Virus-cell membrane fusion does not predict efficient infection of alveolar macrophages by human immunodeficiency virus type 1 (HIV-1)

Mary Jane Potash, Michael Zeira, Zheng Bo Huang, Tillman E. Pearce, Edward Eden, Howard E. Gendelman, David J. Volsky

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Alveolar macrophages (AM) are the principal target cells for HIV-1 in lung tissue. To investigate the mechanisms of HIV-1 infection and efficient replication in these cells we isolated AM from 14 HIV-1 negative donors and exposed them to two virus isolates, either N1T, which replicates well in T lymphocytic and monocytic cell lines, or ADA, a monocytotropic virus. Membrane fluorescence dequenching assays demonstrated that HIV-1/NiT fuses efficiently with AM plasma membranes at neutral pH and that this interaction requires cellular CD4. Despite efficient fusion, AM from eight of 14 donors were not susceptible to productive infection with N1T. In contrast, ADA replicated in all AM populations tested. Soluble CD4 blocked infection of AM by either N1T or ADA, indicating that, like membrane fusion, entry of infectious virus requires an interaction with cellular CD4. Analysis of HIV-1 DNA accumulation in infected cells by enzymatic amplification revealed that productive infection by ADA correlated with a high HIV-1 DNA copy number and abortive infection by NiT was characterized by little or no stable cDNA. These studies suggest that the differences between the two HIV-1 strains studied in their ability to replicate in AM reside in phases of the virus life cycle that follow virus-cell fusion.

Original languageEnglish (US)
Pages (from-to)864-868
Number of pages5
JournalVirology
Volume188
Issue number2
DOIs
StatePublished - Jun 1992

Fingerprint

Virus Internalization
Cell Fusion
Alveolar Macrophages
HIV-1
Cell Membrane
Infection
Viruses
Membrane Fusion
DNA
Virus Diseases
Life Cycle Stages
Complementary DNA
Fluorescence
Cell Line
Lung
Membranes
Population

ASJC Scopus subject areas

  • Virology

Cite this

Virus-cell membrane fusion does not predict efficient infection of alveolar macrophages by human immunodeficiency virus type 1 (HIV-1). / Potash, Mary Jane; Zeira, Michael; Huang, Zheng Bo; Pearce, Tillman E.; Eden, Edward; Gendelman, Howard E.; Volsky, David J.

In: Virology, Vol. 188, No. 2, 06.1992, p. 864-868.

Research output: Contribution to journalArticle

Potash, Mary Jane ; Zeira, Michael ; Huang, Zheng Bo ; Pearce, Tillman E. ; Eden, Edward ; Gendelman, Howard E. ; Volsky, David J. / Virus-cell membrane fusion does not predict efficient infection of alveolar macrophages by human immunodeficiency virus type 1 (HIV-1). In: Virology. 1992 ; Vol. 188, No. 2. pp. 864-868.
@article{e0a86b87a4e546f5aa3221b8938fc5e8,
title = "Virus-cell membrane fusion does not predict efficient infection of alveolar macrophages by human immunodeficiency virus type 1 (HIV-1)",
abstract = "Alveolar macrophages (AM) are the principal target cells for HIV-1 in lung tissue. To investigate the mechanisms of HIV-1 infection and efficient replication in these cells we isolated AM from 14 HIV-1 negative donors and exposed them to two virus isolates, either N1T, which replicates well in T lymphocytic and monocytic cell lines, or ADA, a monocytotropic virus. Membrane fluorescence dequenching assays demonstrated that HIV-1/NiT fuses efficiently with AM plasma membranes at neutral pH and that this interaction requires cellular CD4. Despite efficient fusion, AM from eight of 14 donors were not susceptible to productive infection with N1T. In contrast, ADA replicated in all AM populations tested. Soluble CD4 blocked infection of AM by either N1T or ADA, indicating that, like membrane fusion, entry of infectious virus requires an interaction with cellular CD4. Analysis of HIV-1 DNA accumulation in infected cells by enzymatic amplification revealed that productive infection by ADA correlated with a high HIV-1 DNA copy number and abortive infection by NiT was characterized by little or no stable cDNA. These studies suggest that the differences between the two HIV-1 strains studied in their ability to replicate in AM reside in phases of the virus life cycle that follow virus-cell fusion.",
author = "Potash, {Mary Jane} and Michael Zeira and Huang, {Zheng Bo} and Pearce, {Tillman E.} and Edward Eden and Gendelman, {Howard E.} and Volsky, {David J.}",
year = "1992",
month = "6",
doi = "10.1016/0042-6822(92)90543-X",
language = "English (US)",
volume = "188",
pages = "864--868",
journal = "Virology",
issn = "0042-6822",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Virus-cell membrane fusion does not predict efficient infection of alveolar macrophages by human immunodeficiency virus type 1 (HIV-1)

AU - Potash, Mary Jane

AU - Zeira, Michael

AU - Huang, Zheng Bo

AU - Pearce, Tillman E.

AU - Eden, Edward

AU - Gendelman, Howard E.

AU - Volsky, David J.

PY - 1992/6

Y1 - 1992/6

N2 - Alveolar macrophages (AM) are the principal target cells for HIV-1 in lung tissue. To investigate the mechanisms of HIV-1 infection and efficient replication in these cells we isolated AM from 14 HIV-1 negative donors and exposed them to two virus isolates, either N1T, which replicates well in T lymphocytic and monocytic cell lines, or ADA, a monocytotropic virus. Membrane fluorescence dequenching assays demonstrated that HIV-1/NiT fuses efficiently with AM plasma membranes at neutral pH and that this interaction requires cellular CD4. Despite efficient fusion, AM from eight of 14 donors were not susceptible to productive infection with N1T. In contrast, ADA replicated in all AM populations tested. Soluble CD4 blocked infection of AM by either N1T or ADA, indicating that, like membrane fusion, entry of infectious virus requires an interaction with cellular CD4. Analysis of HIV-1 DNA accumulation in infected cells by enzymatic amplification revealed that productive infection by ADA correlated with a high HIV-1 DNA copy number and abortive infection by NiT was characterized by little or no stable cDNA. These studies suggest that the differences between the two HIV-1 strains studied in their ability to replicate in AM reside in phases of the virus life cycle that follow virus-cell fusion.

AB - Alveolar macrophages (AM) are the principal target cells for HIV-1 in lung tissue. To investigate the mechanisms of HIV-1 infection and efficient replication in these cells we isolated AM from 14 HIV-1 negative donors and exposed them to two virus isolates, either N1T, which replicates well in T lymphocytic and monocytic cell lines, or ADA, a monocytotropic virus. Membrane fluorescence dequenching assays demonstrated that HIV-1/NiT fuses efficiently with AM plasma membranes at neutral pH and that this interaction requires cellular CD4. Despite efficient fusion, AM from eight of 14 donors were not susceptible to productive infection with N1T. In contrast, ADA replicated in all AM populations tested. Soluble CD4 blocked infection of AM by either N1T or ADA, indicating that, like membrane fusion, entry of infectious virus requires an interaction with cellular CD4. Analysis of HIV-1 DNA accumulation in infected cells by enzymatic amplification revealed that productive infection by ADA correlated with a high HIV-1 DNA copy number and abortive infection by NiT was characterized by little or no stable cDNA. These studies suggest that the differences between the two HIV-1 strains studied in their ability to replicate in AM reside in phases of the virus life cycle that follow virus-cell fusion.

UR - http://www.scopus.com/inward/record.url?scp=0026772611&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026772611&partnerID=8YFLogxK

U2 - 10.1016/0042-6822(92)90543-X

DO - 10.1016/0042-6822(92)90543-X

M3 - Article

C2 - 1585653

AN - SCOPUS:0026772611

VL - 188

SP - 864

EP - 868

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -