About: Incorporation of podoplanin into HIV released from HEK-293T cells, but not PBMC, is required for efficient binding to the attachment factor CLEC-2

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About: Incorporation of podoplanin into HIV released from HEK-293T cells, but not PBMC, is required for efficient binding to the attachment factor CLEC-2 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Incorporation of podoplanin into HIV released from HEK-293T cells, but not PBMC, is required for efficient binding to the attachment factor CLEC-2
Creator	Bertram, Stephanie Pöhlmann, Stefan Simmons, Graham Glowacka, Ilona Steffen, Imke Chaipan, Chawaree Gerardy-Schahn, Rita Kato, Yukinari Münch, Jan Schmökel, Jan Tsegaye, Solomon
Source	Medline; PMC
abstract	BACKGROUND: Platelets are associated with HIV in the blood of infected individuals and might modulate viral dissemination, particularly if the virus is directly transmitted into the bloodstream. The C-type lectin DC-SIGN and the novel HIV attachment factor CLEC-2 are expressed by platelets and facilitate HIV transmission from platelets to T-cells. Here, we studied the molecular mechanisms behind CLEC-2-mediated HIV-1 transmission. RESULTS: Binding studies with soluble proteins indicated that CLEC-2, in contrast to DC-SIGN, does not recognize the viral envelope protein, but a cellular factor expressed on kidney-derived 293T cells. Subsequent analyses revealed that the cellular mucin-like membranous glycoprotein podoplanin, a CLEC-2 ligand, was expressed on 293T cells and incorporated into virions released from these cells. Knock-down of podoplanin in 293T cells by shRNA showed that virion incorporation of podoplanin was required for efficient CLEC-2-dependent HIV-1 interactions with cell lines and platelets. Flow cytometry revealed no evidence for podoplanin expression on viable T-cells and peripheral blood mononuclear cells (PBMC). Podoplanin was also not detected on HIV-1 infected T-cells. However, apoptotic bystander cells in HIV-1 infected cultures reacted with anti-podoplanin antibodies, and similar results were obtained upon induction of apoptosis in a cell line and in PBMCs suggesting an unexpected link between apoptosis and podoplanin expression. Despite the absence of detectable podoplanin expression, HIV-1 produced in PBMC was transmitted to T-cells in a CLEC-2-dependent manner, indicating that T-cells might express an as yet unidentified CLEC-2 ligand. CONCLUSIONS: Virion incorporation of podoplanin mediates CLEC-2 interactions of HIV-1 derived from 293T cells, while incorporation of a different cellular factor seems to be responsible for CLEC-2-dependent capture of PBMC-derived viruses. Furthermore, evidence was obtained that podoplanin expression is connected to apoptosis, a finding that deserves further investigation.
has issue date	2010-05-19(xsd:dateTime)
bibo:doi	10.1186/1742-4690-7-47
bibo:pmid	20482880
has license	cc-by
sha1sum (hex)	a5f1fd1f2782b89068dd76bde0acbffc35632895
schema:url	https://doi.org/10.1186/1742-4690-7-47
resource representing a document's title	Incorporation of podoplanin into HIV released from HEK-293T cells, but not PBMC, is required for efficient binding to the attachment factor CLEC-2
has PubMed Central identifier	PMC2885308
has PubMed identifier	20482880
schema:publication	Retrovirology
resource representing a document's body	covid:a5f1fd1f2782b89068dd76bde0acbffc35632895#body_text
is schema:about of	named entity 'PBMC' named entity 'infected' named entity 'individuals' named entity 'HIV' named entity 'ATTACHMENT' named entity 'HIV' named entity 'TRANSMISSION' named entity 'ATTACHMENT' named entity 'PLATELETS' named entity 'MOLECULAR' named entity 'MECHANISMS' named entity 'EXPRESSED' named entity 'MEDIATED' named entity 'VIRUS' named entity 'TRANSMITTED' named entity 'T-CELLS' named entity 'FACTOR' named entity 'MODULATE' named entity 'VIRAL' named entity 'BACKGROUND' named entity 'BLOOD' named entity 'RELEASED' named entity 'BUT' named entity 'CLEC-2' named entity 'OPEN' named entity 'EFFICIENT' named entity 'RESEARCH' named entity 'REQUIRED' named entity 'BINDING' named entity 'PODOPLANIN' named entity '293T CELLS' named entity 'NOVEL' named entity 'HERE' named entity 'INFECTED' named entity 'ASSOCIATED WITH' named entity 'BLOODSTREAM' named entity 'DIRECTLY' named entity 'HIV' named entity 'LECTIN' named entity 'ACCESS' named entity 'INDIVIDUALS' named entity 'HEK' named entity 'FACTOR' named entity 'TYPE' named entity 'CLEC-2' named entity 'HIV-1' named entity 'DC-SIGN' named entity 'DISSEMINATION' covid:arg/a5f1fd1f2782b89068dd76bde0acbffc35632895 named entity 'viral' named entity 'modulate' named entity 'HIV' named entity 'T-cells' named entity 'efficient' named entity 'Platelets' named entity 'virus' named entity 'C-type lectin' named entity '293T cells' named entity 'HIV' named entity 'flow cytometry' named entity 'antibodies' named entity 'CLEC-2' named entity 'viruses' named entity 'transfected' named entity 'Env' named entity 'HIV-1' named entity 'T/B cell' named entity 'antibiotics' named entity 'amyloidogenic' named entity 'ligand' named entity 'DC-SIGN'

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