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

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...

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Published inJournal of Immunology Research Vol. 2021; pp. 1 - 13
Main Authors Lv, Tingxia, Cao, Wei, Li, Taisheng
Format Journal Article
LanguageEnglish
Published Egypt Hindawi 2021
John Wiley & Sons, Inc
Wiley
Subjects
Acquired immune deficiency syndrome
AIDS
Anti-inflammatory agents
Antiretroviral drugs
Antiretroviral therapy
Antiretroviral Therapy, Highly Active - methods
Antiviral agents
Biomarkers
Cardiovascular disease
CD4 antigen
CD4-Positive T-Lymphocytes - drug effects
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - virology
CD8-Positive T-Lymphocytes - drug effects
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - virology
Clinical trials
Cytokines
Cytomegalovirus
Development and progression
Drug therapy
Health aspects
Highly active antiretroviral therapy
HIV
HIV (Viruses)
HIV infection
HIV Infections - drug therapy
HIV Infections - immunology
HIV Infections - virology
HIV-1 - drug effects
HIV-1 - immunology
HIV-1 - physiology
Human immunodeficiency virus
Humans
Immunology
Infections
Inflammation
Inflammation - immunology
Inflammation - prevention & control
Inflammation - virology
Interferon
Lymphocyte Activation - drug effects
Lymphocyte Activation - immunology
Lymphocyte Count
Lymphocytes
Lymphocytes T
Pattern recognition
Proteins
Review
T cells
Virus Replication - drug effects
Virus Replication - immunology
Viruses
China
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Abstract 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.
AbstractList 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.
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.
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[sup.+] 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.
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.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.
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.
Audience Academic
Author Lv, Tingxia
Cao, Wei
Li, Taisheng
AuthorAffiliation 4 Tsinghua-Peking Center for Life Sciences, Beijing 100084, China
2 Department of Infectious Diseases, Beijing Friendship Hospital, Capital Medical University, Beijing, China
3 Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China
1 Department of Infectious Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China
AuthorAffiliation_xml – name: 3 Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China
– name: 1 Department of Infectious Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China
– name: 4 Tsinghua-Peking Center for Life Sciences, Beijing 100084, China
– name: 2 Department of Infectious Diseases, Beijing Friendship Hospital, Capital Medical University, Beijing, China
Author_xml – sequence: 1
  givenname: Tingxia
  orcidid: 0000-0003-1327-8119
  surname: Lv
  fullname: Lv, Tingxia
  organization: Department of Infectious DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences & Peking Union Medical CollegeBeijing 100730Chinapumch.cn
– sequence: 2
  givenname: Wei
  surname: Cao
  fullname: Cao, Wei
  organization: Department of Infectious DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences & Peking Union Medical CollegeBeijing 100730Chinapumch.cn
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  givenname: Taisheng
  orcidid: 0000-0002-7050-5675
  surname: Li
  fullname: Li, Taisheng
  organization: Department of Infectious DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences & Peking Union Medical CollegeBeijing 100730Chinapumch.cn
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34631899$$D View this record in MEDLINE/PubMed
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COPYRIGHT 2021 John Wiley & Sons, Inc.
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– notice: Copyright © 2021 Tingxia Lv et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0
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Snippet Although antiretroviral therapy effectively controls human immunodeficiency virus (HIV) replication, a residual chronic immune activation/inflammation persists...
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SubjectTerms Acquired immune deficiency syndrome
AIDS
Anti-inflammatory agents
Antiretroviral drugs
Antiretroviral therapy
Antiretroviral Therapy, Highly Active - methods
Antiviral agents
Biomarkers
Cardiovascular disease
CD4 antigen
CD4-Positive T-Lymphocytes - drug effects
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - virology
CD8-Positive T-Lymphocytes - drug effects
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - virology
Clinical trials
Cytokines
Cytomegalovirus
Development and progression
Drug therapy
Health aspects
Highly active antiretroviral therapy
HIV
HIV (Viruses)
HIV infection
HIV Infections - drug therapy
HIV Infections - immunology
HIV Infections - virology
HIV-1 - drug effects
HIV-1 - immunology
HIV-1 - physiology
Human immunodeficiency virus
Humans
Immunology
Infections
Inflammation
Inflammation - immunology
Inflammation - prevention & control
Inflammation - virology
Interferon
Lymphocyte Activation - drug effects
Lymphocyte Activation - immunology
Lymphocyte Count
Lymphocytes
Lymphocytes T
Pattern recognition
Proteins
Review
T cells
Virus Replication - drug effects
Virus Replication - immunology
Viruses
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Title HIV-Related Immune Activation and Inflammation: Current Understanding and Strategies
URI https://dx.doi.org/10.1155/2021/7316456
https://www.ncbi.nlm.nih.gov/pubmed/34631899
https://www.proquest.com/docview/2580585545
https://www.proquest.com/docview/2580959768
https://pubmed.ncbi.nlm.nih.gov/PMC8494587
https://doaj.org/article/455d4bb3a58640e1a5cdd595600d5a8f
Volume 2021
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