Transient expression of human immunodeficiency virus type 1 genome results in a nonproductive infection in human fetal dorsal root ganglia glial cells.
Human immunodeficiency virus type 1 (HIV-1), the etiologic agent of acquired immunodeficiency syndrome (AIDS), has been implicated in the generation of AIDS-associated neurologic dysfunction. We are currently examining the replicative processes involved in HIV-1 infection of selected human fetal neural cell populations in vitro. To determine whether infection of the human fetal dorsal root ganglia (DRG) glial cell population culminates in the production and release of infectious HIV-1, cocultivation and reverse transcriptase (RT) assays were performed. Direct assay of HIV-1 infected neural cell supernatants as well as exposure of permissive SupT1 cells to these HIV-1-infected neural cell supernatants detected no RT activity in either the HIV-1-infected DRG glial cell supernatants or the SupT1 cell supernatants. When SupT1 cells were cocultivated with the HIV-1-infected neural cells for 24-hr intervals, RT activity was detected in the SupT1 supernatants from cocultures initiated less than 2 days after infection (most likely resulting from infectious input virus) but not from cocultures initiated on 3, 5, 10, and 30 days after infection. Hybridization analysis demonstrated transient expression of HIV-1 cytoplasmic mRNA with accumulation reaching a maximum level by 2 to 3 days postinfection, declining thereafter with low, but detectable, levels at 16 days postinfection. In addition, polymerase chain reaction amplification in conjunction with DNA blot hybridization detected HIV-1-specific proviral DNA at 3 days postinfection. Cumulatively, these data suggest that HIV-1 infection of human fetal DRG glial cells culminates in a nonproductive infection with expression of at least a fraction of the virus genome but no detectable infectious virus production.
Kunsch
C
C
Department of Microbiology and Immunology, Pennsylvania State University, College of Medicine, Hershey 17038.
Wigdahl
B
B
D002478:Cells, Cultured; D004279:DNA, Viral / Q000032:analysis; D005455:Fluorescent Antibody Technique; D005727:Ganglia, Spinal / Q000382:microbiology*; D015967:Gene Expression Regulation, Viral; D015683:Gene Products, gag / Q000032:analysis / Q000235:genetics; D015488:HIV Antigens / Q000032:analysis / Q000235:genetics; D016655:HIV Core Protein p24; D015497:HIV-1 / Q000235:genetics* / Q000502:physiology; D006801:Humans; D009457:Neuroglia / Q000382:microbiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D012367:RNA, Viral / Q000096:biosynthesis; D014758:Viral Core Proteins / Q000032:analysis / Q000235:genetics; D014764:Viral Proteins; D014779:Virus Replication; D054301:gag Gene Products, Human Immunodeficiency Virus
D004279:DNA, Viral; D015683:Gene Products, gag; D015488:HIV Antigens; D016655:HIV Core Protein p24; D012333:RNA, Messenger; D012367:RNA, Viral; D014758:Viral Core Proteins; D014764:Viral Proteins; D054301:gag Gene Products, Human Immunodeficiency Virus; C054858:p17 protein, Human Immunodeficiency Virus Type 1