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Viruses
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Innate Immune Activation in HIV Disease
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Innate Immune Activation in HIV Disease

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (1 September 2021) | Viewed by 5805

Special Issue Editors

Prof. Dr. Anthony Jaworowski

E-Mail Website
Guest Editor
School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia
Interests: HIV; macrophage; monocyte; NK cell; signal transduction
Dr. Anna C. Hearps

E-Mail Website
Guest Editor
Centre for Biomedical Research, Burnet Institute, Melbourne, Australia
Interests: HIV; immune response; monocyte

Special Issue Information

Dear Colleagues,

An estimated 38 million people are living with HIV, and the provision of life-preserving antiretroviral medication to these individuals is increasing. Currently, HIV is a manageable, chronic health condition, and progression to AIDS is effectively prevented by antiretroviral drugs. Evidence suggests that innate immune dysfunction and inflammation remain elevated in people with HIV who achieve virologic suppression on ART and that this is associated with an increased prevalence of age-related, inflammatory comorbidities such as cardiovascular disease, frailty and neurocognitive impairment. While there is growing evidence that early treatment with ART improves outcomes for people with HIV, its effect on HIV-related inflammation and, hence, the risk of long-term inflammatory comorbidities is less clear.

This Special Issue focuses on the current evidence for innate immune dysfunction and inflammation in virologically suppressed people on ART, its possible mechanisms and causes, the impact on comorbid diseases and potential adjunctive therapeutic strategies to minimise its impact on long-term health outcomes in people with HIV.

Prof. Dr. Anthony Jaworowski
Dr. Anna C. Hearps
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • HIV
  • people with HIV
  • inflammation
  • immune dysfunction
  • innate immune activation
  • age-related comorbidities
  • cardiovascular disease
  • neurological complications

Published Papers (2 papers)

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Research

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11 pages, 1618 KiB  
Article
A Sex-Stratified Analysis of Monocyte Phenotypes Associated with HIV Infection in Uganda
by Moises A. Huaman, Manuel G. Feria, Cissy Kityo, Sophie Nalukwago, Rashidah Nazzinda, David A. Zidar, Markella V. Zanni, Mark J. Siedner, Steven K. Grinspoon and Chris T. Longenecker
Viruses 2021, 13(11), 2135; https://doi.org/10.3390/v13112135 - 22 Oct 2021
Cited by 2 | Viewed by 1800
Abstract
Women with HIV may experience higher rates of non-AIDS comorbidities compared to men with HIV, but the underlying mechanisms are not well understood. We investigated sex-related differences in the effects of HIV on monocyte phenotypes within the Ugandan Study of HIV effects on [...] Read more.
Women with HIV may experience higher rates of non-AIDS comorbidities compared to men with HIV, but the underlying mechanisms are not well understood. We investigated sex-related differences in the effects of HIV on monocyte phenotypes within the Ugandan Study of HIV effects on the Myocardium and Atherosclerosis (mUTIMA). Of 133 participants who provided blood for flow cytometry assays, 86 (65%) were women and 91 (68%) were persons living with HIV (PLWH) on antiretroviral therapy. The median age was 57 (interquartile range, 52–63) years. PLWH exhibited a lower proportion of circulating CD14+CD16- classical monocytes (66.3% vs. 75.1%; p < 0.001), and higher proportion of CD14+CD16+ inflammatory monocytes (17% vs. 11.7%; p = 0.005) compared to HIV-uninfected participants. PLWH had an increased expression of the chemokine receptor CX3CR1 in total monocytes (CX3CR1+ monocytes, 24.5% vs. 4.7%; p < 0.001) and monocyte subsets. These findings were generally similar when analyzed by sex, with no significant interactions between sex and HIV status in adjusted models. Our data show that the inflammatory monocyte subset is expanded and monocyte CX3CR1 chemokine receptor expression is enhanced among PLWH, regardless of sex. Whether these parameters differentially affect risk for non-AIDS comorbidities and clinical outcomes in women with HIV requires additional investigation. Full article
(This article belongs to the Special Issue Innate Immune Activation in HIV Disease)
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Review

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12 pages, 5073 KiB  
Review
Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
by Zoey K. Wallis and Kenneth C. Williams
Viruses 2022, 14(2), 409; https://doi.org/10.3390/v14020409 - 17 Feb 2022
Cited by 11 | Viewed by 3438
Abstract
Before the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive [...] Read more.
Before the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive disorders, lung and kidney disease, and malignancies. The broad evidence suggests that HIV with ART is associated with accentuated aging, and that the age-related comorbidities occur earlier, due in part to chronic immune activation, co-infections, and possibly the effects of ART alone. Normally the immune system undergoes alterations of lymphocyte and monocyte populations with aging, that include diminished naïve T- and B-lymphocyte numbers, a reliance on memory lymphocytes, and a skewed production of myeloid cells leading to age-related inflammation, termed “inflamm-aging”. Specifically, absolute numbers and relative proportions of monocytes and monocyte subpopulations are skewed with age along with myeloid mitochondrial dysfunction, resulting in increased accumulation of reactive oxygen species (ROS). Additionally, an increase in biomarkers of myeloid activation (IL-6, sCD14, and sCD163) occurs with chronic HIV infection and with age, and may contribute to immunosenescence. Chronic HIV infection accelerates aging; meanwhile, ART treatment may slow age-related acceleration, but is not sufficient to stop aging or age-related comorbidities. Overall, a better understanding of the mechanisms behind accentuated aging with HIV and the effects of myeloid activation and turnover is needed for future therapies. Full article
(This article belongs to the Special Issue Innate Immune Activation in HIV Disease)
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