R5 HIV Productively Infects Langerhans Cells, and Infection Levels Are Regulated by Compound CCR5 Polymorphisms

Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4+T cells were both found to depend on CCR5. By contrast, infection of mon...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 100; no. 14; pp. 8401 - 8406
Main Authors Kawamura, Tatsuyoshi, Gulden, Forrest O., Sugaya, Makoto, McNamara, David T., Borris, Debra L., Lederman, Michael M., Orenstein, Jan M., Zimmerman, Peter A., Blauvelt, Andrew
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 08.07.2003
National Acad Sciences
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Abstract Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4+T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4+T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORFΔ 32 revealed that LCs isolated from ORFΔ 32/wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt/wt individuals (P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORFΔ 32/wt heterozygous individuals revealed that LCs isolated from -2459A/G + ORFΔ 32/wt individuals were markedly less susceptible to HIV than were LCs from -2459A/A + ORFΔ 32/wt individuals (P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
AbstractList Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4+ T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4+ T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORF Delta 32 revealed that LCs isolated from ORF Delta 32/wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt/wt individuals (P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORF Delta 32/wt heterozygous individuals revealed that LCs isolated from -2459A/G + ORF Delta 32/wt individuals were markedly less susceptible to HIV than were LCs from -2459A/A + ORF Delta 32/wt individuals (P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4 + T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4 + T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORF Δ 32 revealed that LCs isolated from ORF Δ 32 / wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt / wt individuals ( P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORF Δ 32 / wt heterozygous individuals revealed that LCs isolated from - 2459A / G + ORF Δ 32 / wt individuals were markedly less susceptible to HIV than were LCs from - 2459A / A + ORF Δ 32 / wt individuals ( P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4 + T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4 + T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORF Δ 32 revealed that LCs isolated from ORF Δ 32 / wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt / wt individuals ( P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORF Δ 32 / wt heterozygous individuals revealed that LCs isolated from - 2459A / G + ORF Δ 32 / wt individuals were markedly less susceptible to HIV than were LCs from - 2459A / A + ORF Δ 32 / wt individuals ( P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4+ T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4+ T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORF32 revealed that LCs isolated from ORF32/wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt/wt individuals (P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORF32/wt heterozygous individuals revealed that LCs isolated from -2459A/G + ORF32/wt individuals were markedly less susceptible to HIV than were LCs from -2459A/A + ORF32/wt individuals (P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4+T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4+T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORFΔ 32 revealed that LCs isolated from ORFΔ 32/wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt/wt individuals (P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORFΔ 32/wt heterozygous individuals revealed that LCs isolated from -2459A/G + ORFΔ 32/wt individuals were markedly less susceptible to HIV than were LCs from -2459A/A + ORFΔ 32/wt individuals (P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4 + T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4 + T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORF Δ 32 revealed that LCs isolated from ORF Δ 32 / wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt / wt individuals ( P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORF Δ 32 / wt heterozygous individuals revealed that LCs isolated from - 2459A / G + ORF Δ 32 / wt individuals were markedly less susceptible to HIV than were LCs from - 2459A / A + ORF Δ 32 / wt individuals ( P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV infection of LC ex vivo and LC-mediated transmission of virus to CD4 super(+) T cells were both found to depend on CCR5. By contrast, infection of monocyte-derived dendritic cells and transfer of infection from monocyte-derived dendritic cells to CD4 super(+) T cells were mediated by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways. Furthermore, in 62 healthy individuals, R5 HIV infection levels in LCs ex vivo were associated with CCR5 genotype. Specifically, genotyping for ORF[Delta]32 revealed that LCs isolated from ORF[Delta]32/wt individuals were significantly less susceptible to HIV when compared with LCs isolated from ORFwt/wt individuals (P = 0.016). Strikingly, further genetic analyses of the A-2459G CCR5 promoter polymorphism in ORF[Delta]32/wt heterozygous individuals revealed that LCs isolated from -2459A/G + ORF[Delta]32/wt individuals were markedly less susceptible to HIV than were LCs from -2459A/A + ORF[Delta]32/wt individuals (P = 0.012). Interestingly, these genetic susceptibility data in LCs parallel those of genetic susceptibility studies performed in cohorts of HIV-infected individuals. Thus, we suggest that CCR5-mediated infection of LCs, and not capture of virus by LCs, provides a biologic basis for understanding certain aspects of host genetic susceptibility to initial HIV infection.
Author Kawamura, Tatsuyoshi
Gulden, Forrest O.
Sugaya, Makoto
Blauvelt, Andrew
Lederman, Michael M.
Zimmerman, Peter A.
Borris, Debra L.
Orenstein, Jan M.
McNamara, David T.
AuthorAffiliation Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-1908; † Department of Medicine, Center for AIDS Research, Case Western Reserve University and University Hospitals, Cleveland, OH 44195; and ‡ Department of Pathology, George Washington University, Washington, DC 20037
AuthorAffiliation_xml – name: Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-1908; † Department of Medicine, Center for AIDS Research, Case Western Reserve University and University Hospitals, Cleveland, OH 44195; and ‡ Department of Pathology, George Washington University, Washington, DC 20037
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  surname: Kawamura
  fullname: Kawamura, Tatsuyoshi
– sequence: 2
  givenname: Forrest O.
  surname: Gulden
  fullname: Gulden, Forrest O.
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  givenname: Makoto
  surname: Sugaya
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/12815099$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
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Copyright National Academy of Sciences Jul 8, 2003
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Communicated by Frederick C. Robbins, Case Western Reserve University, Cleveland, OH, April 24, 2003
Abbreviations: LC, Langerhans cell; DC, dendritic cell; mDC, monocyte-derived DC; DC-SIGN, DC-specific ICAM-3-grabbing nonintegrin; SNP, single-nucleotide polymorphism; AZT, 3′-azido-3′-deoxythymidine; RANTES, regulated on activation normal T cell expressed and secreted.
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Snippet Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV...
Langerhans cells (LCs) are suspected to be initial targets for HIV after sexual exposure (by becoming infected or by capturing virus). Here, productive R5 HIV...
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SubjectTerms Alleles
Antibodies, Monoclonal - pharmacology
Biological Sciences
CCR5 Receptor Antagonists
CD4 Antigens - physiology
CD4-Positive T-Lymphocytes - virology
Cell Adhesion Molecules - physiology
Cellular biology
Chemokine CCL5 - physiology
Dendritic Cells - virology
Endocytosis
Epithelial Cells - virology
Female
Genetic Predisposition to Disease
Genotype
Genotypes
Heterocyclic Compounds - pharmacology
HIV
HIV - physiology
HIV infections
HIV Infections - genetics
Human immunodeficiency virus
Humans
Infections
Langerhans Cells - physiology
Langerhans Cells - virology
Lectins, C-Type - physiology
Male
Mannans
Open Reading Frames - genetics
Polymorphism, Genetic
Reagents
Receptors, CCR5 - genetics
Receptors, CCR5 - physiology
Receptors, Cell Surface - physiology
Receptors, CXCR4 - antagonists & inhibitors
Sequence Deletion
T lymphocytes
Virus Replication
Viruses
Volunteerism
Title R5 HIV Productively Infects Langerhans Cells, and Infection Levels Are Regulated by Compound CCR5 Polymorphisms
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http://www.pnas.org/content/100/14/8401.abstract
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