Exogenous tat protein activates central nervous system-derived endothelial cells
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Cited by (92)
Investigating the distribution of HIV-1 Tat lengths present in the Drexel Medicine CARES cohort
2019, Virus ResearchCitation Excerpt :Tat secretion has been shown to occur through an unconventional pathway; passing through the plasma membrane primarily through oligomerization and pore formation (Mele et al., 2018). Once extracellular, Tat can directly cause neurotoxicity by hyper-activation (Fields et al., 2015) and recruitment of additional immune cells to the central nervous system (CNS), causing low levels of chronic inflammation through activation of bystander cells and release of pro-inflammatory cytokines, such as IL1-β from monocytes and macrophages (Albini et al., 1998; Bachani et al., 2013; Hofman et al., 1994; Hudson et al., 2000; Rayne et al., 2010b). Furthermore, Tat produced in the periphery can cross the blood-brain barrier and traffic into the CNS (Banks et al., 2005).
HIV, Tat and dopamine transmission
2017, Neurobiology of DiseaseCitation Excerpt :In vivo, immunohistochemical staining was used to identify Tat protein in monocytes, astrocytes and oligodendrocytes in the frontal cortex and white matter of 3 HIV-infected patients (Del Valle et al., 2000), and in the cytoplasm of astrocytes and microglia in gray and white matter from 10 HIV-infected brains (Bonwetsch et al., 1999). A third study also used immunohistochemistry to identify Tat positive cells in the subcortical frontal white matter of 3 out of 4 HIV-infected brain specimens (Hofman et al., 1994). Although the movement and localization of Tat in vivo are not fully resolved, these data suggest that Tat could be taken up by CNS-specific cells in infected areas of the brain.
Neuropathological sequelae of Human Immunodeficiency Virus and apathy: A review of neuropsychological and neuroimaging studies
2015, Neuroscience and Biobehavioral ReviewsCitation Excerpt :These mechanisms are implicated in the symptoms of dementia observed in older adult patients with AD (Kawahara and Kuroda, 2000; Mattson, 2007). Because HIV viral proliferation is most pronounced within the basal ganglia, viral proteins such as gp120 and Tat are found there in highest concentrations (Aksenov et al., 2001; Hofman et al., 1994; Kruman et al., 1998). Consequentially, Tat has a neurotoxic effect by influencing excitatory properties of neurons that results in cell apoptosis through increased intracellular levels of calcium, glutamate, and inflammatory cytokines (Buonaguro et al., 1992; Ensoli et al., 1993).
Human immunodeficiency virus-1 protein Tat induces excitotoxic loss of presynaptic terminals in hippocampal cultures
2013, Molecular and Cellular NeuroscienceCitation Excerpt :One such toxic protein is the HIV transactivator of transcription (Tat), which is shed by infected cells. Tat mRNA and protein are found in the CNS of HAND patients (Del Valle et al., 2000; Hofman et al., 1994; Hudson et al., 2000; Wiley et al., 1996) and Tat protein induces HAND neuropathologies in vivo (Fitting et al., 2010; Kim et al., 2003). In vitro effects of Tat include dendritic pruning, decreased spine density, and synapse loss (Eugenin et al., 2007; Kim et al., 2008; Liu et al., 2000).
Progressive multifocal leukoencephalopathy: from its origin to 2008
2009, Seminarios de la Fundacion Espanola de ReumatologiaLimited role of COX-2 in HIV Tat-induced alterations of tight junction protein expression and disruption of the blood-brain barrier
2007, Brain ResearchCitation Excerpt :To support the role of Tat in the development of neuropathological changes associated with HIV infection, Tat was detected in AIDS brains with progressive multifocal leukoencephalopathy (Valle et al., 2000; Johnston et al., 2001). Tat positive mononuclear cells have also been localized in the perivascular regions in the brains of patients with HIV encephalitis (Hofman et al., 1994; Bonwetsch et al., 1999) and in rhesus macaques with SHIV encephalitis (Hudson et al., 2000). We, and others, indicated that intracerebral injection of Tat can cause profound inflammatory reactions in the CNS with upregulation of chemokines, inflammatory cytokines, and adhesion molecules (Jones et al., 1998; Pu et al., 2003; Flora et al., 2005).