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Cited by 38HIV Research and TreatmentT-cell and Retrovirus StudiesHIV/AIDS drug development and treatment

Upregulation of human immunodeficiency virus-1 in chronically infected monocytic cell line by both contact with endothelial cells and cytokines

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Fan, ST, Hsia, K, Edgington, TS·1994·Blood
DOI 10.1182/blood.v84.5.1567.1567
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Abstract

Cells of monocytic lineage (Mo) persistently infected with human immunodeficiency virus (HIV) have been suspected to be a major reservoir for in vivo transmission of virus to susceptible target cells. Cellular events and mechanisms that upregulate viral gene expression in such cells are important issues. Because the traffic of such cells is central to biodistribution of HIV, we have explored the impact of interaction of endothelium with HIV-1-infected U1 promonocytic cells. Coculturing of U1 with human umbilical endothelial cells (HUVEC) for 24 to 72 hours in the absence of stimulation induced HIV-1 p24 biosynthesis significantly. Antibody-blocking experiments indicated that CD11/CD18 integrins play a role in upregulation of HIV expression elicited by interaction with HUVEC. Engagement of CD11b/CD18 by adherence of U1 to surfaces coated with either the cognate ligand fibrinogen or monoclonal antibody specific for CD11b/CD18 also enhanced p24 biosynthesis. Furthermore, endothelial cells were found to constitutively synthesize and secrete soluble factors that enhanced HIV- 1 synthesis. The enhancing factors, of estimated size 10 to 45 kD, were induced in HUVEC to high levels by monokines or by lipopolysaccharide, resulting in markedly enhanced HIV-1 expression by U1. These endothelial cell-derived HIV-1-enhancing factors consist of, among others, interleukin-6 (IL-6), IL-1 beta, and granulocyte-macrophage CSF (GM-CSF). Our results suggest that activation of HIV biosynthesis in infected Mo via interaction with endothelium may impact significantly on the tissue distribution and pathogenesis of HIV infections.

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  • Contacts with EC enhanced HIV-1 replication in infected monocytes and macrophages.

    “These findings corroborate in vitro studies on HIV, demonstrating that contacts with EC enhanced HIV-1 replication in infected monocytes and macrophages (39, 40).”

    From Equine Herpesvirus Type 1 Enhances Viral Replication in CD172a <sup>+</sup> Monocytic Cells upon Adhesion to Endothelial Cells (2015) · cites this paper as [39]

    The ‘Induction of HIV-I expression by endothelial cell’ section reports increased HIV-1 p24 production when infected U1 cells were cocultured with endothelial monolayers. The paper identifies U1 as a promonocytic cell line; it does not establish the same result in infected macrophages. (LLM, conf=0.86)

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Research works printed but not linked: 2

  1. [4]4. Wiley CA, Schrier RD, Nelson JA, Lampert PW, Oldstone MBA: Cellular localization of human immunodeficiency virus infec- tion within the brains of acquired immunodeficiency syndrome pa- tients. Proc Natl Acad Sci USA 83:7089, 1986
  2. [21]21. Ho MK, Springer TA: Biosynthesis and assembly of the 01 and p subunits of Mac-l, a macrophage glycoproteins associated with complement receptor function. J Biol Chem 258:2766, 1983

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Authors
Fan, S., Hsia, K., & Edgington, T.
Affiliations
Scripps Research Institute (US)
Venue
Blood
Publisher
American Society of Hematology
Published
1994-09-01
Volume
84
Issue
5
Pages
1567-1572
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
DOI
10.1182/blood.v84.5.1567.1567
OpenAlex
W268447036
Cited by
38
References
39
Citations by year
2020: 1 · 2015: 1
FWCI
1.60
Type
journal article
Language
en
Open access
Locations
  • Blood (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of California, San Diego
  • National Institute of Mental Health (MH47680, P50MH047680)
Topics
  • Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
  • Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
Keywords
HIV-1, human umbilical vein endothelial cells, CD11b/CD18 integrin, fibrinogen, monokines, lipopolysaccharide, interleukin-6, IL-1β, GM-CSF, HIV reservoir, HIV pathogenesis
MeSH terms
Antibodies, Monoclonal, Cell Line, Cells, Cultured, Endothelium, Vascular, Humans, Kinetics, Lipopolysaccharides, Monocytes, Time Factors, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Umbilical Veins, Virus Replication, HIV-1, Antigens, CD, Interleukin-6, Granulocyte-Macrophage Colony-Stimulating Factor, Cytokines, HIV Core Protein p24, CD18 Antigens, CD11 Antigens

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