HIV and Drugs of Abuse, 3rd Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 209

Special Issue Editors


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Guest Editor
San Diego Biomedical Research Institute (SDBRI), 3525 John Hopkins Ct., San Diego, CA 92121, USA
Interests: neuroinflammation; neuro-immunemodulation; chronic inflammation; brain pathogenesis; HIV associated neurological disorders; drugs of abuse; innate immune response
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Division of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, CA 92521, USA
Interests: neuroinflammation; neurodegenerative disease; host-pathogen interactions; HIV-1; drug abuse; innate immunity; microglia/macrophages; neuroprotection; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Substance use disorders and HIV infection are long-standing public health concerns and frequent comorbidities. HIV continues to cause neurocognitive deficits despite highly effective anti-retroviral therapies that lead to viral suppression. Combined with the neurobehavioral factors underlying substance use and the neurological consequences of addictive drugs, HIV-associated neurological disorders present a range of distinctive characteristics, and there is still no treatment available. The modulation of immune functions by the actions of neurotransmitters released under the influence of such drugs may be one reason for the aggravating effects of addiction on HIV-associated disorders in the central nervous system. Among the addictive drugs, methamphetamine and other stimulants are highly detrimental due to the associated risky behaviors, and due to their effects on neurotransmitters interfering with cellular responses. Given that innate and adaptive immune cells express neurotransmitter receptors, HIV target cells in the context of substance use respond differently than in non-users, particularly in the brain. Polysubstance use is highly prevalent among individuals with addictive behaviors, further complicating the picture. In this Special Issue of Viruses, we aim at integrating information derived from research with humans and animal models, as well as in cells of the immune system, thus providing a unique multidimentional and translational perspective of the clinical and mechanistic interactions between HIV and drugs of abuse that contribute to neurological disorders. Original work performed by interdisciplinary teams will be showcased.

Dr. Maria Cecilia Garibaldi Marcondes
Prof. Dr. Marcus Kaul
Guest Editors

Manuscript Submission Information

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Keywords

  • substance use disorders
  • HIV
  • HAND
  • methamphetamine

Published Papers (1 paper)

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Research

14 pages, 4143 KiB  
Article
HIV-1 Tat-Mediated Human Müller Glial Cell Senescence Involves Endoplasmic Reticulum Stress and Dysregulated Autophagy
by Uma Maheswari Deshetty, Nivedita Chatterjee, Shilpa Buch and Palsamy Periyasamy
Viruses 2024, 16(6), 903; https://doi.org/10.3390/v16060903 - 3 Jun 2024
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Abstract
Antiretroviral treatments have notably extended the lives of individuals with HIV and reduced the occurrence of comorbidities, including ocular manifestations. The involvement of endoplasmic reticulum (ER) stress in HIV-1 pathogenesis raises questions about its correlation with cellular senescence or its role in initiating [...] Read more.
Antiretroviral treatments have notably extended the lives of individuals with HIV and reduced the occurrence of comorbidities, including ocular manifestations. The involvement of endoplasmic reticulum (ER) stress in HIV-1 pathogenesis raises questions about its correlation with cellular senescence or its role in initiating senescent traits. This study investigated how ER stress and dysregulated autophagy impact cellular senescence triggered by HIV-1 Tat in the MIO-M1 cell line (human Müller glial cells). Cells exposed to HIV-1 Tat exhibited increased vimentin expression combined with markers of ER stress (BiP, p-eIF2α), autophagy (LC3, Beclin-1, p62), and the senescence marker p21 compared to control cells. Western blotting and staining techniques like SA-β-gal were employed to examine these markers. Additionally, treatments with ER stress inhibitor 4-PBA before HIV-1 Tat exposure led to a decreased expression of ER stress, senescence, and autophagy markers. Conversely, pre-treatment with the autophagy inhibitor 3-MA resulted in reduced autophagy and senescence markers but did not alter ER stress markers compared to control cells. The findings suggest a link between ER stress, dysregulated autophagy, and the initiation of a senescence phenotype in MIO-M1 cells induced by HIV-1 Tat exposure. Full article
(This article belongs to the Special Issue HIV and Drugs of Abuse, 3rd Edition)
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