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Article: DC-specific ICAM-3-grabbing nonintegrin mediates internalization of HIV-1 into human podocytes

TitleDC-specific ICAM-3-grabbing nonintegrin mediates internalization of HIV-1 into human podocytes
Authors
Issue Date2010
Citation
American Journal of Physiology - Renal Physiology, 2010, v. 299 n. 3, p. F664-F673 How to Cite?
AbstractHuman immunodeficiency virus (HIV)-1 has been demonstrated to contribute to the pathogenesis of HIV-associated nephropathy. In renal biopsy studies, podocytes have been reported to be infected by HIV-1. However, the mechanism involved in HIV-1 internalization into podocytes is not clear. In the present study, we evaluated the occurrence of HIV-1 internalization into conditionally immortalized human podocytes and the mechanism involved. Human podocytes rapidly internalized R5 and X4 HIV-1 primary strains via an endocytosis-dependent pathway, without establishing a productive infection. The HIV-1 internalization was dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) receptor mediated. The role of DC-SIGN was confirmed by using specific blocking antibodies and transfection with small interfering (si) RNA/ DC-SIGN. Since podocyte HIV-1 trafficking was not altered by pH-modulating agents, it appeared that HIV-1 routing occurred through nonacid vesicular compartments. Interestingly, transfection of podocytes with neither siRNA/caveolin-1 nor siRNA/clathrin heavy chain inhibited podocyte viral accumulation. Thus it appears that clathrin-coated vesicles and caveosomes may not be contributing to HIV-1-associated membrane traffic. DC-SIGN; DEC 205; HIV-1 receptor; HIV-associated nephropathy Copyright © 2010 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/195489
ISSN
2008 Impact Factor: 3.89
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMikulak, J-
dc.contributor.authorTeichberg, S-
dc.contributor.authorArora, S-
dc.contributor.authorKumar, D-
dc.contributor.authorYadav, A-
dc.contributor.authorSalhan, D-
dc.contributor.authorPullagura, S-
dc.contributor.authorMathieson, PW-
dc.contributor.authorSaleem, MA-
dc.contributor.authorSinghal, PC-
dc.date.accessioned2014-02-28T06:12:14Z-
dc.date.available2014-02-28T06:12:14Z-
dc.date.issued2010-
dc.identifier.citationAmerican Journal of Physiology - Renal Physiology, 2010, v. 299 n. 3, p. F664-F673-
dc.identifier.issn0363-6127-
dc.identifier.urihttp://hdl.handle.net/10722/195489-
dc.description.abstractHuman immunodeficiency virus (HIV)-1 has been demonstrated to contribute to the pathogenesis of HIV-associated nephropathy. In renal biopsy studies, podocytes have been reported to be infected by HIV-1. However, the mechanism involved in HIV-1 internalization into podocytes is not clear. In the present study, we evaluated the occurrence of HIV-1 internalization into conditionally immortalized human podocytes and the mechanism involved. Human podocytes rapidly internalized R5 and X4 HIV-1 primary strains via an endocytosis-dependent pathway, without establishing a productive infection. The HIV-1 internalization was dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) receptor mediated. The role of DC-SIGN was confirmed by using specific blocking antibodies and transfection with small interfering (si) RNA/ DC-SIGN. Since podocyte HIV-1 trafficking was not altered by pH-modulating agents, it appeared that HIV-1 routing occurred through nonacid vesicular compartments. Interestingly, transfection of podocytes with neither siRNA/caveolin-1 nor siRNA/clathrin heavy chain inhibited podocyte viral accumulation. Thus it appears that clathrin-coated vesicles and caveosomes may not be contributing to HIV-1-associated membrane traffic. DC-SIGN; DEC 205; HIV-1 receptor; HIV-associated nephropathy Copyright © 2010 the American Physiological Society.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Renal Physiology-
dc.titleDC-specific ICAM-3-grabbing nonintegrin mediates internalization of HIV-1 into human podocytes-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajprenal.00629.2009-
dc.identifier.pmid20630938-
dc.identifier.scopuseid_2-s2.0-77956456793-
dc.identifier.volume299-
dc.identifier.issue3-
dc.identifier.spageF664-
dc.identifier.epageF673-
dc.identifier.isiWOS:000281537700020-

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