title: HIV-1 and kidney cells: better understanding of viral interaction.
abstract: HIV-associated nephropathy (HIVAN) is the most common disease affecting untreated seropositive patients of African descent. Besides genetic (African descent) and HIV-1 infection (environmental), specific host factors such as activation of renin-angiotensin-aldosterone system (RAAS) have also been demonstrated to play a role in the manifestation of HIVAN. The recent identification of MYH9 as susceptible allele is a key step forward in our understanding for the pathogenesis of focal glomerulosclerosis in people of African-American descent. HIV-1 transgenic models have significantly advanced our knowledge base in terms of role of HIV-1 genes in general and individual gene in particular in the development of renal lesions mimicking HIVAN. These studies suggest that viral replication is not needed for the development of renal lesions. Renal biopsy data from HIVAN patients suggest that renal epithelial cells express HIV-1 genes and thus it may be sufficient to invoke HIVAN phenotype in the presence of specific host and genetic factors. On the other hand, immune response to infection may be required to induce HIV-1 associated immune complex kidney disease (HIVICK). Since renal cell lack conventional HIV-1 receptors, HIV-1 entry into renal cells has been a mystery. Recently, non-conventional pathways have been demonstrated to facilitate HIV-1 entry into renal cells in in vitro studies. These include presence of DEC-205 receptors in renal tubular cells and lipid rafts in podocytes. However, HIV-1 entry through these pathways only allows non-productive infection. It appears that the presence of specific genetic and host factors in in vivo conditions may be facilitating the development of the productive HIV-1 infection in kidney cells.
authors.affiliation: Feinstein Institute for Medical Research and Long Island Jewish Medical Center, New Hyde Park, NY, USA.
authors.forename: Joanna
authors.initials: J
authors.lastname: Mikulak
authors.forename: Pravin C
authors.initials: PC
authors.lastname: Singhal
mesh_terms: D016263:AIDS-Associated Nephropathy / Q000821:virology*; D001741:Black or African American; D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D001057:Apolipoproteins E / Q000502:physiology; D017209:Apoptosis; D002455:Cell Division; D002648:Child; D042783:Endothelial Cells / Q000821:virology; D004847:Epithelial Cells / Q000821:virology; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology / Q000473:pathology / Q000821:virology; D015497:HIV-1 / Q000502:physiology*; D054884:Host-Pathogen Interactions; D054298:Human Immunodeficiency Virus Proteins / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000166:cytology / Q000821:virology*; D007684:Kidney Tubules / Q000166:cytology / Q000821:virology; D037181:Lectins, C-Type / Q000502:physiology; D021962:Membrane Microdomains; D050527:Mesangial Cells / Q000821:virology; D051379:Mice; D008822:Mice, Transgenic; D015778:Minor Histocompatibility Antigens; D020409:Molecular Motor Proteins / Q000502:physiology; D018995:Myosin Heavy Chains / Q000502:physiology; D018384:Oxidative Stress; D050199:Podocytes / Q000473:pathology / Q000821:virology; D011956:Receptors, Cell Surface / Q000502:physiology; D014281:Trihexosylceramides / Q000502:physiology; D053586:Virus Internalization
chemical_list: D015703:Antigens, CD; D001057:Apolipoproteins E; C093569:DEC-205 receptor; D054298:Human Immunodeficiency Virus Proteins; D037181:Lectins, C-Type; C103814:MYH9 protein, human; D015778:Minor Histocompatibility Antigens; D020409:Molecular Motor Proteins; D011956:Receptors, Cell Surface; D014281:Trihexosylceramides; C018549:globotriaosylceramide; D018995:Myosin Heavy Chains
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