West Nile Virus inactivation by the solvent/detergent steps of the second and third generation manufacturing processes for B-domain deleted recombinant factor VIII.

West Nile Virus (WNV) was immediately and completely inactivated to below assay detection limits upon addition of solvent/detergent (S/D) to intermediate process pools of second and third generation B-domain deleted recombinant Factor VIII (BDDrFVIII; ReFacto, Wyeth, Cambridge, MA, USA). We verify that the S/D step provides robust enveloped virus inactivation (>5 log(10)) and functions as a WNV barrier.

Immune complexes containing human immunodeficiency virus type 1 primary isolates bind to lymphoid tissue B lymphocytes and are infectious for T lymphocytes.

This study investigated the interaction of tonsil B lymphocytes with immune complexes containing human immunodeficiency virus (HIV IC) primary isolates and the infectivity of the B cell-bound HIV IC. Treatment of virus with a source of antibody and complement increased HIV IC binding to B cells by 5.6-fold. Most of the HIV IC that bound to B cells were not internalized but remained on the cell surface and were gradually released over 72 h. Cell-bound HIV IC were highly infectious for T cells while virus released by cultured B cells was only slightly infectious. Removal of HIV IC from the B-cell surface by protease treatment reduced the infection of T cells to near-background levels, indicating that infectious virus remained on the B-cell surface. These studies show that B lymphocytes can carry and transfer infectious HIV IC to T cells and thus suggest a novel mode of infection of T cells in lymphoid tissue that could be important for pathogenesis during HIV infection.

B lymphocytes in lymph nodes and peripheral blood are important for binding immune complexes containing HIV-1.

We investigated the interaction of HIV immune complexes (HIV IC) with mononuclear cells from lymph nodes and blood. While antibody alone did not affect binding of HIV IC to mononuclear cells, antibody plus complement increased binding by as much as 10-fold and complement alone also increased binding slightly. Most of the increased binding of HIV IC to mononuclear cells was blocked by heat-inactivation of complement and by OKB7 monoclonal antibody, indicating that virus binding was to CR2 on B cells. A similar pattern of antibody and complement dependence for binding of HIV IC was observed with two model systems; Raji and Arent B-cell lines. Most of the HIV IC that bound to lymph node cells were not internalized, but remained on the cell surface and were gradually released. However, even after 48 hr some HIV IC could be detected bound to cells. Under certain conditions, HIV IC were infectious for T cells if bound to B cells but not infectious if added directly to T cells. Additionally, HIV IC bound to B cells led to higher virus replication. These studies show that B lymphocytes from blood and lymph nodes can transfer infectious HIV IC to T cells.