Restricted replication of the HIV-1 T-lymphotropic isolate NL4-3 in HL-60 cells.
To understand how different cell types might influence the generation of viral variants, we have examined the differences in the viral life cycle of the HIV-1 isolate, NL4-3, in the human promyelocytic cell line, HL-60, and the human T cell line, H9. NL4-3 harvested from H9 cells productively infected and was cytopathic to H9 and HL-60 cells. However, the cytopathic effect was delayed in HL-60 cells compared to that seen in H9 cells, suggesting that NL4-3 replication was restricted in myeloid cells. This restriction was overcome by production of a variant virus, NL4-3 (M), which replicated efficiently in HL-60 cells. Measurements of the kinetics of entry of NL4-3 in H9 and HL-60 cells and NL4-3 (M) in HL-60 cells demonstrated that the timing of viral entry into each cell line was similar. However, quantitation of the amount of newly reverse-transcribed NL4-3 DNA in H9 and HL-60 cells revealed that NL4-3-infected H9 cells and NL4-3 (M)-infected HL-60 cells contained consistently more newly reverse-transcribed DNA than NL4-3-infected HL-60 cells. This difference was further amplified by inefficient spread of the virus throughout the HL-60 culture. Together these results suggest that the efficiency of NL4-3 infection of HL-60 cells is restricted at early steps in the viral life cycle and may be restricted at late steps as well.
Pise-Masison
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CA
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical Center, Worcester.
Holland
C A
CA
D001483:Base Sequence; D002460:Cell Line; D003588:Cytopathogenic Effect, Viral; D017931:DNA Primers; D004279:DNA, Viral / Q000032:analysis; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D008561:Membrane Fusion; D008969:Molecular Sequence Data; D013601:T-Lymphocytes / Q000821:virology*; D014779:Virus Replication
D017931:DNA Primers; D004279:DNA, Viral