Trained Immunity and HIV Infection

Sviridov, Dmitri; Miller, Yury I.; Bukrinsky, Michael

doi:10.3389/fimmu.2022.903884

Cited by 8 publications

(6 citation statements)

References 67 publications

(70 reference statements)

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“…Interestingly, epigenetic changes appear to suppress the expression of ABCA1 in Nef EVs‐treated cells, the effect that was not described for β‐glucan and which may further enhance ABCA1 inhibition induced by Nef EVs 128 . This concept is yet to be tested in brain cells, but if confirmed, this finding opens a possibility that chronic neuroinflammation may be maintained in HIV‐infected individuals even when all HIV‐specific factors are eliminated 130 …”

Section: Trained Innate Immunity—a Possible Contributor To Handmentioning

confidence: 96%

Neuro‐HIV—New insights into pathogenesis and emerging therapeutic targets

Sviridov,

Bukrinsky

2023

The FASEB Journal

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HIV‐associated neurocognitive disorders (HAND) is a term describing a complex set of cognitive impairments accompanying HIV infection. Successful antiretroviral therapy (ART) reduces the most severe forms of HAND, but milder forms affect over 50% of people living with HIV (PLWH). Pathogenesis of HAND in the ART era remains unknown. A variety of pathogenic factors, such as persistent HIV replication in the brain reservoir, HIV proteins released from infected brain cells, HIV‐induced neuroinflammation, and some components of ART, have been implicated in driving HAND pathogenesis in ART‐treated individuals. Here, we propose another factor—impairment of cholesterol homeostasis and lipid rafts by HIV‐1 protein Nef—as a possible contributor to HAND pathogenesis. These effects of Nef on cholesterol may also underlie the effects of other pathogenic factors that constitute the multifactorial nature of HAND pathogenesis. The proposed Nef‐ and cholesterol‐focused mechanism may provide a long‐sought unified explanation of HAND pathogenesis that takes into account all contributing factors. Evidence for the impairment by Nef of cellular cholesterol balance, potential effects of this impairment on brain cells, and opportunities to therapeutically target this element of HAND pathogenesis are discussed.

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Section: Trained Innate Immunity—a Possible Contributor To Handmentioning

confidence: 96%

Neuro‐HIV—New insights into pathogenesis and emerging therapeutic targets

Sviridov,

Bukrinsky

2023

The FASEB Journal

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“…Following an initial infection, long-term epigenetic reprogramming allows innate immune cells to provide enhanced response to subsequent infections. Although only a few studies have focused on trained immunity in the context of HIV infection, 171 trained immunity has received growing attention in atherosclerosis 172 and may represent an important missing link to explain HIV-associated cardiovascular comorbidities.…”

Section: Immunologic Evidencementioning

confidence: 99%

HIV-Associated Cardiovascular Disease Pathogenesis: An Emerging Understanding Through Imaging and Immunology

Hudson,

Ferrand,

Gitau

et al. 2024

Circulation Research

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Cardiac abnormalities were identified early in the epidemic of AIDS, predating the isolation and characterization of the etiologic agent, HIV. Several decades later, the causation and pathogenesis of cardiovascular disease (CVD) linked to HIV infection continue to be the focus of intense speculation. Before the widespread use of antiretroviral therapy, HIV-associated CVD was primarily characterized by HIV-associated cardiomyopathy linked to profound immunodeficiency. With increasing antiretroviral therapy use, viral load suppression, and establishment of immune competency, the effects of HIV on the cardiovascular system are more subtle. Yet, people living with HIV still face an increased incidence of cardiovascular pathology. Advances in cardiac imaging modalities and immunology have deepened our understanding of the pathogenesis of HIV-associated CVD. This review provides an overview of the pathogenesis of HIV-associated CVD integrating data from imaging and immunologic studies with particular relevance to the HIV population originating from high-endemic regions, such as sub-Saharan Africa. The review highlights key evidence gaps in the field and suggests future directions for research to better understand the complex HIV-CVD interactions.

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“…Before the 2022 MPXV outbreak, most of the PWH populations had not received the smallpox vaccine, which not only provides protection against MPXV but may also induce "trained immunity" to fend off other infections. The concept of trained immunity was introduced by Netea et al [62][63][64] to describe the ability of innate immune cells (e.g., NK, dendritic cells, and monocytes/macrophages) to acquire an immunological memory to a "priming" pathogen (e.g., viruses, bacteria or fungi), a stimulus (e.g., TLR agonists, oxidized low-density lipoprotein, and aldosterone) or a vaccine (e.g., VACV-based smallpox vaccine), allowing them to trigger enhanced response to subsequent infection/stimulation by the same or unrelated agents/stimuli [65]. For example, innate immune responses associated with "trained immunity" persist after certain infections or vaccinations, e.g., with the smallpox vaccine.…”

Section: Pathogenesis Of Human Mpxv and Its Co-infection With Hiv Sti...mentioning

confidence: 99%

Mpox (Monkeypox) Virus and Its Co-Infection with HIV, Sexually Transmitted Infections, or Bacterial Superinfections: Double Whammy or a New Prime Culprit?

Liu,

Rakhmanina,

Yang

et al. 2024

Viruses

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Epidemiologic studies have established that mpox (formerly known as monkeypox) outbreaks worldwide in 2022–2023, due to Clade IIb mpox virus (MPXV), disproportionately affected gay, bisexual, and other men who have sex with men. More than 35% and 40% of the mpox cases suffer from co-infection with HIV and sexually transmitted infections (STIs) (e.g., Chlamydia trachomatis, Neisseria gonorrhoeae, Treponema pallidum, and herpes simplex virus), respectively. Bacterial superinfection can also occur. Co-infection of MPXV and other infectious agents may enhance disease severity, deteriorate outcomes, elongate the recovery process, and potentially contribute to the morbidity and mortality of the ensuing diseases. However, the interplays between MPXV and HIV, bacteria, other STI pathogens and host cells are poorly studied. There are many open questions regarding the impact of co-infections with HIV, STIs, or bacterial superinfections on the diagnosis and treatment of MPXV infections, including clinical and laboratory-confirmed mpox diagnosis, suboptimal treatment effectiveness, and induction of antiviral drug resistance. In this review article, we will discuss the progress and knowledge gaps in MPXV biology, antiviral therapy, pathogenesis of human MPXV and its co-infection with HIV, STIs, or bacterial superinfections, and the impact of the co-infections on the diagnosis and treatment of mpox disease. This review not only sheds light on the MPXV infection and co-infection of other etiologies but also calls for more research on MPXV life cycles and the molecular mechanisms of pathogenesis of co-infection of MPXV and other infectious agents, as well as research and development of a novel multiplex molecular testing panel for the detection of MPXV and other STI co-infections.

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Trained Immunity and HIV Infection

Cited by 8 publications

References 67 publications

Neuro‐HIV—New insights into pathogenesis and emerging therapeutic targets

Neuro‐HIV—New insights into pathogenesis and emerging therapeutic targets

HIV-Associated Cardiovascular Disease Pathogenesis: An Emerging Understanding Through Imaging and Immunology

Mpox (Monkeypox) Virus and Its Co-Infection with HIV, Sexually Transmitted Infections, or Bacterial Superinfections: Double Whammy or a New Prime Culprit?

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