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      Feline Immunodeficiency Virus Neuropathogenesis: A Model for HIV-Induced CNS Inflammation and Neurodegeneration

      review-article
      Author(s): 1 , * , 2
      Editor(s):
      Publication date (Electronic):
      Journal: Veterinary Sciences
      Publisher: MDPI
      Keywords: AIDS, human immunodeficiency virus, dementia, neurons, microglia, macrophages

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          Abstract

          Feline Immunodeficiency virus (FIV), similar to its human analog human immunodeficiency virus (HIV), enters the central nervous system (CNS) soon after infection and establishes a protected viral reservoir. The ensuing inflammation and damage give rise to varying degrees of cognitive decline collectively known as HIV-associated neurocognitive disorders (HAND). Because of the similarities to HIV infection and disease, FIV has provided a useful model for both in vitro and in vivo studies of CNS infection, inflammation and pathology. This mini review summarizes insights gained from studies of early infection, immune cell trafficking, inflammation and the mechanisms of neuropathogenesis. Advances in our understanding of these processes have contributed to the development of therapeutic interventions designed to protect neurons and regulate inflammatory activity.

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          Most cited references134

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          Recruitment of beneficial M2 macrophages to injured spinal cord is orchestrated by remote brain choroid plexus.

          Ravid Shechter, Omer Miller, Gili Yovel … (2013)
          Monocyte-derived macrophages are essential for recovery after spinal cord injury, but their homing mechanism is poorly understood. Here, we show that although of common origin, the homing of proinflammatory (M1) and the "alternatively activated" anti-inflammatory (M2) macrophages to traumatized spinal cord (SC) was distinctly regulated, neither being through breached blood-brain barrier. The M1 macrophages (Ly6c(hi)CX3CR1(lo)) derived from monocytes homed in a CCL2 chemokine-dependent manner through the adjacent SC leptomeninges. The resolving M2 macrophages (Ly6c(lo)CX3CR1(hi)) derived from monocytes trafficked through a remote blood-cerebrospinal-fluid (CSF) barrier, the brain-ventricular choroid plexus (CP), via VCAM-1-VLA-4 adhesion molecules and epithelial CD73 enzyme for extravasation and epithelial transmigration. Blockage of these determinants, or mechanical CSF flow obstruction, inhibited M2 macrophage recruitment and impaired motor-function recovery. The CP, along with the CSF and the central canal, provided an anti-inflammatory supporting milieu, potentially priming the trafficking monocytes. Overall, our finding demonstrates that the route of monocyte entry to central nervous system provides an instructional environment to shape their function. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Isolation of a T-lymphotropic virus from domestic cats with an immunodeficiency-like syndrome.

            Hector Ho, J Yamamoto, M Wiktor … (1987)
            A highly T-lymphotropic virus was isolated from cats in a cattery in which all the animals were seronegative for feline leukemia virus. A number of cats in one pen had died and several had an immunodeficiency-like syndrome. Only 1 of 18 normal cats in the cattery showed serologic evidence of infection with this new virus, whereas 10 of 25 cats with signs of ill health were seropositive for the virus. Tentatively designated feline T-lymphotropic lentivirus, this new feline retrovirus appears to be antigenically distinct from human immunodeficiency virus. There is no evidence for cat-to-human transmission of the agent. Kittens experimentally infected by way of blood or plasma from naturally infected animals developed generalized lymphadenopathy several weeks later, became transiently febrile and leukopenic, and continued to show a generalized lymphadenopathy 5 months after infection.
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              HIV-associated cognitive impairment before and after the advent of combination therapy.

              Karen Marder, Karl Kieburtz, Donna Palumbo … (2002)
              The objective of this study was to describe the occurrence of HIV dementia and neuropsychological testing abnormalities in a new cohort of HIV-seropositive individuals at high risk for HIV dementia and to compare these results to a cohort before the advent of highly active antiretroviral therapy (HAART). HAART has been associated with improvements in cognitive performance in some HIV-infected patients. However, it is uncertain whether HAART has changed the frequency of specific neurocognitive abnormalities. Baseline data from 272 HIV-seropositive subjects in the Dana cohort recruited from January, 1994, to December, 1995, and 251 HIV-seropositive subjects in the Northeastern AIDS Dementia Consortium (NEAD) cohort recruited from April, 1998, to August, 1999, were compared. Participants in both cohorts received nearly identical assessments. After adjusting for differences in age, education, gender, race, and CD4 count between the two cohorts, there were no differences in the occurrence of HIV dementia or abnormalities either 1 SD or 2 SDs below established norms for any of the neuropsychological tests. Even though HAART has reduced the incidence of HIV dementia, HIV-associated cognitive impairment continues to be a major clinical problem among individuals with advanced infection.
              Article 0 comments Cited 87 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Patrick Butaye: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Vet Sci
                Journal ID (iso-abbrev): Vet Sci
                Journal ID (publisher-id): vetsci
                Title: Veterinary Sciences
                Publisher: MDPI
                ISSN (Electronic): 2306-7381
                Publication date (Electronic): 06 March 2017
                Publication date Collection: March 2017
                Volume: 4
                Issue: 1
                Electronic Location Identifier: 14
                Affiliations
                [1 ]Department of Neurology, University of North Carolina, Chapel Hill, NC 27599, USA
                [2 ]Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27607, USA; lola_hudson@ 123456ncsu.edu
                Author notes
                [* ]Correspondence: meekerr@ 123456neurology.unc.edu ; Tel.: +1-919-966-5512
                Article
                Publisher ID: vetsci-04-00014
                DOI: 10.3390/vetsci4010014
                PMC ID: 5606611
                SO-VID: 5edf81b9-b50f-4253-ad17-5fbb50e341b0
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 12 January 2017
                Date accepted : 01 March 2017
                Categories
                Subject: Review

                Keywords: aids,human immunodeficiency virus,dementia,neurons,microglia,macrophages
                Data availability:
                Keywords: aids, human immunodeficiency virus, dementia, neurons, microglia, macrophages

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