1,721,063 research outputs found
Cell-to-cell vs. cell-free HIV-1 transmission from macrophages to CD4(+) T lymphocytes: lessons from the virology textbook
No full text
THE EFFECT OF CYTOKINES AND PHARMACOLOGICAL AGENTS ON CHRONIC HIV-INFECTION
No full textThe ability of the human immunodeficiency virus (HIV) to replicate in CD4+ T lymphocytes and mononuclear phagocytes(MP) is strongly influenced by immunoregulatory cytokines. In the T cell system, interleukin-2 (IL-2) provides a mitogenic signal leading to both cell proliferation and virus replication. Among other HIV-inductive cytokines, only tumor necrosis factor-alpha or -beta (TNF-alpha/-beta) have been shown thus far to trigger virus expression both in T cells and MP. The mechanism of action of TNF involves the activation of the cellular transcription factor NF-kB which binds to specific consensus sequences present in the enhancer region of the HIV proviral LTR. In addition, several other cytokines (including colony stimulating factors, IL-1, IL-3, and IL-6) have demonstrated upregulatory effects on HIV production in MP, whereas nonimmune interferons (INF-alpha/-beta) have been shown to suppress HIV replication in T cells and MP by acting at different phases in the virus life cycle. Finally, cytokines such as TGF-beta, IFN-gamma, and IL-4 have demonstrated either upregulatory or suppressive effects on virus expression depending on the experimental conditions. This scenario indicates that HIV expression is under the control of a complex network of immunoregulatory cytokines, in addition to its own endogenous regulatory proteins, suggesting that new pharmacologic strategies may be aimed at either mimicking or interrupting cytokine-dependent virus expression. In this regard, a number of different physiologic and pharmacologic agents capable of interfering with cytokine-mediated events, including glucocorticoids, anti-oxidants, such as N-Acetyl-L-Cysteine (NAC), and retinoic acid (RA) have already been shown to profoundly affect HIV replication in vitro
Novel factors interfering with human immunodeficiency virus-type 1 replication in vivo and in vitro
No full textEditorial: New frontiers in HIV antiretroviral treatment: from the management of metabolic complications and chronic inflammation to new long-acting regimens
Full text linkPertussis toxin (PTX) and its non-toxic Derivatives as vaccine adjuvant and microbicides
No full textALPHA-INTERFERON SUPPRESSES VIRION BUT NOT SOLUBLE HUMAN-IMMUNODEFICIENCY-VIRUS ANTIGEN PRODUCTION IN CHRONICALLY INFECTED T-LYMPHOCYTIC CELLS
No full textAlpha interferon (IFN-alpha) is effective in preventing the release of human immunodeficiency virus (HIV) from chronically infected T-lymphocytic (ACH-2) and promonocytic (U1) cell lines stimulated with the phorbol ester phorbol-12-myristate-13 acetate (PMA). In the present study, we observed that together with particle production, shedding of HIV antigen (p24gag) occurs in the T-cell line ACH-2 both constitutively and after stimulation with PMA. IFN-alpha, although effective in suppressing the release of HIV particles, did not inhibit shedding of p24gag into the culture supernatants of either unstimulated or PMA-stimulated cells. These observations may be of relevance in the evaluation of the in vivo efficacy of IFN-alpha-treatment of HIV-infected individuals as determined by levels of p24 antigen in plasma
The nef gene of human immunodeficiency virus type-1 (HIV1) is required for optimal virus replication in fully activated primary T lymphocytes
No full textIL-10 SYNERGIZES WITH MULTIPLE CYTOKINES IN ENHANCING HIV PRODUCTION IN CELLS OF MONOCYTIC LINEAGE
No full textSeveral cytokines, whose expression is increased in human immunodeficiency virus (HIV)-infected individuals, can enhance virus replication in CD4(+) T lymphocytes and mononuclear phagocytes (MP). We have previously reported that interleukin (IL)-10 inhibited HIV replication in acutely infected monocyte-derived macrophages (MDM) at concentrations that completely blocked the production of endogenous tumor necrosis factor-alpha (TNF-alpha) and IL-6 from infected cells. In the present study, lower concentrations of IL-10, which were unable to completely suppress endogenous cytokines, paradoxically enhanced HIV replication in MDM induced by other cytokines. This synergistic induction of HIV expression by IL-10 in combination with TNF-alpha, IL-6, and other cytokines was also observed in the chronically infected promonocytic cell line, U1. The enhancing effect of IL-10 was correlated with an increase in HIV mRNA accumulation and potentiation of phorbol ester-induced long terminal repeat-driven transcription that was independent of the NF-kappa B and Spl transcription factors. Thus, IL-10 is a cytokine capable of exerting complex regulatory effects on HIV expression in MP as a function of its own concentration and of the presence of other HIV regulatory cytokines
- …
