HIV receptors within the brain: A study of CD4 and MHC-II on human neurons, astrocytes and microglial cells

Peudenier, Sylviane; Héry, Christiane; Ng, Kim Heng; Tardieu, Marc

doi:10.1016/0923-2516(91)90051-4

Cited by 56 publications

(28 citation statements)

References 8 publications

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“…Further, these experiments clarify the importance of amino acid differences between the nonneurovirulent SIVmac239 and the neurovirulent SIV/17E-Fr in Env and Nef that are characteristic of the neurovirulent phenotype (1,28,47). Specifically, these results strongly suggest that key residues within the TM portion of Env are required for CD4-independent Env protein function that in turn is necessary for the efficient infection of CNS cells, such as astrocytes, that express extremely low levels of CD4 (38). Treatment of virus with sCD4 prior to infection of astrocytes greatly enhanced the replicative capacity of the molecular clones containing full-length cytoplasmic tails of TM, while clones expressing truncated TM proteins were only slightly enhanced by sCD4.…”

Section: Discussionmentioning

confidence: 89%

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CD4-Independent Entry and Replication of Simian Immunodeficiency Virus in Primary Rhesus Macaque Astrocytes Are Regulated by the Transmembrane Protein

Overholser

Babas

Zink

et al. 2005

J Virol

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Previous studies have demonstrated that the genetic determinants of simian immunodeficiency virus (SIV) neurovirulence map to the env and nef genes. Recent studies from our laboratory demonstrated that SIV replication in primary rhesus macaque astrocyte cultures is dependent upon the nef gene. Here, we demonstrate that macrophage tropism is not sufficient for replication in astrocytes and that specific amino acids in the transmembrane (TM) portion of Env are also important for optimal SIV replication in astrocytes. Specifically, a Gly at amino acid position 751 and truncation of the cytoplasmic tail of TM are required for efficient replication in these cells. Studies using soluble CD4 demonstrated that these changes within the TM protein regulate CD4-independent, CCR5-dependent entry of virus into astrocytes. In addition, we observed that two distinct CD4-independent, neuroinvasive strains of SIV/DeltaB670 also replicated efficiently in astrocytes, further supporting the role of CD4 independence as an important determinant of SIV infection of astrocytes in vitro and in vivo.

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Section: Discussionmentioning

confidence: 89%

“…CD4 is expressed at relatively low levels in cells of the CNS (38); thus, viruses with reduced dependence on CD4 likely have a selective advantage for replication in the brain. Notably, SIV/17E-Fr, in addition to being reproducibly neurovirulent, infects cells via a CD4-independent mechanism in vitro (14,28,40,47).…”

mentioning

confidence: 99%

CD4-Independent Entry and Replication of Simian Immunodeficiency Virus in Primary Rhesus Macaque Astrocytes Are Regulated by the Transmembrane Protein

Overholser

Babas

Zink

et al. 2005

J Virol

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“…It has been proposed that galactosylceramide or its derivative may play a role as a receptor for the binding of HIV-1 to neuronal cells, whereas the CD4 antigen is the receptor for the binding of virus to reticuloendothelial cells (Bhat et al, 1991 ;Parmantier et al, 1995 ;Peudenier et al, 1991). Since proteoglycans are complex and structurally diverse, it is possible that for HSV either a different family of GAGs might mediate virus binding to neurons or the structural sequences within the GAG might differ for neuronal cells compared to epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells.

Immergluck

Domowicz

Schwartz

et al. 1998

Journal of General Virology

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Herpes simplex virus (HSV) causes many disease states including mucosal lesions, encephalitis or disseminated infection in the immunocompromised host. These diverse clinical manifestations reflect the capacity of the virus to infect both epithelial and neuronal cell types. Determining the requirements for virus entry into both cell types may provide insights into the pathogenesis of HSV. Previous studies have focused on identifying viral and cellular requirements for entry using epithelial cells. However, little is known about the requirements for binding and entry into neuronal cells. The purpose of the studies reported here was to identify viral and cellular components involved in entry of HSV-1 into primary neuronal cells. Heparan sulfate glycosaminoglycans were found to serve as a receptor for entry of HSV-1 into primary neuronal cells. Evidence

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“…on May 10, 2018 by guest http://jvi.asm.org/ neurons was not detected by a luciferase assay (data not shown), likely because of the absence of CD4 on these cells (26,65,83). To determine if the neurotoxicity induced by these recombinant virus strains was mediated through CCR5, CXCR4, or other chemokine receptors, LAN-2 cells (for the direct neurotoxicity assay) and primary human macrophages (for the indirect neurotoxicity assay) were pretreated with anti-CCR5 or anti-CXCR4 antibodies or the G-protein-coupled receptor inhibitor PTX before virus infection and subsequent neurotoxicity was investigated with assays of total (Fig.…”

Section: Vol 77 2003 Hiv-1 Envelope-mediated Neuronal Death 6905mentioning

confidence: 97%

Human Immunodeficiency Virus Type 1 Envelope-Mediated Neuronal Death: Uncoupling of Viral Replication and Neurotoxicity

Zhang

Rana

Silva³

et al. 2003

J Virol

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HIV receptors within the brain: A study of CD4 and MHC-II on human neurons, astrocytes and microglial cells

Cited by 56 publications

References 8 publications

CD4-Independent Entry and Replication of Simian Immunodeficiency Virus in Primary Rhesus Macaque Astrocytes Are Regulated by the Transmembrane Protein

CD4-Independent Entry and Replication of Simian Immunodeficiency Virus in Primary Rhesus Macaque Astrocytes Are Regulated by the Transmembrane Protein

Viral and cellular requirements for entry of herpes simplex virus type 1 into primary neuronal cells.

Human Immunodeficiency Virus Type 1 Envelope-Mediated Neuronal Death: Uncoupling of Viral Replication and Neurotoxicity

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