Cell counts (Fig. 1a) and CD4 : CD8 T cell ratio (Fig. 1a), but not correlated with viral load (Fig. 1c). Positive correlation was observed between sCD40L plasma levels and T cell immune activation defined by co-expression of CD38/HLA-DR on CD4 and CD8 T cells (Fig. 1d,e), as well as IDO-mRNA expression in ARTnaive patients ([7] and Fig. 1f). However, no correlation was observed between sCD40L and

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Ir Immune Defic Syndr. Author manuscript; available in PMC 2013 June 01.Mosam et al.Pagena e, 89 had advanced (but not immediately life threatening) KS and 58 had CD4

S, a link between CD40 and microglia has been established. Upregulation of CD40 expression has been detected on microglia of HIV-1-infected brain tissues [28]. CD40L was also shown to potentiate the ability of HIV-1 Tat to activate monocytes and microglia leading to the overproduction of inflammatory proteins such as cytokines and chemokines [122]. Furthermore HAART is unable to modulate blood bra

S, a link between CD40 and microglia has been established. Upregulation of CD40 expression has been detected on microglia of HIV-1-infected brain tissues [28]. CD40L was also shown to potentiate the ability of HIV-1 Tat to activate monocytes and microglia leading to the overproduction of inflammatory proteins such as cytokines and chemokines [122]. Furthermore HAART is unable to modulate blood bra

Ith Erk2 and PLA2 phosphorylation (Fig. 5A). Indeed, vimentin has previously been shown to interact with PLA2 (52); therefore, it is reasonable to believe that they could be involved in similar cellular signaling pathways. Furthermore, previous studies indicate that vimentin filaments are regulated by phosphorylation (53). To test whether intermediate filaments and microtubules have a function in

Ied [31,32]. These compounds, which include the prototypic compound NBD556 and its derivatives, mimic the effects of CD4 by inducing the exposure of the coreceptor-binding site on gp120 [31,33]. Although NBD-556 inhibits HIV-1 infection of CD4+CCR5+ cells, it can replace CD4 and thus enhance HIV-1 infection of CD42CCR5+ cells [31]. In view of their capacity to enhance infectivity, any potential ap