Mechanism(s) Involved in HIV-1 and Drug Abuse-Mediated Neuroinflammation

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 221

Special Issue Editor


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Guest Editor
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 69198, USA
Interests: HIV-1 and inflammaging; drug abuse and HIV-1 morbidity; endoplasmic reticulum stress and autophagy; inflammasome; mitochondrial dysfunction

Special Issue Information

Dear Colleagues,

HIV-1 infection and drug abuse are two intertwined epidemics. Despite the effectiveness of combination antiretroviral therapy (cART) in suppressing virus replication, chronic inflammation remains one of the cardinal features intersecting HIV-1, cART, and drug abuse, and likely contributes to the accelerated neurocognitive decline and inflammation-mediated aging in people living with HIV-1 that abuse drugs. Recent years have also seen an explosive surge in research on inflammation and its effects on aging, now referred to as “inflammaging.” While there is extensive literature on inflammaging in response to lifestyle stressors during normal aging, there is a knowledge gap in our understanding of how HIV-1, cART, and drug abuse contribute to accelerated aging. This Special Issue on “Mechanism(s) Involved in HIV-1 and Drug-Abuse-Mediated Neuroinflammation” focuses on multiple aspects of neuroinflammation mediated by HIV-1, cART, and drug abuse, and will provide innovative research updates on the underpinnings of HIV-1 and drug abuse intersection in mediating “inflammaging.” The major themes of the Special Issue include: a) inflammatory mechanisms of HIV-1/HIV-1 proteins and drug-abuse-mediated cognitive aging; b) effects of drugs abuse on premature aging; c) neuroimmune interactions, including bidirectional cross-talk between periphery and CNS and between CNS cells in the context of addiction, HIV-1 infection, and inflammation; d) involvement of reactive oxygen species, endoplasmic reticulum stress, mitochondrial dysfunction, and autophagy in the context of inflammaging associated with drug abuse, HIV-1, and cART. This Special Issue will hopefully address these issues by linking neuroinflammation with aging in the context of HIV-1, cART, and drug abuse.

Prof. Shilpa Buch
Guest Editor

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Keywords

  • neuroinflammation
  • drug abuse
  • viruses and viral proteins
  • aging
  • inflammasome
  • autophagy/mitophagy

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