Immunologic havoc induced by the 60 kD Gag protein of the MAIDS defective virus.
The mechanisms responsible for development of profound immunodeficiency and extensive lymphoproliferation that characterize infection of different species with retroviruses are only partially understood. In mice, it has been shown the activities of an unusual Gag protein are necessary and sufficient to induce these abnormalities in a syndrome designated mouse AIDS (MAIDS). Current studies suggest that complex, antigen-driven interactions between T cells and B cells result in polyclonal activation of both types of lymphocytes, aberrant cytokine production and late lymphomas.
Morse
H C
HC
Laboratory of Immunopathology, NIAID, NIH, Bethesda, MD 20892, USA.
Morawetz
R A
RA
Giese
N A
NA
Chattopadhyay
S K
SK
Tang
Y
Y
Fredrickson
T N
TN
Hartley
J W
JW
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics; D003673:Defective Viruses / Q000276:immunology; D015683:Gene Products, gag / Q000276:immunology*; D009052:Leukemia Virus, Murine / Q000276:immunology* / Q000378:metabolism; D008213:Lymphocyte Activation; D051379:Mice; D018345:Mice, Knockout; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology* / Q000821:virology*; D014158:Transcription, Genetic; D014764:Viral Proteins / Q000276:immunology*
D016207:Cytokines; D015683:Gene Products, gag; C107020:Pr60(gag) protein, murine AIDS virus; D014764:Viral Proteins