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Symposium on Neurovirology June 2–6, 2015, San Diego, California, USA

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Symposium on Neurovirology June 2–6, 2015, San Diego, California, USA J. Neurovirol. (2015) 21 (Suppl 1):S1–S87 DOI 10.1007/s13365-015-0345-z Abstracts from the 13th International Symposium on NeuroVirology June 2–6, 2015, San Diego, California, USA Published online: 5 May 2015 # Journal of NeuroVirology, Inc. 2015 P1 increased in the brains of Tat transgenic mice. Our in vitro Replication independent functions of Tat may contribute studies indicate that Tat-mediated changes in PINCH-PP1-al- to hpTau pha and downstream AKT-GSK3-beta signaling are responsi- ble in part for hpTau formation in HIV CNS disease. Radhika Adiga1,WilliamYen1, Anthony Adame2,Kori Kosberg2,EdwardRockenstein2, Satish Deshmane1, Prasun Datta1, Eliezer Masliah2,DianneLangford1 P2 (corresponding author: [email protected]) Astrocytes Activation Induced by a Neuroadapted Dengue Virus Strain 1Temple University School of Medicine, Department of Neuroscience, Philadelphia, PA, USA; Sandra Elizabeth Aguilera Rojas, Maria Angélica Calderón 2University of California, San Diego, CA, USA Pelaez, Julieth Pardo, Edgar Orlando Beltran, Jaime Castellanos, Myriam Lucia Velandia Even though HIV does not infect neurons, extracellular Tat is (corresponding author: [email protected]) internalized by neurons, localizes to the nucleus and can in- teract with numerous neuronal proteins to impact a variety of Grupo de Virología, Vicerrectoría de Investigaciones, cellular processes. The serine/threonine-protein phosphatase Universidad El Bosque, Bogotá, Colombia PP1 (PP1) is among the numerous host proteins to which Tat can bind. PP1-alpha contributes to the regulation of Little is known about the cellular and molecular mechanisms AKT and GSK3-beta activity and can de-phosphorylate the involved in neurological symptoms during dengue infection. microtubule binding protein Tau at residues associated with It seems that astrocyte cell activation could play an important tauopathy. PP1-alpha’s activity is regulated in part by its in- role, as occurred in other neurotropic flavivirus infections. teraction with the PINCH protein. Previous studies report the The aim of this work was to study the in vitro response of robust expression of PINCH in the neurons of HIV patients, astrocytes during an infection with a neuroadapted dengue whereas, PINCH is nearly undetectable in healthy adult brain. virus strain (D4MB-6). Primary astrocytes cell cultures ob- Given the significant level of overlap among PINCH, PP1- tained from 7-day-old Balb/C mice with 95 % of purity were alpha and kinases with hyperphosphorylation of Tau (hpTau) inoculated at MOI:1 with dengue virus serotype 4 (DENV-4) and Tat, we hypothesized that replication independent func- or D4MB-6 during 24, 48, or 72 h. Then, the cells were proc- tions of Tat may contribute to hpTau. To assess the potential essed using immunofluorescence assay (IFI) to evaluate the importance of Tat in the PP1-alpha/PINCH pathway in neu- expression of GFAP, and DENVenvelope protein. The results rons, we investigated these pathways in HIV patient brains, in showed that the astrocytes were not susceptible to the infec- HIV Tat transgenic mice and in neurons in vitro. Our results tion with neither of the evaluated virus (infection <1.0 %). show that PP1-alpha levels are increased and co-localize in the However, the astrocytes changed their morphology, showing nucleus of neurons in HIVE patients compared to HIV+ pa- long and numerous cytoplasmic extensions mainly in the tients with out encephalitis. PINCH and PP1-alpha are also D4MB-6 infected cultures, suggesting a glial activation S2 J. Neurovirol. (2015) 21 (Suppl 1):S1–S87 process. It was also observed a higher proportion of cell mi- that freshly isolated human microglia from brain can be pro- tosis at 24 h and chromatin condensation at 72 h in infected ductively infected with HIV, suggesting a key role of HIV- cultures. TUNEL assay did not demonstrate an increase in infected resident cells in HIV-related neurologic disorders. apoptotic cells regarding infected and non-infected cultures. Primary microglia can also be immortalized and infected with Astrocyte proliferation was only corroborated by MTT assay pseudo-HIVs to study molecular events associated with HIV at 48 h in D4MB-6 with an increase of 10 % in infected entry and emergence from latency. cultures but there were not changes in mitochondrial metabol- ic rate measured by resazurine assay. Concomitantly D4MB-6 infection induced a 50-fold increase in GFAP transcripts at 24 P4 hpi with an evident raise in protein fluorescence intensity. We Detection of Human T-cell Lymphotropic Virus Type I could suggest that astrocytes cells are activated by the proteins in exosomes from HAM/TSP patient CSF by nov- neuroadapted virus, producing a response, leading to physio- el nanotrap technology or morphological nervous system damage. Future studies re- garding this topic should be conducted. Monique Anderson1, Benjamin Lepene2, Joan Ohayon1, Fatah Kashanchi3, Steven Jacobson1 (corresponding author: [email protected]) P3 HIV Infection and Immortalization of Freshly Isolated 1Neuroimmunology Branch, NINDS, NIH; Human Microglial Cells 2Ceres Nanosciences; 3National Center for Biodefense and Infectious Diseases, David Alvarez-Carbonell, Mary-Ann Checkley, Benjamin George Mason University Luttge, Jonathan Karn (corresponding author: [email protected]) There has been increasing evidence for the role of microvesicles (MV) in CNS inflammation and viral disease. Case Western Reserve University HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neuroinflammatory disease that affects a sub- During HAART, microglial cells become a reservoir of HIV in set of virus-infected infected individuals. This disorder is brain. However, reliable methodologies and cellular models to immunopathologically mediated since virus-specific immune study molecular events involved in HIV infection of microglia cells can be found in both the CSF and in the CNS of patients and in establishment/emergence of latency are practically non- although HTLV-I virus has been difficult to isolate in CNS existent. Fresh CNS cortical tissue from patients undergoing resident cells. The possibility of transfer of viral proteins via brain surgery was dissociated with the Neural Tissue MV from viral reservoirs to uninfected cells in the absence of Dissociation Kit (Miltenyi Biotec), and CD11b+cells cultured virus is an intriguing mechanism by which this might occur. for 5 days prior to infection with replication competent R5 Recently, HTLV-1 tax proteins have been shown in exosomes HIV (AD8gNef-GFP) particles. After virus removal, cells (EX), a type of MV,from HTLV-1 infected cell lines (Jaworski were insulted with Raltegravir, followed by treatment with et al., 2014). Therefore, we examined if similar MVs were TNF-alpha. Fixed/permeabilized cells were stained for actin present in the CNS of HAM/TSP patients, and if these MVs and nucleus, and Deltavision® pictures were taken to detect also carried HTLV-1 proteins and genes. Using a novel HIV expression (GFP), stained actin, and nuclei. Primary nanotrap (NT) technology, exosomes containing HTLV-1 tax microglial cells were also infected with VSVG SV40- were successfully isolated specifically from HTLV-1 infected puromycin virus by spinoculation to induce immortalization. cell lines. Moreover, CSF from HAM/TSP patients but not Transformed cells were infected with VSVG-GFP-HIVs, and from HTLV-1 seronegative multiple sclerosis (MS) patients, latency tested with TNF-alpha, LPS, or IL-1beta. The yield of also demonstrated exosomes that were HTLV-I tax positive by CD11b+cells from brain tissue was between 1,300 and 3,000 Western blot. These results suggest the possibility that HTLV- cells per mg. Observational analysis indicated that these cells 1 proteins present in virus-free CSF can be a potential source had a typical ramified morphology. Incubation with R5 HIVs of antigen in an inflammatory neuropathological disease. resulted in HIV expression 7 days post-viral exposure in a Given the implication that regulatory T cells (Tregs) fraction of cells. Exposure of primary microglia to SV40 virus and other immune subsets are prolific producers of resulted in cell expansion 6 to 8 weeks post-immortalization. exosomes (Okoye et al., 2014), we are investigating the pro- A CD11b+clonal population with ramified morphology was duction of MVs and exosomes in ex vivo culture of HAM/ infected with VSVG-GFP-HIVand monitored for HIVexpres- TSP peripheral blood mononuclear cells (PBMCs) and sion. Our initial studies indicate that HIV expression is in- virally-transduced normal donor (ND) PBMCs after the intro- duced in by typical pro-inflammatory stimuli. We show here duction of HTLV-1 genes. J. Neurovirol. (2015) 21 (Suppl 1):S1–S87 S3 P5 relation to neurocognitive impairment and CNS com- HIV-1 Tat genetic polymorphisms associated with partmentalization, which may contribute to the neurocognitive impairment impact NMDA receptor excitotoxicity of Tat and HIV-1 neuropathogenesis. docking This work is supported by R01 NS32092, R01 DA19807, P30 MH092177, T32 MH079785, and R01 Gregory Antell1,UriHershberg2, Sandhya Kortagere1, Vanessa NS089435. Pirrone1, William Dampier1, Gregory Schwartz2,Benjamas Aiamkitsumrit1, Jean Williams1, Shendra Passic1, Katherine Kercher1, Wen Zhong1, Jeffrey Jacobson3,BrianWigdahl1, P6 Michael Nonnemacher1 Plasma MicroRNA profiling predicts HIV-Associated (corresponding author: [email protected]) Neurocognitive Disorder 1Department of Microbiology and Immunology and Institute
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