HIV replication can be blocked by recombinant human interferon beta

Michaelis, Barbara; Levy, Jay A.

doi:10.1097/00002030-198901000-00006

Cited by 21 publications

(16 citation statements)

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“…Efforts have been made to identify and characterize the anti-HIV tymphokine produced by CD8ĉ ells. None of a panel of known lymphokines tested inhibited HIV replication in vitro in a manner consistent with that of the CD8^ cell-produced factor [29][30][31][32]. These findings suggest that this activity is mediated by a novel cytokine.…”

Section: Introductionmentioning

confidence: 84%

Inhibition of HIV replication by CD8+ T cells correlates with CD4 counts and clinical stage of disease

Gómez

Smaill

Rosenthal

1994

Clinical and Experimental Immunology

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SUMMARY We sought to evaluate the relationship of CD8+ T cell‐mediated inhibition of autologous HIV replication in vitro to disease stage in HIV+ individuals. Depletion of CD8+ T cells from peripheral blood lymphocytes of 16 HIV+ subjects increased the percentage of virus‐producing cultures from 56% to 81%. CD4+ T cells were purified from 52 HIV+ individuals and cultured alone or in the presence of autologous CD8+ T cells. In 13 (25%) subjects HIV replication was only detected in the absence of CD8+ T cells (inhibition positive); in 26 (50%) viral replication occurred both in the absence and presence of CD8+ cells (inhibition negative). In the remaining 13 (25%) subjects, CD8+ T cell‐mediated inhibitory activity could not be evaluated because stimulation of their purified CD4+ T cells did not result in p24 production. In some virus culture‐negative individuals, the inability to demonstrate HIV replication was due to the presence of low numbers of CD8+ T cells that co‐purified with CD4+ T cells. Detection of inhibitory CD8+ T cells was associated with significantly higher CD4 counts and better clinical status compared with inhibition‐negative subjects. These results demonstrate that CD8+ T cell‐mediated inhibition of HIV replication correlates with disease stage, and thus may play a role in preventing disease progression. CD8+ T cells did not inhibit autologous HIV replication across a semipermeable membrane. Further, the ability of CD8+ T cells to prevent HIV replication did not correlate with lysis of autologous CD4+ T cells. Thus, CD8+ T cells inhibited autologous HIV replication in vitro through a contact mediated non‐lytic mechanism.

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Section: Introductionmentioning

confidence: 84%

Inhibition of HIV replication by CD8+ T cells correlates with CD4 counts and clinical stage of disease

Gómez

Smaill

Rosenthal

1994

Clinical and Experimental Immunology

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“…Type I IFNs are known to contribute to HIV control by increasing the IFN‐γ secreting ability of CD4+ T cells (59, 60). Recombinant human IFN‐β and IFN‐α are effective in suppressing HIV (61). One study suggests a therapeutic role for PEG‐IFN in primary HIV infection when the numbers of IFN‐α producing‐pDC start to decline (62, 63).…”

Section: Plasmacytoid Dendritic Cellsmentioning

confidence: 99%

Recent advances targeting innate immunity‐mediated therapies against HIV‐1 infection

Shankar

Velu

Vignesh

et al. 2012

Microbiology and Immunology

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Early defence mechanisms of innate immunity respond rapidly to infection against HIV‐1 in the genital mucosa. Additionally, innate immunity optimises effective adaptive immune responses against persistent HIV infection. Recent research has highlighted the intrinsic roles of apolipoprotein B mRNA‐editing, enzyme‐catalytic, polypeptide‐like 3G, tripartite motif‐containing protein 5, tetherin, sterile α‐motif and histidine/aspartic acid domain‐containing protein 1 in restricting HIV‐1 replication. Likewise, certain endogenously secreted antimicrobial peptides, namely α/β/θ‐defensins, lactoferrins, secretory leukocyte protease inhibitor, trappin‐2/elafin and macrophage inflammatory protein‐3α are reportedly protective. Whilst certain factors directly inhibit HIV, others can be permissive. Interferon‐λ3 exerts an anti‐HIV function by activating Janus kinase‐signal transducer and activator of transcription‐mediated innate responses. Morphine has been found to impair intracellular innate immunity, contributing to HIV establishment in macrophages. Interestingly, protegrin‐1 could be used therapeutically to inhibit early HIV‐1 establishment. Moreover, chloroquine inhibits plasmacytoid dendritic cell activation and improves effective T‐cell responses. This minireview summarizes the recently identified targets for innate immunity‐mediated therapies and outlines the challenges that lie ahead in improving treatment of HIV infection.

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“…In this context, cytokines produced in response to a variety of stimuli, including viral and bacterial infections, have been considered to play important roles in the clinical progression of AIDS (38). Some cytokines, such as tumor necrosis factor (TNF), interleukin 1 (IL-1), and colony-stimulating factors, have been shown to enhance HIV expression in different cell systems (reviewed in reference 38), whereas other cytokines, such as interferons (IFNs) have been reported to exhibit some anti-HIV activity in vitro (3,30,36). In particular, it has been found that TNF-a is capable of increasing viral production in activated macrophages, possibly through the action of the NF-KB protein (18).…”

Section: )mentioning

confidence: 99%

Increased human immunodeficiency virus (HIV) expression in chronically infected U937 cells upon in vitro differentiation by hydroxyvitamin D3: roles of interferon and tumor necrosis factor in regulation of HIV production

Locardi

Petrini

Boccoli

et al. 1990

J Virol

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We have investigated the roles of cytokines in the modulation of human immunodeficiency virus (HIV) production in chronically infected U937 cells upon in vitro differentiation by hydroxyvitamin D3. HIV-infected U937 cells exhibited markedly lower levels of CD4 and HLA-DR antigens than uninfected cells did. Vitamin D3 induced a time-dependent macrophagelike differentiation, as determined by monitoring the expression of some surface antigens by means of the monoclonal antibodies OKM1, OKM5, OKM13, OKM14, OKT4, anti-HLA-DR, TecMG2, TecMG3, LeuM3, LeuMl, anti-HLA-DP, and anti-HLA-DQ. Treatment with hydroxyvitamin D3 resulted in a marked increase in HIV production compared with control cultures. Interleukin 1I (IL-1fi) and tumor necrosis factor a (TNF-a) were detected in the culture media, whereas interferon (IFN) was not generally found. Using the polymerase chain reaction technique, we found HIV-infected U937 cells to express detectable levels of mRNAs for alpha interferon (IFN-a), IFN-0, TNF-ax, and IL-1,. The addition of TNF resulted in a marked increase of HIV production, whereas IL-1p was ineffective. In contrast, both IFN-ot and IFN-,(exerted some inhibitory effect on HIV production, which was more marked in vitamin D3-treated cultures than in untreated cultures. HIV production was significantly increased by antibodies to IFN-ot in both untreated and vitamin D3-treated cultures. Anti-IFN-0 antibody increased HIV production only in vitamin D3-treated cells. In contrast, anti-TNF-ot antibodies markedly decreased HIV production in both control and differentiating U937 cells. Vitamin D3 treatment resulted in a higher expression of TNF receptors in differentiating cells than in control HIV-infected cells. These data demonstrate a strong correlation between HIV production and macrophagelike differentiation in chronically infected U937 cells and suggest that endogenous IFN and TNF exert opposite effects in the regulation of virus production in both undifferentiated and vitamin D3-treated cell cultures. Many experimental and clinical data indicate that macrophages play a crucial role in the pathogenesis of acquired immunodeficiency syndrome (AIDS) (reviewed in reference

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HIV replication can be blocked by recombinant human interferon beta

Cited by 21 publications

References 0 publications

Inhibition of HIV replication by CD8+ T cells correlates with CD4 counts and clinical stage of disease

Inhibition of HIV replication by CD8+ T cells correlates with CD4 counts and clinical stage of disease

Recent advances targeting innate immunity‐mediated therapies against HIV‐1 infection

Increased human immunodeficiency virus (HIV) expression in chronically infected U937 cells upon in vitro differentiation by hydroxyvitamin D3: roles of interferon and tumor necrosis factor in regulation of HIV production

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