Inhibition of CMV replication in human fibroblasts by human monocyte-derived macrophages: implication for CMV persistent infection

E. Manor, I. Sarov

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

The effect of monocytes (M) and monocyte-derived macrophages (MdM) on cytomegalovirus (CMV) replication in human fibroblasts (HF) was studied by one step growth experiments, plaque formation and dot hybridization with a labeled CMV DNA probe. HF were infected with CMV at multiplicities of infection (mol) of 0.001 to 1. After virus adsorption, M or MdM were added at an effector target ratio of 2:1. MdM reduced both infectious viral yield and the quantity of viral DNA and inhibited viral plaque formation. M, however, affected these parameters to a lesser extent. Electron microscopic studies showed that MdM treated CMF-infected HF, 4 days pi, contained only a few capsids in their nuclei and many vacuoles in their cytoplasm as compared to CMV infected HF (control). A reduction of CMV DNA inhibition was observed upon incubation of the infected HF cells with MdM separated from the infected cells by a membrane. Addition of tumor necrosis factor (TNF) antibody to CMV-infected HF incubated with MdM either in direct contact or separated by a membrane from the infected cells reduced the inhibition of CMV-DNA production. The results of this study suggest that MdM may modulate CMV replication in vivo and may also have a role in CMV persistence or chronic infection.

Original languageEnglish
Pages (from-to)97-107
Number of pages11
JournalMicrobial Pathogenesis
Volume5
Issue number2
DOIs
StatePublished - 1 Jan 1988

Keywords

  • Cytomegalovirus
  • macrophages
  • monocytes
  • tumor necrosis factor

ASJC Scopus subject areas

  • Microbiology
  • Infectious Diseases

Fingerprint

Dive into the research topics of 'Inhibition of CMV replication in human fibroblasts by human monocyte-derived macrophages: implication for CMV persistent infection'. Together they form a unique fingerprint.

Cite this