COMPLEX EFFECTS OF INTERFERON-α ON THE CYTOKINE NETWORK IN HIV INFECTION—POSSIBLE CONTRIBUTION TO IMMUNOSUPPRESSION

Cytokine ◽  
2001 ◽  
Vol 14 (1) ◽  
pp. 56-62 ◽  
Author(s):  
Eva Stylianou ◽  
Pål Aukrust ◽  
Fredrik Müller ◽  
Ingvild Nordøy ◽  
Stig S. Frøland
Keyword(s):  
Hiv Infection ◽  
Interferon Α ◽  
Cytokine Network

The Cytokine Network in HIV Infection

2002 ◽  
Vol 2 (8) ◽  
pp. 677-689 ◽  
Author(s):  
M. Alfano ◽  
G. Poli
Keyword(s):  
Hiv Infection ◽  
Cytokine Network

scholarly journals HIV infection does not alter interferon α/β receptor 2 expression on mucosal immune cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. e0218905 ◽  
Author(s):  
Julia Ickler ◽  
Sandra Francois ◽  
Marek Widera ◽  
Mario L. Santiago ◽  
Ulf Dittmer ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Immune Cells ◽  
Interferon Α ◽  
Β Receptor

scholarly journals The breakdown of the cytokine network subsequent to human immunodeficiency virus infection

1995 ◽  
Vol 4 (5) ◽  
pp. 315-321
Author(s):  
M. Clerici ◽  
M. L. Villa ◽  
D. Trabattoni ◽  
G. M. Shearer
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Hiv Infection ◽  
Hiv Disease ◽  
Cytokine Network ◽  
Type 2 Cytokines ◽  
Immunodeficiency Virus ◽  
Hiv Seropositive

The acquired immunodeflciency syndrome (AIDS) is a clinically multifaceted disease induced by infection with the human immunodeficiency virus (HIV). HIV infection results in a complex pattern of immunologic alterations that leads to the development of AIDS in the majority of HIV seropositive (HIV+) individuals. The reduction in CD4 T lymphocyte counts is the hallmark of HIV infection; nevertheless, long before the reduction in CD4 counts reaches critical levels, a series of profound and complex defects that impair the function of CD4 T lymphocytes can be detected. Thus, HIV infection is characterized by quantitative and qualitative defects affecting CD4 T lymphocytes. It was suggested recently that programmed cell death (PCD) is an important mechanism leading to CD4 depletion in HIV infection, and that susceptibility of peripheral lymphocytes to PCD is differentially regulated by diverse cytokines. Thus, type 1 cytokines would protect CD4 lymphocytes against PCD, whereas type 2 cytokines would not protect against, and could augment, PCD. We suggest that the qualitative alterations of the immune response provoke the CD4 depletion characteristic of HIV disease via type 2 cytokinemediated augmentation of PCD, and are therefore ultimately responsible for the progression of HIV infection. Finally, we summarize recent data showing that three correlates of disease progression: emergence of HIV strains with syncitium-inducing ability (SI), type 1-to-type 2 cytokine shift, and CD4 depletion, are significantly associated, suggesting a complex interconnected virologic-immunologic pathogenesis of HIV infection.

scholarly journals Monocyte Activation from Interferon-α in HIV Infection Increases Acetylated LDL Uptake and ROS Production

2014 ◽  
Vol 34 (10) ◽  
pp. 822-828 ◽  
Author(s):  
Lynn Pulliam ◽  
Cyrus Calosing ◽  
Bing Sun ◽  
Carl Grunfeld ◽  
Hans Rempel
Keyword(s):  
Hiv Infection ◽  
Interferon Α ◽  
Ros Production ◽  
Monocyte Activation ◽  
Ldl Uptake

scholarly journals HIV disease progression correlates with the generation of dysfunctional naive CD8low T cells

Blood ◽  
2011 ◽  
Vol 117 (7) ◽  
pp. 2189-2199 ◽  
Author(s):  
David Favre ◽  
Cheryl A. Stoddart ◽  
Brinda Emu ◽  
Rebecca Hoh ◽  
Jeffrey N. Martin ◽  
...  
Keyword(s):  
T Cells ◽  
Hiv Infection ◽  
Cd8 T Cells ◽  
Mononuclear Cells ◽  
Cell Receptor ◽  
Interferon Α ◽  
Hiv Disease ◽  
Peripheral Blood Mononuclear ◽  
Class I Mhc ◽  
Mhc I

Abstract HIV infection can result in depletion of total CD4+ T cells and naive CD8+ T cells, and in the generation of dysfunctional effector CD8+ T cells. In this study, we show that naive CD8+ T cells in subjects with progressive HIV disease express low levels of CD8α and CD8β chains. Such naive CD8low T cells display broad signaling defects across the T-cell receptor complex, and their appearance correlates with generalized up-regulation of major histocompatibility complex class I (MHC-I) antigens on peripheral blood mononuclear cells (PBMCs). To explore a causal link between increased MHC-I up-regulation and the generation of naive CD8low T cells, we used the humanized SCID-hu Thy/Liv mouse model to show that HIV infection of the thymus and interferon α (IFNα) treatment alone result in MHC-I up-regulation and in the generation of dysfunctional CD3highCD8+CD4− single-positive 8 (SP8) thymocytes with low expression of CD8. We suggest that dysfunctional naive CD8low T cells are generated as a result of IFNα-mediated up-regulation of MHC-I on stromal cells in the thymus and antigen-presenting cells in the periphery, and that dysfunction in this naive compartment contributes to the immunodeficiency of HIV disease. This study is registered at www.clinicaltrials.gov as NCT00187512.

scholarly journals Interferon-α alters host glycosylation machinery during treated HIV infection

EBioMedicine ◽  
2020 ◽  
Vol 59 ◽  
pp. 102945 ◽  
Author(s):  
Leila B. Giron ◽  
Florent Colomb ◽  
Emmanouil Papasavvas ◽  
Livio Azzoni ◽  
Xiangfan Yin ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Interferon Α

scholarly journals HIV infection does not alter Interferon α/β receptor expression on mucosal immune cells

2019 ◽  
Author(s):  
Julia Ickler ◽  
Sandra Francois ◽  
Marek Widera ◽  
Mario L. Santiago ◽  
Ulf Dittmer ◽  
...  
Keyword(s):  
T Cells ◽  
Hiv Infection ◽  
Immune Cells ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Critical Role ◽  
Receptor Expression ◽  
Interferon Α ◽  
Target Cells ◽  
Type I

AbstractThe innate immune response induced by type I interferons (IFNs) play a critical role in the establishment of HIV infection. IFNs are induced early in HIV infection and trigger an antiviral defense program by signaling through the IFNa/b receptor (IFNAR), which consists of two subunits, IFNAR1 and IFNAR2. Changes in IFNAR expression in HIV target cells, as well as other immune cells, could therefore have important consequences for initial HIV spread. It was previously reported that IFNAR2 expression is increased in peripheral blood CD4+CXCR4+T cells of HIV+patients compared to HIV uninfected controls, suggesting that HIV infection may alter the IFN responsiveness of target cells. However, the earliest immune cells affected by HIVin vivoreside in the gut-associated lymphoid tissue (GALT). To date, it remains unknown if IFNAR expression is altered in GALT immune cells in the context of HIV infection and exposure to IFNs, including the 12 IFNa subtypes. Here, we analyzed the expression of surface bound and soluble IFNAR2 on Lamina propria mononuclear cells (LPMCs) isolated from the GALT of HIV−individuals and in plasma samples of HIV+patients. IFNAR2 expression varied between different T cells, B cells and natural killer cells, but was not altered following HIV infection. Furthermore, expression of the soluble IFNAR2a isoform was not changed in HIV+patients compared to healthy donors, nor in LPMCs after HIV-1 infectionex vivo. Even though the 12 human IFNα subtypes trigger different biological responses and vary in their affinity to both receptor subunits, stimulation of LPMCs with different recombinant IFNα subtypes did not result in any significant changes in IFNAR2 surface expression. Our data suggests that potential changes in the IFN responsiveness of mucosal immune cells during HIV infection is unlikely dictated by changes in IFNAR2 expression.

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