Neurovirology and Brain Health—A Microglial Perspective DOI

Anindya Kishor Biswas,

Jayasri Das Sarma

Healthy ageing and longevity, Journal Year: 2024, Volume and Issue: unknown, P. 119 - 142

Published: Jan. 1, 2024

Language: Английский

Bidirectional Relationship between HIV/HBV Infection and Comorbid Depression and/or Anxiety: A Systematic Review on Shared Biological Mechanisms DOI Open Access
Michele Fabrazzo, Salvatore Cipolla, Mariantonietta Pisaturo

et al.

Journal of Personalized Medicine, Journal Year: 2023, Volume and Issue: 13(12), P. 1689 - 1689

Published: Dec. 5, 2023

Mental disorders that are comorbid with chronic infectious diseases may worsen clinical outcomes and patients' quality of life. We hypothesized depression and/or anxiety syndromes or symptoms human immunodeficiency virus (HIV) hepatitis B (HBV) infection might stem from shared biological mechanisms. conducted a systematic review applying the PRISMA statement by searching into PubMed, APA PsycInfo, Scopus databases. examined literature on HIV/HBV in adults ≥18 years. Thirty-one studies HIV three HBV were analyzed. The Tat protein contributed to HIV-associated mood due protein's ability cause neurodegeneration induce hypothalamic-pituitary-adrenal (HPA) axis dysregulation response natural stressors. decreased brain-derived neurotrophic factor (BDNF) levels also emerged as mechanism involved neuropathogenesis associated symptoms. Neuroinflammation was implicated onset patients infections. Microglial activation release cytokines, particular, appeared potential pathogenetic Furthermore, an altered balance between quinolinic acid kynurenic production depression, indicating glutamatergic dysfunction. Inflammatory cytokine downregulation cellular immune responses persisting inflammation, delayed healing, functional decline (CHB) infection. A shift type 1-type 2 be HBV-related pathogenesis, considered immunomodulatory factors. Cytokines caused HPA hyperactivity, frequently observed depression/anxiety. present showed, for first time, have several mechanisms common denominators. longitudinal course highlighted should explored establish causative interrelationship among In addition, future research investigate possibility patient's outcome improve using pharmacological treatments acting we described denominators inflammatory infective

Language: Английский

Citations

4

α-Synuclein fibrils enhance HIV-1 infection of human T cells, macrophages and microglia DOI Creative Commons
Frank Kirchhoff, Lia‐Raluca Olari, Sichen Liu

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: May 14, 2024

Abstract HIV-associated neurocognitive disorders (HAND) and viral reservoirs in the brain remain a significant challenge. Despite their importance, mechanisms allowing HIV-1 entry replication central nervous system (CNS) are poorly understood. Here, we show that α-synuclein (to lesser extent) Aβ40 fibrils associated with neurological diseases, enhance human T cells, macrophages, microglia. Additionally, an Env-derived amyloidogenic peptide accelerated amyloid formation by Aβ peptides. Mechanistic studies showed interact particles promote virion attachment fusion target cells. overall negative surface charge, these facilitate interactions between cellular membranes. Enhancing effects of extracts on infection correlated binding to Thioflavin commonly used stain amyloids. Our results suggest detrimental interplay amyloids may contribute development neurodegenerative diseases.

Language: Английский

Citations

0

MITOCHONDRIAL ANTIVIRAL PATHWAYS CONTROL ANTI-HIV RESPONSES AND ISCHEMIC STROKE OUTCOMES VIA THE RIG-1 SIGNALING AND INNATE IMMUNITY MECHANISMS DOI Creative Commons
Silvia Torices,

T Lázaro Moreno,

Sita Ramaswamy

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: June 8, 2024

Occludin (ocln) is one of the main regulatory cells blood-brain barrier (BBB). Ocln silencing resulted in alterations gene expression signatures a variety genes innate immunity system, including IFN-stimulated (ISGs) and antiviral retinoic acid-inducible gene-1 (RIG-1) signaling pathway, which functions as regulator cytoplasmic sensors upstream mitochondrial protein (MAVS). Indeed, we observed dysfunctional bioenergetics, dynamics, autophagy our system. Alterations bioenergetics immune protection translated into worsened ischemic stroke outcomes EcoHIV-infected ocln deficient mice. Overall, these results allow for better understanding molecular mechanisms viral infection brain describe previously unrecognized role key factor control responses affect cerebral vascular diseases such stroke.

Language: Английский

Citations

0

Neurovirology and Brain Health—A Microglial Perspective DOI

Anindya Kishor Biswas,

Jayasri Das Sarma

Healthy ageing and longevity, Journal Year: 2024, Volume and Issue: unknown, P. 119 - 142

Published: Jan. 1, 2024

Language: Английский

Citations

0