IL-16 anti-HIV-1 therapy

Viglianti, Gregory A.; Parada, Nereida A.; Maciaszek, Joseph Walter; Kornfeld, Hardy; Center, David M.; Cruikshank, William W.

doi:10.1038/nm0997-938

Cited by 11 publications

(7 citation statements)

References 3 publications

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“…Under the conditions used, normal cell growth and the percentage of viable cells throughout the 2-week culture period were found to be identical in the absence or the presence of IL-16. Similar observations on the lack of rIL-16-mediated toxicity have been previously reported, and even an increase in cell number was observed in long-term cultures (4-6 weeks) maintained in the presence of IL-16 and IL-2 [25]. Based on these latter findings, an argument was made to suggest a potential therapeutic benefit of the administration of rIL-16 to HIV-infected subjects.…”

Section: Discussionsupporting

confidence: 84%

“…This discordance between natural IL-16 serum levels and the virus-suppressive concentration of rIL-16 in vitro may also be explained by the possibility that circulating cytokine levels do not necessarily reflect the actual local levels released in major sites for viral replication, which are the lymphoid tissues. Nevertheless, with the recombinant cytokine presenting potent HIV-suppressive effects, protective activity against apoptosis of infected lymphocytes [4], and enhanced CD4 cell expansion when associated with IL-2 [25,39], it would seem highly valid to evaluate the therapeutic potential of rIL-16 in HIV disease.…”

Section: Discussionmentioning

confidence: 99%

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Interleukin‐16 (IL‐16) Inhibits Human Immunodeficiency Virus Replication in Cells from Infected Subjects, and Serum IL‐16 Levels Drop with Disease Progression

et al. 1999

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The role of recombinant interleukin-16 (rIL-16) in regulating human immunodeficiency virus type 1 (HIV-1) replication in endogenously infected cells has been investigated. Cultures of CD8 cell-depleted mitogen-activated lymphocytes from 22 of 26 HIV-1-infected subjects presented variable levels of secreted p24 antigen. The presence of rIL-16 throughout the 14-day culture period dramatically inhibited p24 release into the culture supernatants. This effect was found to be mediated through inhibition of viral transcription but to be independent of the induced levels of other cytokines or chemokines known to regulate viral replication. Analysis of serum samples from HIV-1-infected subjects over a period of 8 years showed maintained or even increased IL-16 levels during the whole asymptomatic phase and a significant drop on progression to disease. These results strongly support a potential therapeutic value of rIL-16 in HIV-1 infection and the use of serum IL-16 levels to monitor disease progression.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Interleukin‐16 (IL‐16) Inhibits Human Immunodeficiency Virus Replication in Cells from Infected Subjects, and Serum IL‐16 Levels Drop with Disease Progression

et al. 1999

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“…It has been reported that IL-16 derived from the AGM, which is a soluble factor produced by CD8 cells, has the effect of suppressing HIV replication in activated human CD4 cells [42]. Human IL-16 also suppresses HIV replication [43,44] and acts as a growth factor speci®c for CD4 cells in cooperation with IL-2 [45,46]. A new ®eld of AIDS therapy has clearly been opened up by IL-16.…”

Section: Discussionmentioning

confidence: 99%

An African green monkey lacking peripheral CD4 lymphocytes that retains helper T cell activity and coexists with SIVagm

Murayama

Mukai

Inoue‐Murayama

et al. 1999

Clinical and Experimental Immunology

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Natural infection with simian immunodeficiency virus (SIV) is known to occur in the African green monkey (AGM). The actual onset of the disease has not been recognized in SIVagm infected AGM, and the precise reason for such apathogenicity in the AGM remains unclear. We reported previously that AGM peripheral CD4 lymphocytes underwent a peculiar differentiation from CD4+ to CD4- cells after in vitro activation, and we inferred that the AGM does not fall into a fatal immunodeficient state because of the generation of CD4- helper T cells in vivo. To evaluate this possibility, we examined the relationship between CD4 expression and helper T cell activity in the naturally infected AGM. We identified a healthy monkey almost lacking CD4 T cells in the periphery. This AGM showed no signs and symptoms of immunodeficiency and retained a helper T cell activity in antibody production comparable to those of CD4+ AGMs. In addition, SIVagm could be isolated from CD8+ lymphocytes in the CD4- AGM. These observations suggest that a unique host-virus adaptation has developed in the AGM, and may be helpful in explaining the fundamental reason for the apathogenicity occurring in this monkey.

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“…In contrast, IL-15 stimulation of NK cells has resulted in a much more substantial release of these chemokines up to levels effective in suppressing R5 HIV infection [230,231]. unlike anti-CD4 Ab, chemokines and other agents, its antiviral activity does not affect viral entry, but mostly occurs at the transcriptional level, at least in T cells [244][245][246]. Thus, IL-16 resembles the HIV suppressive effects observed when cells were exposed to certain anti-CD4 Ab directed against the CD3 region [247].…”

Section: Il-15mentioning

confidence: 99%

Cytokine and Chemokine Based Control of HIV Infection and Replication

Alfano

Poli

2001

CPD

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HIV infects and propagates into CD4+ T lymphocytes and macrophages, although many other cell types play an important role in virus spreading and pathogenesis. In addition to regulatory viral proteins, the cytokine network has early been implicated as a major controller of the plastic capacity of HIV to spread productively or rather remain silently integrated in the chromosomes of infected cells. The recent discovery of CCR5 and CXCR4 as essential entry co-receptors together with CD4 has highlighted a novel and potentially important step in the pharmacological hunt for more effective antiviral agents. In addition to regulate HIV expression and replication, several cytokines have demonstrated the capacity of up- or down-modulating chemokine receptors including CCR5 and CXCR4 with the consequence of influencing the susceptibility of T cells and macrophages to HIV infection. Pharmacological agents such as pertussis toxin B-oligomer have demonstrated HIV suppressive effects via non competitive binding of CCR5, whereas interferons or interleukin-16 (IL-16) can prevent post-entry steps in HIV expression. At the clinical level, several cytokines or their receptors are useful markers for monitoring disease progression and its consequence on the immune system. Cytokine-based therapy represents a realistic complementary approach to traditional antiretroviral therapy potentially capable of restoring important adaptive or innate immune functions ultimately curtailing HIV spreading and its consequences on the immune system, as exemplified by the experimental clinical use of IL-2.

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IL-16 anti-HIV-1 therapy

Cited by 11 publications

References 3 publications

Interleukin‐16 (IL‐16) Inhibits Human Immunodeficiency Virus Replication in Cells from Infected Subjects, and Serum IL‐16 Levels Drop with Disease Progression

Interleukin‐16 (IL‐16) Inhibits Human Immunodeficiency Virus Replication in Cells from Infected Subjects, and Serum IL‐16 Levels Drop with Disease Progression

An African green monkey lacking peripheral CD4 lymphocytes that retains helper T cell activity and coexists with SIVagm

Cytokine and Chemokine Based Control of HIV Infection and Replication

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