Morphology andphenotype ofdendritic cells fromperipheral blood andtheir productive andnon-productive infection withhuman immunodeficiency virus type1
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SUMMARY Immununoelectron microscopy ofhumanperipheral bloodmononuclear cells enriched forthe presenceofantigen-presenting dendritic cells (DC)hasrevealed twomorphologically distinct cell typesbothexpressing DR andDQ majorhistocompatibility complex (MHC)class II antigens but lacking T,B,natural killer (NK)andmonocyte/macrophage markers. Thefirst (type 1)hasan irregular surface with numerous projections andshowscytoplasmic vacuoles. Thesecond (type 2)has apaler nucleus showing only athinrimofdenseheterochromatin, large expansesofcytoplasm devoid oforganelles, fewer vacuoles andasmoothcell boundary withfewprocesses. Inaddition afewcells with amorphology similar toveiled cells oftheafferent lymphatics (type 3DC)wereobserved. Cells with amorphology intermediate between these three types wereobserved, suggesting thatthey may represent stages oftheveiled cell differentiation pathway. Type2and3DC were shownbyelectron microscopy tobesusceptible toproductive infection withhumanimmunodeficiency virus(HIV), whilst type1 DC didnotsupportvirus growth. Examination ofinfected DC preparations byinsitu hybridization revealed ahigher numberofDC positive forviral DNA andRNA thanforRNA alone. Thus, inaddition toproductively infected DC,there may besome that arelatently infected, contain defective virus genome orreplicate virus ata verylowlevel.Cite
NIH3T3cellsinfected withMoloney murine sarcoma virus (murine leukemia virus) produce virions whichcontain about99%murine sarcoma virus RNA and 1%murine leukemia virus RNA.Thisreport describes experiments which measured intracellular concentrations ofproviral DNA andRNA transcripts foreach oftheviruses. We foundthatthreetofourcopies ofproviral DNA fromeach virus were integrated intothecellular DNA.Measurements ofRNA specific for eachofthegenomesbyhybridization tospecific cDNAreagents revealed a 10-to 15-fold difference inconcentration inbothnuclear andpolysomal RNA fractions, withmurine sarcoma virus RNA predominating inbothcases.Unless there are majordifferences instability between thetwoviral RNAs,our results suggest thattranscriptional control isresponsible formuchofthedifference infinal levels ofvirus synthesis. RNA tumorviruses caninfect cells, integrate intothehostDNA asdouble-stranded DNA proviruses, betranscribed bycellular polymerases(23, 33,38), andbereleased into themedium without killing their hosts. Theseproperties makethemparticularly attractive asmodelsystemsforstudying thecontrol ofgeneexpression. Expression ofviral genetic information canbe monitored byusing specific viral cDNAprobes. Examples ofthis approach include theworkby Boettinger (5), Bishop etal.(4), andDengetal. (9, 10)onRoussarcoma virus-transformed BHK
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