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Cited by 360

The DOI matches its Crossref record; 165 of the 165 references it cites were found in a registry or an index.

Role of the immune system in HIV-associated neuroinflammation and neurocognitive implications

Open access
Hong, Suzi, Banks, William A.·2015·Brain, Behavior, and Immunity
DOI 10.1016/j.bbi.2014.10.008
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Abstract

Individuals living with HIV who are optimally treated with combination antiretroviral therapy (cART) can now lead an extended life. In spite of this remarkable survival benefit from viral suppression achieved by cART in peripheral blood, the rate of mild to moderate cognitive impairment remains high. A cognitive decline that includes impairments in attention, learning and executive function is accompanied by increased rates of mood disorders that together adversely impact the daily life of those with chronic HIV infection. The evidence is clear that cells in the brain are infected with HIV that has crossed the blood-brain barrier both as cell-free virus and within infected monocytes and T cells. Viral proteins that circulate in blood can induce brain endothelial cells to release cytokines, invoking another source of neuroinflammation. The difficulty of efficient delivery of cART to the central nervous system (CNS) contributes to elevated viral load in the CNS, resulting in a persistent HIV-associated neurocognitive disorders (HAND). The pathogenesis of HAND is multifaceted, and mounting evidence indicates that immune cells play a major role. HIV-infected monocytes and T cells not only infect brain resident cells upon migration into the CNS but also produce proinflammatory cytokines such as TNF and IL-1β, which in turn, further activate microglia and astrocytes. These activated brain resident cells, along with perivascular macrophages, are the main contributors to neuroinflammation in HIV infection and release neurotoxic factors such as excitatory amino acids and inflammatory mediators, resulting in neuronal dysfunction and death. Cytokines, which are elevated in the blood of patients with HIV infection, may also contribute to brain inflammation by entering the brain from the blood. Host factors such as aging and co-morbid conditions such as cytomegalovirus co-infection and vascular pathology are important factors that affect the HIV-host immune interactions in HAND pathogenesis. By these diverse mechanisms, HIV-1 induces a neuroinflammatory response that is likely to be a major contributor to the cognitive and behavior changes seen in HIV infection.

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Metadata

Authors
Hong, S., & Banks, W. A.
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2015-03
Volume
45
Pages
1-12
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2014.10.008
OpenAlex
W2000868000
Cited by
360
References
165
FWCI
10.77
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Role of the immune system in HIV-associated neuroinflammation and neurocognitive implications. https://app.cochat.ai/papers/10.1016/j.bbi.2014.10.008
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Hong, S., & Banks, W. A. (2015). Role of the immune system in HIV-associated neuroinflammation and neurocognitive implications. Brain, Behavior, and Immunity. https://doi.org/10.1016/j.bbi.2014.10.008

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.