Most　HIV-1-infected　patients　experience　hematopoiesis　suppression　complications.　Bone　marrow　mesenchymal　stem　cells　(BMSCs)　are　involved　in　regulation　of　hematopoietic　homeostasis,　so　we　investigated　the　role　of　Tat,　a　protein　released　by　infected　cells　in　bone　marrow　and　impacted　differentiation　potential　of　mesenchymal　stem　cells,　in　the　BMSC　hematopoietic　support　function.　BMSCs　were　treated　with　HIV-1　Tat　protein　(BMSCTat-p),　transfected　with　HIV-1　Tat　mRNA　(BMSCTat-m)　or　treated　with　solvent　(PBS)　(BMSCcon)　for　20　days.　Then,　the　hematopoietic　support　function　of　BMSCTat-p,　BMSCTat-m　and　BMSCcon,　was　analyzed　via　ex　vivo　expansion　of　hematopoietic　stem　cells　(HSCs)　grown　on　the　BMSCs　and　via　in　vivo　cotransplantation　of　HSCs　and　BMSCs.　In　addition,　the　hematopoiesis-supporting　gene　expression　patterns　of　BMSCTat-p,　BMSCTat-m　and　BMSC(con　)were　compared.　The　results　showed　that　BMSCTat-p,　BMSCTat-m,　displayed　reduced　expansion,　a　decline　in　the　number　of　colony　forming　units　(CFUs)　and　a　decreased　proportion　of　the　primitive　subpopulation　of　hematopoietic　stem　cells　under　coculture　conditions　compared　with　BMSCcon　.　The　ability　of　BMSCTat-p,　to　support　hematopoietic　recovery　was　also　impaired,　which　was　further　confirmed　by　the　patterns　in　gene　expression　analysis.　In　conclusion,　Tat　treatment　reduced　the　function　of　BMSCs　in　hematopoietic　support,　likely　by　downregulating　the　expression　of　a　series　of　hematopoietic　cytokines.