CommentarySynaptodendritic injury with HIV-Tat protein: What is the therapeutic target?
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Cited by (24)
Endolysosome dysfunction in HAND
2024, HIV-Associated Neurocognitive DisordersUp-regulation of the p75 neurotrophin receptor is an essential mechanism for HIV-gp120 mediated synaptic loss in the striatum
2020, Brain, Behavior, and ImmunityCitation Excerpt :Common features of HAND pathology include dendritic damage, broad dendritic spine loss, and overall synaptic simplification. Both the simplification and loss of synapses may be due to neuroinflammation (Hong and Banks, 2015), comorbid conditions (McArthur et al., 2010), aging (Smail and Brew, 2018), drug addiction (Letendre et al., 2005), and viral proteins such as gp120 and Tat (Kaul et al., 2007; Nath and Steiner, 2014). However, multiple proteins and interwoven signaling mechanisms are involved in the formation and lifelong plasticity of adult synapses.
HIV and opiates dysregulate K<sup>+</sup>- Cl<sup>−</sup> cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice
2020, Neurobiology of DiseaseCitation Excerpt :It is widely accepted that neurons are not infected by HIV-1. Neurological deficits in patients receiving combined antiretroviral therapy (cART) are likely due to sublethal neuronal stress and injury induced by viral proteins released from infected cells and persistent neuroinflammation, resulting in hyperexcitability (Anthony et al., 2005; Everall et al., 2009; Nath and Steiner, 2014; Neuenburg et al., 2002). Exposure to HIV-1 transactivator of transcription (Tat) depolarizes neurons and leads to electrophysiological dysfunction and hyperexcitability, partly through interactions with N-methyl-D-aspartic acid (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (Krogh et al., 2014; Philippon et al., 1994).
HIV-Associated Cardiovascular Disease: Role of Connexin 43
2017, American Journal of PathologyCitation Excerpt :However, our data on astrocytes in the context of HIV infection indicate that the HIV protein, tat, the transactivator of the virus, binds to the Cx43 promoter, increasing Cx43 expression and gap junctional coupling to enable the spread of toxic intracellular second messengers among coupled cells, resulting in bystander apoptosis and inflammation.18,58 HIV-tat, like other viral proteins, is secreted into the extracellular space even in the presence of effective ART59,60 and may enter and affect cells that do not express HIV-tat. Our data indicate that in all of the heart tissues analyzed from HIV-infected individuals Cx43 was increased in abundance and was anomalously distributed along the lateral membranes.
Reduced neural specificity in middle-aged HIV+ women in the absence of behavioral deficits
2015, NeuroImage: ClinicalCitation Excerpt :Computational simulation and theoretical works of cognitive aging have proposed that increased neuronal noise due to reduced dopamine activity (Li et al., 2001) and decreased neuronal selectivity due to age-related synaptic injury (Morrison and Baxter, 2012) might be responsible for age-related reduction in neural specificity. Coincidently, HIV infection is known to impair dopamine transporter functions (Purohit et al., 2011) and synaptic functions (Atluri et al., 2013; Ellis et al., 2007; Ellis, 2010; Everall et al., 1999; Masliah et al., 1992; Nath and Steiner, 2014). For instance, dopamine reduction has been found in the HIV-infected brain (Wang et al., 2004) and is related to the concentration of HIV-1 RNA (Kumar et al., 2009) and cognitive impairments (Nath et al., 2000).