Shedding and Interspecies Type Sero-reactivity of the Envelope Glycopolypeptide gp120 of the Human Immunodeficiency Virus

Schneider, Josef; Kaaden, Oskar‐Rüger; Copeland, Terry D.; Oroszlan, Stephen; Hunsmann, Gerhard

doi:10.1099/0022-1317-67-11-2533

Cited by 176 publications

(95 citation statements)

References 32 publications

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“…This effect has mostly been shown in vitro using relatively high concentrations of gp120, which leads to the question whether these effects might similarly operate in an in vivo scenario. Gp120 can be shed from the virion or from infected cells (18,19) and is detectable in the plasma of HIV-1 patients, albeit there is some uncertainty about the actual gp120 concentrations (48). Levels in the plasma, however, might be much lower compared with those in lymphoid tissues where gp120 is thought to accumulate (23,24).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, the extent of qualitative (14) and quantitative (5,15) defects within the CD4 + T cell population in HIV-1-infected individuals is disproportionally high in comparison with the levels of infectious virus and productively infected cells (16,17), arguing against the fact that CD4 + T cell-directed viral cytopathicity is the major contributor to disease progression. However, HIV-1 replication, which is fundamental to disease progression, is not only associated with virion-associated envelope glycoprotein but also with soluble gp120 and gp160 due to shedding from the virus or from infected cells (18,19). Consequently, soluble gp120 is present in the plasma (20)(21)(22) or lymphoid tissues of HIV + patients (23,24), and together with the appearance of dysfunctional CD4 + T cells, it is conceivable that binding of soluble gp120 to CD4 + T cells may be a central parameter in HIV-1 pathogenesis that could at least partially explain the high proportion of dysfunctional CD4 + T cells.…”

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confidence: 99%

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The Orientation of HIV-1 gp120 Binding to the CD4 Receptor Differentially Modulates CD4+ T Cell Activation

Zimmermann

Liechti

Haas

et al. 2015

The Journal of Immunology

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Progressive quantitative and qualitative decline of CD4+ T cell responses is one hallmark of HIV-1 infection and likely depends on several factors, including a possible contribution by the HIV-1 envelope glycoprotein gp120, which binds with high affinity to the CD4 receptor. Besides virion-associated and cell-expressed gp120, considerable amounts of soluble gp120 are found in plasma or lymphoid tissue, predominantly in the form of gp120–anti-gp120 immune complexes (ICs). Because the functional consequences of gp120 binding to CD4+ T cells are controversially discussed, we investigated how gp120 affects TCR-mediated activation of human CD4+ T cells by agonistic anti-CD3 mAb or by HLA class II–presented peptide Ags. We show that the spatial orientation of gp120–CD4 receptor binding relative to the site of TCR engagement differentially affects TCR signaling efficiency and hence CD4+ T cell activation. Whereas spatially and temporally linked CD4 and TCR triggering at a defined site promotes CD4+ T cell activation by exceeding local thresholds for signaling propagation, CD4 receptor engagement by gp120-containing ICs all around the CD4+ T cell undermine its capacity in supporting proximal TCR signaling. In vitro, gp120 ICs are efficiently captured by CD4+ T cells and thereby render them hyporesponsive to TCR stimulation. Consistent with these in vitro results we show that CD4+ T cells isolated from HIV+ individuals are covered with ICs, which at least partially contain gp120, and suggest that IC binding to CD4 receptors might contribute to the progressive decline of CD4+ T cell function during HIV-1 infection.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The Orientation of HIV-1 gp120 Binding to the CD4 Receptor Differentially Modulates CD4+ T Cell Activation

Zimmermann

Liechti

Haas

et al. 2015

The Journal of Immunology

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“…Lecatsas et al (1986) also examined unfixed preparations and found spike-free particles with an elongated nucleoid similar to those seen in the present study. The loss of spikes from mature HIV has been reported by Schneider et al (1986) andGelderblom et al (1987).…”

Section: Negative Staining Temmentioning

confidence: 99%

Electron Microscopy of Human Immunodeficiency Virus

Hockley¹,

Wood²,

Jacobs

et al. 1988

Journal of General Virology

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SUMMARYTwo cell lines of human T lymphocytes (H9 and CEM) chronically infected with isolates of human or simian immunodeficiency viruses were examined by electron microscopy. Scanning electron microscopy of H9 cells showed characteristic morphological changes in the cells after infection with human T cell lymphotropic virus type III (HTLV-IIIB); these included loss of cell microvilli and their replacement by rounded surface protrusions. Virus particles were present over the whole cell surface, but were more numerous between, rather than on, surface protrusions. In contrast, CEM cells infected with three other isolates of the virus showed little change in morphology compared with uninfected cells; they typically had a single large aggregate of virus particles at the posterior end of the cell. Transmission electron microscopy of sections of infected cells showed budding virus in only a small proportion of cells although many had mature virus particles on their surface. The immature particles released by budding had a ring-like morphology in contrast to the mature virus with its characteristic elongated nucleoid. Surface spikes were rarely seen on sectioned virus particles, but were more obvious on the simian immunodeficiency virus than on human isolates. Negative staining of purified virus preparations showed that the peripheral dense material of immature particles had a striated structure. Surface spikes were not seen by negative staining on either immature or mature virus particles. A third type of smaller particle with surface spikes was found in all negatively stained preparations.

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“…2B). This is due to the fact that gp120 being associated non-covalently with gp41 becomes readily shed off the HIV particles during manipulation (35,36), particularly during washing virus particles by centrifugation. In our experimental procedures, there were 12 steps of centrifugation of HIV-infected cells before processing for electron microscopy.…”

Section: Several Componentsmentioning

confidence: 99%

The Anti-HIV Pentameric Pseudopeptide HB-19 Binds the C-terminal End of Nucleolin and Prevents Anchorage of Virus Particles in the Plasma Membrane of Target Cells

Nisole¹,

Said²,

Mische³

et al. 2002

Journal of Biological Chemistry

101

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Shedding and Interspecies Type Sero-reactivity of the Envelope Glycopolypeptide gp120 of the Human Immunodeficiency Virus

Cited by 176 publications

References 32 publications

The Orientation of HIV-1 gp120 Binding to the CD4 Receptor Differentially Modulates CD4+ T Cell Activation

The Orientation of HIV-1 gp120 Binding to the CD4 Receptor Differentially Modulates CD4+ T Cell Activation

Electron Microscopy of Human Immunodeficiency Virus

The Anti-HIV Pentameric Pseudopeptide HB-19 Binds the C-terminal End of Nucleolin and Prevents Anchorage of Virus Particles in the Plasma Membrane of Target Cells

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