DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells.

DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Research Abstract Details 

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DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Abstract Text:

Ikusuke Hatsukari,Priyanka Singh,Naoko Hitosugi,Davorka Messmer,Elsa Valderrama,Saul Teichberg,Wayne Chaung,Eleanore Gross,Helena Schmidtmayerova,Pravin C Singhal,

HIV-1 infection of renal cells has been proposed to play a role in HIV-1-associated nephropathy. Renal biopsy data further suggest that renal tubular cells may serve as reservoir for HIV-1. The mechanism by which HIV-1 enters these cells has not been identified. Renal tubular cells do not express any of the known HIV-1 receptors, and our results confirmed lack of the expression of CD4, CCR5, CXCR4, DC-SIGN, or mannose receptors in tubular cells. The aim of this study, therefore, was to determine the mechanism that enables viral entry into renal tubular cells. An in vitro model was used to study the HIV-1 infection of human kidney tubular (HK2) cells and to identify the receptor that enables the virus to enter these cells. Results of these studies demonstrate that the C-type lectin DEC-205 acts as an HIV-1 receptor in HK2 cells. Interaction of HIV-1 with DEC-205 results in the internalization of the virus and establishment of a nonproductive infection. HIV-1-specific strong-stop DNA is detected in the infected HK2 cells for at least 7 d, and the virus can be transmitted in trans to sensitive target cells. HIV-1 entry is blocked by pretreatment with specific anti-DEC-205 antibody. Moreover, expression of DEC-205 in cells that lack the DEC-205 receptors renders them susceptible to HIV-1 infection. These findings suggest that DEC-205 acts as an HIV-1 receptor that mediates internalization of the virus into renal tubular cells, from which the virus can be rescued and disseminated by encountering immune cells.

DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Publishing Authors By Initials

I Hatsukari,P Singh,N Hitosugi,D Messmer,E Valderrama,S Teichberg,W Chaung,E Gross,H Schmidtmayerova,PC Singhal,

For similar proteins: membrane proteins: receptors, cell surface research abstracts see: proteins: membrane proteins: receptors, cell surface research

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DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of the American Society of Nephrology : JA

VOLUME: 18

Page Numbers: 780-7

Journal Abbreviation: J. Am. Soc. Nephrol.

ISSN: 1046-6673

DAY: 7

MONTH: 02

YEAR: 2007

DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Information

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LANGUAGE: eng

NlmUniqueID: 9013836

DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Keywords Mesh Terms:

KEYWORDS: Receptors, Cell Surface

MESH TERMS: metabolism

Chemical & Substance for Abstract: DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells. Information

Substance Name: Receptors, Cell Surface

Registry Number: 0

Grant and Affiliation Information for DEC-205-mediated internalization of HIV-1 results in the establishment of silent infection in renal tubular cells.

AFFILIATION: Center for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA.

Country: United States

AGENCY: United States NIDA

GRANT: DA12111

ACRONYM: DA

MEDLINETA: J Am Soc Nephrol

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