Increased Mycobacterium tuberculosis growth in HIV-1-infected human macrophages: role of tumour necrosis factor-alpha.

Synergism between Mycobacterium tuberculosis (M. tuberculosis) and HIV-1 infections was demonstrated in several in vitro models and clinical studies. Here, we investigated their reciprocal effects on growth in chronically HIV-1-infected promonocytic U1 cells and in acutely infected monocyte-derived macrophages (MDM).

Alpha-melanocyte-stimulating hormone peptides inhibit HIV-1 expression in chronically infected promonocytic U1 cells and in acutely infected monocytes.

The purpose of the present research was to determine if alpha-melanocyte-stimulating hormone (alpha-MSH) and its C-terminal tripeptide [alpha-MSH (11-13), KPV] alter HIV expression in infected cells. The results indicate that chronically HIV-1-infected promonocytic U1 cells produce alpha-MSH and that immunoneutralization of the endogenous peptide enhances HIV expression. Because U1 cells express the alpha-MSH receptor 1 (MC1R), an autocrine-inhibitory circuit based on the peptide and its receptor likely occurs in these cells.

The thalidomide analogue CC-3052 inhibits HIV-1 and tumour necrosis factor-alpha (TNF-alpha) expression in acutely and chronically infected cells in vitro.

We investigated the in vitro effect of the water-soluble, highly stable thalidomide analogue CC-3052 on HIV-1 expression and TNF-alpha production in latently infected promonocytic U1 cells, acutely infected T cells and monocyte-derived human macrophages (MDM), and in mitogen-stimulated ex vivo cultures from patients with primary acute HIV-1 infection. HIV-1 expression was assessed by Northern blot analysis of RNAs, and ELISA for p24 antigen release and reverse transcriptase (RT) activity. TNF-alpha expression was evaluated by RT-polymerase chain reaction (PCR)-ELISA for mRNA and ELISA for protein secretion.

Soluble CD30, tumour necrosis factor (TNF)-alpha, and TNF receptors in primary HIV-1 infection: relationship with HIV-1, RNA, clinical outcome and early antiviral therapy.

The natural course of human immunodeficiency type 1 (HIV-1) infection varies considerably. The identification of laboratory disease markers has become critically important to patient management. This study, carried out on 37 patients with primary HIV-1 infection (PHI), shows that, along with plasma HIV-1 RNA and CD4+ T cell counts, evaluation of plasma levels of some immune activation markers (sCD30, TNF-alpha, and sTNFR-I) may help to identify patients at risk of a more rapid disease progression, suggesting that immune activation is among the factors who determine the rate of disease progression.

omega-Conotoxin GVIA binds to and blocks rat neuromuscular junction.

The effect of omega-conotoxin GVIA, a specific blocker of N-type calcium channels, on the synaptic transmission at the mammalian neuromuscular junction is controversial. We have found that 125I-omega-conotoxin binds to rat tibialis muscle end-plate; that omega-conotoxin blocks the neuromuscular transmission both in vivo, in the sciatic nerve-tibialis anterior muscle, and in vitro in the isolated phrenic nerve-diaphragm preparation; and does not affect muscle nicotinic receptors. We conclude that in rat neuromuscular junctions N-type calcium channels are important for neurotransmitter secretion.