ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Differential type 1 interferon-regulated gene expression in the brain during AIDS: interactions with viral diversity and neurovirulence.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Persistent type I interferon signaling within the brain of people with HIV on ART with cognitive impairment.PLoS pathogens · 2025Article
- Animal models for studies of HIV-1 brain reservoirs.Journal of leukocyte biology · 2022Review
- Acute TBK1/IKK-ε Inhibition Enhances the Generation of Disease-Associated Microglia-Like Phenotype Upon Cortical Stab-Wound Injury.Frontiers in aging neuroscience · 2021Article
- Transcriptomic Analysis of Age-Associated Periventricular Lesions Reveals Dysregulation of the Immune Response.International journal of molecular sciences · 2020Article
- Gene Expression: the Key to Understanding HIV-1 Infection?Microbiology and molecular biology reviews : MMBR · 2020Review
- Human Interleukin-34 facilitates microglia-like cell differentiation and persistent HIV-1 infection in humanized mice.Molecular neurodegeneration · 2019Article
- Morphine-potentiated cognitive deficits correlate to suppressed hippocampal iNOS RNA expression and an absent type 1 interferon response in LP-BM5 murine AIDS.Journal of neuroimmunology · 2018Article
- Neurologic disease in feline immunodeficiency virus infection: disease mechanisms and therapeutic interventions for NeuroAIDS.Journal of neurovirology · 2018Review
- Insulin Treatment Prevents Neuroinflammation and Neuronal Injury with Restored Neurobehavioral Function in Models of HIV/AIDS Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- HIV life cycle, innate immunity and autophagy in the central nervous system.Current opinion in HIV and AIDS · 2014Review
- Rapid inflammasome activation in microglia contributes to brain disease in HIV/AIDS.Retrovirology · 2014Article
- The Significance of Interferon-γ in HIV-1 Pathogenesis, Therapy, and Prophylaxis.Frontiers in immunology · 2014Review
- Inflammasome induction in Rasmussen's encephalitis: cortical and associated white matter pathogenesis.Journal of neuroinflammation · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
The lentiviruses, human and feline immunodeficiency viruses (HIV-1 and FIV, respectively), infect the brain and cause neurovirulence, evident as neuronal injury, inflammation, and neurobehavioral abnormalities with diminished survival. Herein, different lentivirus infections in conjunction with neural cell viability were investigated, concentrating on type 1 interferon-regulated pathways. Transcriptomic network analyses showed a preponderance of genes involved in type 1 interferon signaling, which was verified by increased expression of the type 1 interferon-associated genes, Mx1 and CD317, in brains from HIV-infected persons (P<0.05). Leukocytes infected with different strains of FIV or HIV-1 showed differential Mx1 and CD317 expression (P<0.05). In vivo studies of animals infected with the FIV strains, FIV(ch) or FIV(ncsu), revealed that FIV(ch)-infected animals displayed deficits in memory and motor speed compared with the FIV(ncsu)- and mock-infected groups (P<0.05). TNF-α, IL-1β, and CD40 expression was increased in the brains of FIV(ch)-infected animals; conversely, Mx1 and CD317 transcript levels were increased in the brains of FIV(ncsu)-infected animals, principally in microglia (P<0.05). Gliosis and neuronal loss were evident among FIV(ch)-infected animals compared with mock- and FIV(ncsu)-infected animals (P<0.05). Lentiviral infections induce type 1 interferon-regulated gene expression in microglia in a viral diversity-dependent manner, representing a mechanism by which immune responses might be exploited to limit neurovirulence.
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