Inhibition of HIV-1 replication in alveolar macrophages by adenovirus gene transfer vectors. Academic Article uri icon

Overview

MeSH

  • Flow Cytometry
  • Gene Transfer Techniques
  • Humans
  • Receptors, CCR5
  • Receptors, CXCR4
  • Transgenes

MeSH Major

  • Adenoviridae
  • Genetic Vectors
  • HIV-1
  • Macrophages, Alveolar
  • Virus Replication

abstract

  • To assess the hypothesis that infection of alveolar macrophages (AM) with adenovirus (Ad) gene transfer vectors might prevent subsequent human immunodeficiency virus (HIV)-1 replication in AM, AM isolated from normal volunteers were infected with increasing doses of first generation (E1(-)) Ad vectors, followed 72 h later by infection with HIV-1(JRFL), an R5/M-tropic strain that preferentially uses the CCR5 coreceptor. As a measure of HIV-1 replication, p24 Ag was quantified by enzyme-linked imunosorbent assay in supernatants on Days 4 to 14 after HIV-1infection. Pretreatment of the AM with an Ad vector resulted in a dose- and time-dependent suppression of subsequent HIV-1 replication. The Ad vector inhibition of HIV-1 replication was independent of the transgene in the Ad vector expression cassette and E4 genes in the Ad backbone. Moreover, it did not appear to be secondary to a soluble factor released by the AM, nor was it overridden by the concomitant transfer of the CCR5 or CXCR4 receptors to the AM before HIV-1 infection. These observations have implications regarding pulmonary host responses associated with HIV-1 infection, as well as possibly uncovering new therapeutic strategies against HIV-1 infection.

publication date

  • August 2002

has subject area

  • Adenoviridae
  • Flow Cytometry
  • Gene Transfer Techniques
  • Genetic Vectors
  • HIV-1
  • Humans
  • Macrophages, Alveolar
  • Receptors, CCR5
  • Receptors, CXCR4
  • Transgenes
  • Virus Replication

Research

keywords

  • Journal Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1165/ajrcmb.27.2.4696

PubMed ID

  • 12151313

Additional Document Info

start page

  • 214

end page

  • 219

volume

  • 27

number

  • 2