Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
Molecular diversity of SIVsm/PBj and a cognate variant (SIVsm/PGg).
Symp Nonhum Primate Models AIDS. 1990 Nov 28-30;8:17 (abstract no. 1). Unique Identifier : AIDSLINE PRIM8/900001 Novembre FJ; Hirsch VM; McClure HM; Johnson PR; Department of Microbiology, Georgetown University, and Laboratory; of Infectious Diseases, NIAID/NIH, Rockville, Md.
Abstract:
Experimental inoculation of SIVsm/PBj (PBj) into pig-tail macaques induces an acute syndrome characterized by fulminant diarrhea, acid-base imbalance, and death. This outcome is in distinct contrast to the more protracted immunodeficiency syndrome (AIDS) caused by other SIVsm isolates, including the PBj parental strain, SIVsmm9. Thus, by defining the viral properties responsible for the acute syndrome phenotype, we may further our understanding of viral determinants important for AIDS. The starting materials for our studies were tissues taken from a pig-tail macaque (PGg) that died after inoculation with PBj. Subgenomic molecular clones were derived (by PCR) from three sources of genomic DNA: (i) splenic tissue; (ii) ileum (Peyer's patch); and, (iii) CEMX174 cells infected by cocultivation with a filtrate from a Peyer's patch homogenate. Analyses of nucleotide sequences from clones of LTR, envelope, and the entire 3' half of the genome revealed the following findings. By comparison with clones from SIVsmm9 and SIVsmH-4 (a molecular clone of SIVsm that does not induce acute disease), two areas of primary structural divergence were observed: an envelope region analogous to the peptide T domain in HIV-1, and the U3 region in the LTR. The peptide T region in gp120 in most PGg clones contained an insertion of 6 to 9 amino acids relative to smm9 or smH-4. For the LTR, an insertion of 22 nucleotides representing a duplication of the NF-kB enhancer element was present in 5 of 22 clones sequenced. Overall, clones derived from CEMX174 cells were generally reflective of sequences present in tissues. Comparative analyses of clones of the 5' half of the PGg genome (gag/pol) did not reveal any distinctive findings (except the duplicated core enhancer). To define regions of the PGg genome important for induction of acute disease, chimeric molecular clones have been constructed using the 5' half of smH-4 and various 3' halves of PGg. Several biologically-active proviral clones have been generated, some of which contain the distinctive primary structural features described above. Characterization of the biological properties of these clones in cells in culture and in experimentally-inoculated macaques should allow a dissection of the determinants responsible for the acute disease syndrome.
Keywords: Acquired Immunodeficiency Syndrome/GENETICS Animal Cells, Cultured Chimera Clone Cells DNA, Viral/BIOSYNTHESIS HIV Enhancer/GENETICS HIV Envelope Protein gp120/GENETICS HIV Long Terminal Repeat HIV-1/GENETICS Macaca nemestrina Peyer's Patches/MICROBIOLOGY Phenotype Polymerase Chain Reaction Proviruses/GENETICS Simian Acquired Immunodeficiency Syndrome/*GENETICS SIV/*GENETICS *Variation (Genetics) Virus Cultivation ABSTRACT
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
