Immune Responses in the Central Nervous System Are Anatomically Segregated in a Non-Human Primate Model of Human Immunodeficiency Virus Infection

The human immunodeficiency virus (HIV) accesses the central nervous system (CNS) early during infection, leading to HIV-associated cognitive impairment and establishment of a viral reservoir. Here, we describe a dichotomy in inflammatory responses in different CNS regions in simian immunodeficiency...

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Published inFrontiers in immunology Vol. 8; p. 361
Main Authors Tavano, Barbara, Tsipouri, Vicky, Hardy, Gareth A D, Royle, Caroline M, Keegan, Michael R, Fuchs, Dietmar, Patterson, Steven, Almond, Neil, Berry, Neil, Ham, Claire, Ferguson, Deborah, Boasso, Adriano
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 30.03.2017
Subjects
central nervous system
Immunology
indoleamine (2,3)-dioxygenase
neuroinflammation
neurotoxicity
simian immunodeficiency virus
simian immunodeficiency virus
neurotoxicity
neuroinflammation
indoleamine (2,3)-dioxygenase
central nervous system
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Summary:The human immunodeficiency virus (HIV) accesses the central nervous system (CNS) early during infection, leading to HIV-associated cognitive impairment and establishment of a viral reservoir. Here, we describe a dichotomy in inflammatory responses in different CNS regions in simian immunodeficiency virus (SIV)-infected macaques, a model for HIV infection. We found increased expression of inflammatory genes and perivascular leukocyte infiltration in the midbrain of SIV-infected macaques. Conversely, the frontal lobe showed downregulation of inflammatory genes associated with interferon-γ and interleukin-6 pathways, and absence of perivascular cuffing. These immunologic alterations were not accompanied by differences in SIV transcriptional activity within the tissue. Altered expression of genes associated with neurotoxicity was observed in both midbrain and frontal lobe. The segregation of inflammatory responses to specific regions of the CNS may both account for HIV-associated neurological symptoms and constitute a critical hurdle for HIV eradication by shielding the CNS viral reservoir from antiviral immunity.
Bibliography:Reviewed by: Joern E. Schmitz, Fraunhofer Institute for Molecular Biology and Applied Ecology (FHG), Germany; Seema N. Desai, Rush University, USA
Specialty section: This article was submitted to HIV and AIDS, a section of the journal Frontiers in Immunology
Present address: Caroline M. Royle, Centenary Institute, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
These authors have contributed equally to this work.
Edited by: Clive Maurice Gray, University of Cape Town, South Africa
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2017.00361