scholarly journals Mucosal and Systemic Immune Activation Is Present in Human Immunodeficiency Virus–Exposed Seronegative Women

2000 ◽  
Vol 182 (5) ◽  
pp. 1365-1374 ◽  
Author(s):  
Mara Biasin ◽  
Sergio Lo Caputo ◽  
Livianna Speciale ◽  
Fulvia Colombo ◽  
Luigi Racioppi ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune Activation ◽  
Systemic Immune Activation ◽  
Immunodeficiency Virus

scholarly journals HIV-Related Immune Activation and Inflammation: Current Understanding and Strategies

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Tingxia Lv ◽  
Wei Cao ◽  
Taisheng Li
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune Activation ◽  
Driving Forces ◽  
Intervention Strategy ◽  
Clinical Intervention ◽  
Cd4 T Cell ◽  
Chronic Immune Activation ◽  
Hiv Replication ◽  
Systemic Immune Activation ◽  
Immunodeficiency Virus

Although antiretroviral therapy effectively controls human immunodeficiency virus (HIV) replication, a residual chronic immune activation/inflammation persists throughout the disease. This aberrant immune activation and inflammation are considered an accelerator of non-AIDS-related events and one of the driving forces of CD4+ T cell depletion. Unfortunately, HIV-associated immune activation is driven by various factors, while the mechanism of excessive inflammation has not been formally clarified. To date, several clinical interventions or treatment candidates undergoing clinical trials have been proposed to combat this systemic immune activation/inflammation. However, these strategies revealed limited results, or their nonspecific anti-inflammatory properties are similar to previous interventions. Here, we reviewed recent learnings of immune activation and persisting inflammation associated with HIV infection, as well as the current directions to overcome it. Of note, a more profound understanding of the specific mechanisms for aberrant inflammation is still imperative for identifying an effective clinical intervention strategy.

scholarly journals Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection

Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
Mahmoud Mohammad Yaseen ◽  
Nizar Mohammad Abuharfeil ◽  
Homa Darmani
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Hiv Infection ◽  
Immune Activation ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Chronic Immune Activation ◽  
Immune Suppressor Cells ◽  
Immunodeficiency Virus ◽  
Immune Suppressor

There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.

scholarly journals Differential Plasma Protein Regulation and Statin Effects in Human Immunodeficiency Virus (HIV)-Infected and Non-HIV-Infected Patients Utilizing a Proteomics Approach

2020 ◽  
Vol 222 (6) ◽  
pp. 929-939 ◽  
Author(s):  
Chris deFilippi ◽  
Mabel Toribio ◽  
Lai Ping Wong ◽  
Ruslan Sadreyev ◽  
Ida Grundberg ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Human Immunodeficiency Virus ◽  
Endothelial Function ◽  
Immune Activation ◽  
Atherosclerotic Cardiovascular Disease ◽  
Type I ◽  
Integrin Subunit ◽  
Central Adiposity ◽  
Proteomic Approach ◽  
Immunodeficiency Virus

Abstract Background People with human immunodeficiency virus (PWH) demonstrate increased atherosclerotic cardiovascular disease (ASCVD). Statins are being studied to prevent ASCVD in human immunodeficiency virus (HIV), but little is known regarding the effects of statins on a broad range of inflammatory and cardiovascular proteins in this population. Methods We used a highly specific discovery proteomic approach (Protein Extension Assay), to determine statin effects on over 350 plasma proteins in relevant ASCVD pathways among HIV and non-HIV groups. Responses to pitavastatin calcium were assessed in 89 PWH in the INTREPID trial and 46 non-HIV participants with features of central adiposity and insulin resistance. History of cardiovascular disease was exclusionary for both studies. Results Among participants with HIV, PCOLCE (enzymatic cleavage of type I procollagen) significantly increased after pitavastatin therapy and PLA2G7 (systemic marker of arterial inflammation) decreased. Among participants without HIV, integrin subunit alpha M (integrin adhesive function) and defensin alpha-1 (neutrophil function) increased after pitavastatin therapy and PLA2G7 decreased. At baseline, comparing participants with and without HIV, differentially expressed proteins included proteins involved in platelet and endothelial function and immune activation. Conclusions Pitavastatin affected proteins important to platelet and endothelial function and immune activation, and effects differed to a degree within PWH and participants without HIV.

Cellular immune activation in the brain and human immunodeficiency virus infection

1988 ◽  
Vol 24 (2) ◽  
pp. 289-289 ◽  
Author(s):  
Dietmarch Fuchs ◽  
Ernst R. Werner ◽  
Manfred P. Dierich ◽  
Helmut Wachter
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
Immune Activation ◽  
Immunodeficiency Virus ◽  
Cellular Immune ◽  
The Brain

scholarly journals Chronic Immune Activation Associated with Chronic Helminthic and Human Immunodeficiency Virus Infections: Role of Hyporesponsiveness and Anergy

2004 ◽  
Vol 17 (4) ◽  
pp. 1012-1030 ◽  
Author(s):  
Gadi Borkow ◽  
Zvi Bentwich
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Immune Activation ◽  
Current Knowledge ◽  
Human Populations ◽  
Chronic Immune Activation ◽  
Virus Infections ◽  
Chronic Infections ◽  
Helminth Infections ◽  
Immunodeficiency Virus

SUMMARY Chronic immune activation is one of the hallmarks of human immunodeficiency virus (HIV) infection. It is present also, with very similar characteristics, in very large human populations infested with helminthic infections. We have tried to review the studies addressing the changes in the immune profiles and responses of hosts infected with either one of these two chronic infections. Not surprisingly, several of the immune derangements and impairments seen in HIV infection, and considered by many to be the “specific” effects of HIV, can be found in helminth-infected but HIV-noninfected individuals and can thus be accounted for by the chronic immune activation itself. A less appreciated element in chronic immune activation is the immune suppression and anergy which it may generate. Both HIV and helminth infections represent this aspect in a very wide and illustrative way. Different degrees of anergy and immune hyporesponsiveness are present in these infections and probably have far-reaching effects on the ability of the host to cope with these and other infections. Furthermore, they may have important practical implications, especially with regard to protective vaccinations against AIDS, for populations chronically infected with helminths and therefore widely anergic. The current knowledge of the mechanisms responsible for the generation of anergy by chronic immune activation is thoroughly reviewed.

scholarly journals Lymphatic Tissue Fibrosis Is Associated with Reduced Numbers of Naïve CD4+ T Cells in Human Immunodeficiency Virus Type 1 Infection

2006 ◽  
Vol 13 (5) ◽  
pp. 556-560 ◽  
Author(s):  
Timothy W. Schacker ◽  
Jason M. Brenchley ◽  
Gregory J. Beilman ◽  
Cavan Reilly ◽  
Stefan E. Pambuccian ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immune Activation ◽  
Cellular Interactions ◽  
Collagen Deposition ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The organized structure of lymphatic tissues (LTs) constitutes a microenvironment referred to as a niche that plays a critical role in immune system homeostasis by promoting cellular interactions and providing access to cytokines and growth factors on which cells are dependent for survival, proliferation, and differentiation. In chronic human immunodeficiency virus type 1 (HIV-1) infection, immune activation and inflammation result in collagen deposition and disruption of this LT niche. We have previously shown that these fibrotic changes correlate with a reduction in the size of the total population of CD4+ T cells. We now show that this reduction is most substantial within the naïve CD4+ T-cell population and is in proportion to the extent of LT collagen deposition in HIV-1 infection. Thus, the previously documented depletion of naïve CD4+ T cells in LTs in HIV-1 infection may be a consequence not only of a decreased supply of thymic emigrants or chronic immune activation but also of the decreased ability of those cells to survive in a scarred LT niche. We speculate that LT collagen deposition might therefore limit repopulation of naïve CD4+ T cells with highly active antiretroviral therapy, and thus, additional treatments directed to limiting or reversing inflammatory damage to the LT niche could potentially improve immune reconstitution.

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