting partner as compared to recipient envelopes replicated more efficiently in CD4+ T cells, monocyte derived dendritic cell (MDDC) - CD4+ T cell co-cultures, Langerhans cells (LCs) - CD4+ T cell co-cultures and CD4+ T cells expressing high levels of the gut homing receptor, alpha4beta7, and demonstrated greater binding to alpha4beta7 high / CD8+ T cells. These transmitter versus recipient envelope virus phenotypic differences, however, were not always consistent among the primary cells from all the different blood or skin donation volunteers.
Although genotypically unique variants are present in newly infected individuals compared to the diverse swarm circulating in the chronically infected transmitting partner, replication in potential early target cells and receptor utilization either do not completely dictate this genetic selection, or these potential transmission phenotypes are lost very soon after HIV-1 acquisition.
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