MicroRNA regulation of STAT4 protein expression: rapid and sensitive modulation of IL-12 signaling in human natural killer cells.

IL-12 exerts several regulatory effects on natural killer (NK) cells by activating IL-12 signaling. IL-12 signaling is tightly auto-regulated to control its onset and termination, with prolonged IL-12 treatment resulting in IL-12 hyporesponsiveness. However, the mechanisms underlying IL-12 auto-regulation are still unclear.

Matrin 3 and HIV Rev regulation of mRNA.

The nuclear matrix protein, MATR3, is a newly-described Rev cofactor whose mechanism of action is only starting to be revealed.

Quantitative estimate of the risks and benefits of possible alternative blood donor deferral strategies for men who have had sex with men.

Background: Implementation of sensitive screening methods for human immunodeficiency virus (HIV) and hepatitis viruses prompts the question of what quantitative risks may result from altered deferral strategies for donation of blood by men who have had sex with men (MSM).

Study Design And Methods: Quantitative probabilistic models were developed to assess changes in the residual risk of transfusion-transmitted HIV and hepatitis B virus (HBV) associated with blood testing and quarantine release errors (QREs) in the initial year of two hypothetical policy scenarios that would allow donations from donors who have abstained from MSM behavior for at least 5 years (MSM5) or at least 1 year (MSM1).

Results: The MSM5 and MSM1 models, respectively, predicted annual increases in units of HIV-infected blood of 0.

beta-Estradiol attenuates the anti-HIV-1 efficacy of Stavudine (D4T) in primary PBL.

Background: Female hormones are known to play an important role in predisposition for many infectious diseases. Recent work suggests there are gender effects in HIV/AIDS progression. Here we ask whether the sex steroid hormone beta-estradiol affects the replication of HIV-1 or the efficacy of a common anti-retroviral drug, Stavudine (D4T).

Hitting HIV where it hides.

The recent finding that inhibitors of PI3/Akt can sensitize HIV infected macrophages to oxidative stress-induced cell death suggest a potential new therapeutic approach to targeting HIV reservoirs.

Beyond open access: open discourse, the next great equalizer.

The internet is expanding the realm of scientific publishing to include free and open public debate of published papers. Journals are beginning to support web posting of comments on their published articles and independent organizations are providing centralized web sites for posting comments about any published article. The trend promises to give one and all access to read and contribute to cutting edge scientific criticism and debate.

HIV regulation of the IL-7R: a viral mechanism for enhancing HIV-1 replication in human macrophages in vitro.

We report a novel mechanism, involving up-regulation of the interleukin (IL)-7 cytokine receptor, by which human immunodeficiency virus (HIV) enhances its own production in monocyte-derived macrophages (MDM) in vitro. HIV-1 infection or treatment of MDM cultures with exogenous HIV-1 Tat(86) protein up-regulates the IL-7 receptor (IL-7R) alpha-chain at the levels of steady-state RNA, protein, and functional IL-7R on the cell surface (as measured by ligand-induced receptor signaling). This IL-7R up-regulation is associated with increased amounts of HIV-1 virions in the supernatants of infected MDM cultures treated with exogenous IL-7 cytokine.

Monocytes-macrophages are a potential target in human infection with West Nile virus through blood transfusion.

Background: West Nile virus (WNV) transmission by transfusion was documented in 2002. Approximately 80 percent of WNV infections are asymptomatic and 1 percent develop severe neurological illness. In animals, Langerhans-dendritic cells support initial viral replication, followed by replication in lymphoid tissues and dissemination to organs and possibly to the CNS.

Human immunodeficiency virus type 1 Vpr interacts with antiapoptotic mitochondrial protein HAX-1.

Human immunodeficiency virus type 1 viral protein R (Vpr) is required for viral pathogenesis and has been implicated in T-cell apoptosis through its activation of caspase 3 and caspase 9 and perturbation of mitochondrial membrane potential. To understand better Vpr-mitochondria interaction, we report here the identification of antiapoptotic mitochondrial protein HAX-1 as a novel Vpr target. We show that Vpr and HAX-1 physically associate with each other.

Within you, without you: HIV-1 Rev and RNA export.

Nucleo-cytoplasmic transport of RNA is one of many cellular pathways whose illumination has progressed hand in hand with understanding of retroviral mechanisms. A recent paper in Cell reports the involvement of an RNA helicase in the pathway by which HIV exports partially spliced and unspliced RNA out of the nucleus. This suggests the ubiquity of RNA helicases in RNA export from the nucleus, and has novel mechanistic implications.

Polyarginine inhibits gp160 processing by furin and suppresses productive human immunodeficiency virus type 1 infection.

Correct endoproteolytic maturation of gp160 is essential for the infectivity of human immunodeficiency virus type 1. This processing of human immunodeficiency virus-1 envelope protein, gp160, into gp120 and gp41 has been attributed to the activity of the cellular subtilisin-like proprotein convertase furin. The prototypic furin recognition cleavage site is Arg-X-Arg/Lys-Arg.

Bcl-2 upregulation by HIV-1 Tat during infection of primary human macrophages in culture.

The ability of cells of the human monocyte/macrophage lineage to host HIV-1 replication while resisting cell death is believed to significantly contribute to their ability to serve as a reservoir for viral replication in the host. Although macrophages are generally resistant to apoptosis, interruption of anti-apoptotic pathways can render them susceptible to apoptosis. Here we report that HIV-1(BAL )infection of primary human monocyte-derived macrophages (MDM) upregulates the mRNA and protein levels of the anti-apoptic gene, Bcl-2.