IAS 2007 - Immune Activation in HIV Pathogenesis

Immune Activation in HIV Pathogenesis

MOAA1

Type:

Oral abstract session

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Venue:

Parkside Ballroom B

Time:

11:00 - 12:30, Monday, 23.07.2007

Code:

MOAA1

Co-Chairs:

Susan Plaeger, United States
Patricia Price, Australia

Presentations in this session:
11:00
MOAA101
Abstract
Powerpoint (646 KB) Persistent HIV-1 infection in duodenal mucosa and memory CD8+ T cell differentiation
Presented by Liliana Belmonte, Argentina
Belmonte L.¹, Zalar A.², Bare P.³, Badano N.¹, Araya V.², Piskorz E.², Figueroa M.I.⁴, Parodi C.¹, Ruibal-Ares B.¹, Cahn P.⁴, de Bracco M.M.¹
¹Academia Nacional de Medicina, Immunology, Buenos Aires, Argentina, ²Hospital Juan A Fernandez, Gastroenterology, Buenos Aires, Argentina, ³Academia Nacional de Medicina, Virology, Buenos Aires, Argentina, ⁴Hospital Juan A Fernandez, Infectology, Buenos Aires, Argentina

11:15
MOAA102
Abstract Regulatory T cells in infant macaques suppress anti-SIV responses among CD4+ T cells
Hartigan-OConnor D.¹, Abel K.², McCune J.M.¹
¹University of California, Division of Experimental Medicine, San Francisco, United States, ²University of California, California National Primate Research Center, Davis, United States

11:30
MOAA103
Abstract HIV-1 Nef is a critical regulator of PD-1 upregulation during HIV-1 infection
Presented by Karuppiah Muthumani, United States
Muthumani K.¹, Choo A.Y.², Sundaram S.G.¹, Laddy D.J.¹, Hokey D.A.¹, Kutzler M.A.¹, Weiner D.B.¹
¹University of Pennsylvania School of Medicine, Pathology and Lab. Medicine, Philadelphia, PA, United States, ²Harvard Medical School, Department of Cell Biology, Boston, United States

11:45
MOAA104
Abstract Increased viral set point following IL-15 treatment of acute SIV infection
Presented by Peter Katsikis, United States
Katsikis P.¹, Mueller Y.¹, Do D.¹, Altork S.¹, Katsetos C.¹, Legido A.¹, Villinger F.², Altman J.¹, Lewis M.³
¹Drexel University College of Medicine, Philadelphia, United States, ²Emory University School of Medicine, Atlanta, United States, ³BIOQUAL, Rockville, United States

12:00
MOAA105
Abstract
Powerpoint (1.35 MB) GBV-C infection is associated with less T cell activation in recently HIV-1-infected subjects and is independent of HIV-1 viral load
Presented by Maria Teresa Maidana Giret, Brazil
Maidana Giret M.T.¹, Silva T.M.¹, Levi J.E.², Bassichetto K.C.³, Ana N.⁴, Sabino E.⁴, Palácios R.¹, Kallás E.G.¹
¹Federal University of São Paulo, Medicine, São Paulo, Brazil, ²Institute of Tropical Diseases of São Paulo, São Paulo, Brazil, ³Public Health Department of São Paulo, São Paulo, Brazil, ⁴Blood Center of São Paulo, São Paulo, Brazil

12:15
MOAA1LB
Abstract
Powerpoint (2.5 MB) Naïve CD4+ T cell homeostasis during HIV infection
Presented by Tammy M. Rickabaugh
Rickabaugh T.M.¹, Kilpatrick R.², Fauce S.R.³, Hultin L.¹, Hultin P.¹, Hausner M.A.¹, Effros R.B.³, Detels R.², Phair J.⁴, Jamieson B.D.¹
¹University of California, David Geffen School of Medicine, Los Angeles, United States, ²University of California, School of Public Health, Los Angeles, United States, ³University of California, Department of Pathology and Laboratory Medicine, Los Angeles, United States, ⁴Northwestern University, Feinberg School of Medicine, Chicago, United States

Audio files:

audio file - high quality (mp3 format, 80.4 MB)
audio file - low quality (mp3 format, 20.1 MB)

Rapporteur report

Track A: HIV Basic Science report by John Zaunders
Following on from Michael Lederman's plenary, studies presented in this session examine factors that contribute and prevent immune activation in HIV infected individuals.

Belmonte et al studied the phenotype of CD8+ T cells in duodenal mucosa. There was an increased proportion of late differentiated CD27-CD28- CD8+ T cells, but this was not related to whether there were detectable p24+ infected cells in the biopsies. In fact, CD4+ T cells were greatly depleted and infected cells were CD64+ and CD68+ mature macrophages. These cells may be a critical HAART-resistant reservoir of HIV-1.

Hartigan-O’Connore et al studied SIV primary infection in infant rhesus macaques, which have twice as many suppressive T regulatory CD4+ T cells (Tregs) as adults. Infant macaques only have a transient CD8+ T cell response to SIV. In vitro, the Tregs appeared to act on other IL-2 and IFN-gamma producing CD4+ T cells, which may in turn lead to sub-optimal CD8 responses.

Muthuman et al studied the effect of HIV nef protein on T cell PD-1 expression which is associated with “exhausted” CD8+ T cells in chronic viral infections. This appearance of PD-1 may be regulated by extracellular nef protein via activation of the MAP kinase p38. Nef-mediated induction of PD-1 in vitro was reversed by deletion of the SH3 domain motif PxxP in nef, and was also reduced by inhibition of p38 activation by siRNA or specific inhibitors. In patients, circulating soluble nef levels and the activated phosphorylated state of p38 were highly correlated with PD-1 expression on CD8+ T cells.

Katsikis et al studied treatment of SIV-infected rhesus macaques with the cytokine IL-15, which has been shown to prevent apoptosis of antiviral CD8+ T cells in vitro. Rhesus macaques were treated with IL-15, which led to a doubling of SIV-specific CD8+ T cells. However, there was a 1,000-fold increase in the set point plasma viral load in the treated animals, and 2 out of 6 animals progressed to simian AIDS within 25 weeks. IL-15 treatment rapidly increased the Ki-67+ subset of CD4+ T cells, probably increasing susceptibility to infection and hastening CD4 decline.

Giret et al studied immune activation levels of T cells in recently HIV-infected subjects, with and without GBV-C co-infection. GBV-C infected subjects had significantly lower CD38 expression, and also significantly lower expression of CCR5, on both CD4+ and CD8+ T cells, independently of HIV viral loads and CD4 cell counts. This may lead to a protection against HIV progression afforded by GBV-C co-infection.

Rickabaugh et al studied the subdivision of naïve CD4+ T cells into a less-differentiated, more recent thymic emigrant CD31+ phenotype, and a more differentiated CD31- phenotype. HIV-infected subjects had decreased numbers of both subsets of naïve CD4+ T cells, such that they were comparable to subjects who were 30 years older. Similarly, telomere lengths in these cells were much shorter, again suggesting premature aging of the immune system. HAART treatment led to increases in the CD31+, but not the CD31- subset. The latter subset is maintained in older subjects, and low CD31 naïve cells may impair full immune reconstitution.

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