Distinctive pattern of infection and replication of HIV1 strains in blood-derived macrophages Article

Schmidtmayerova, H, Bolmont, C, Baghdiguian, S et al. (1992). Distinctive pattern of infection and replication of HIV1 strains in blood-derived macrophages . VIROLOGY, 190(1), 124-133. 10.1016/0042-6822(92)91198-4

cited authors

  • Schmidtmayerova, H; Bolmont, C; Baghdiguian, S; Hirsch, I; Chermann, JC

abstract

  • The macrophage-tropic virus HIV1-PAR, isolated from cerebrospinal fluid of HIV1-seropositive man, induced cytopathic effect accompanied by different magnitude of the virus production in blood-derived macrophages (BDM) obtained from different donors. HIV1-PAR-specific RNA was detected by in situ hybridization in 15 and 66% of BDM producing low and high levels of virus, respectively. In contrast with HIV1-PAR, infection of BDM with two laboratory strains adapted to T-cell lines, HIV1-LAV prototype and HIV1-NDK, a Zairian virus that is highly cytopathic for T-lymphocytes, resulted in a low production of HIV1 p24gag in culture fluid. Expression of HIV1-LAV and HIV1-NDK RNA was detected by in situ hybridization in a maximum of 1% of macrophages. Only HIV1-NDK, and not HIV1-LAV, induced ultrastructural alterations in BDM. In contrast with a striking difference in the production of macrophage-tropic and T-lymphotropic viruses, no significant differences were found in the proportion of macrophages containing retrotranscribed genomes of HIV1. HIV1 DNA was detected by in situ hybridization in 93, 100, and 80% of macrophages infected with HIV1-PAR, HIV1-LAV, and HIV1-NDK, respectively. A higher level of HIV1 DNA was detected by polymerase chain reaction in the BDM infected with HIV1-PAR than in that infected with HIV1-LAV and HIV1-NDK. The results indicate that both macrophage-tropic as well as T-lymphotropic viruses can enter and retrotranscribe their genomes in a vast majority of macrophages. © 1992.

publication date

  • January 1, 1992

published in

Digital Object Identifier (DOI)

start page

  • 124

end page

  • 133

volume

  • 190

issue

  • 1