Abstract
Non-human primates (NHPs) are the most relevant model of Acquired Immunodeficiency Syndrome (AIDS) and neuroAIDS, being of great importance in explaining the pathogenesis of HIV-induced nervous system damage. Simian Immunodeficiency Virus (SIV)/ Simian-Human Immunodeficiency Virus (SHIV)-infected monkeys have provided evidence of complex interactions between the virus and host that include host immune response, viral genetic diversity, and genetic susceptibility, which may explain virus-associated central nervous system (CNS) pathology and HIV-associated neurocognitive disorders (HAND). In this article, we review the recent progress contributions obtained using monkey models of HIV infection of the CNS, neuropathogenesis and SIV encephalitis (SIVE), with an emphasis on pharmacologic therapies and dependable markers that predict development of CNS AIDS.
Highlights
Pathogens 2021, 10, 1018. https://Human Immunodeficiency Virus (HIV)-related cognitive impairments persist with effective antiretroviral therapy (ART) and remain a clinical concern for people with HIV (PWH)
Productive infection is difficult to be revealed during the macrophages, multi-nucleated giant cells (MNGC) andof inAIDS, some the cases parenchymal miasymptomatic phase of infection, while following the development virus is croglia [5,6,7,8,9,10].macrophages, Factors that control the development of encephalitis andin giant cell formation detected in perivascular multi-nucleated giant cells (MNGC) and some in the central nervous system (CNS)
Brain macrophages of ART-suppressed Simian Immunodeficiency Virus (SIV)-infected macaques harbor latent viral genomes that can be reactivated during treatment with the protein kinase C (PKC) agonist ingenol-B and the histone deacetylase (HDAC) inhibitor vorinostat, and that are infectious in peripheral blood mononuclear cells (PBMCs) [43]
Summary
Human Immunodeficiency Virus (HIV)-related cognitive impairments persist with effective antiretroviral therapy (ART) and remain a clinical concern for people with HIV (PWH). Despite use of ART results in effective viral suppression within the systemic circulation, the virus persists in the central nervous system (CNS), as a site of viral reservoir, due to limited ART penetrance, thereby hampering efforts to eradicate HIV. After crossing the BBB, viral particles are able to infect resident cells such as microglia and macrophages contributing to establishing a persistent infection (Figure 1). In the CNS latent integrated HIV DNA can potentially reactivate and replicate viral. An important unsolved question is whether virus originating in the CNS can reseed the periphery and even cause failure of systemic control in otherwise virologically suppressed individuals, contributing to the development of HIV-associated neurocognitive disorder (HAND) in the course of their life [1,2].
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