DOI Seite / Zitierlink:
https://doi.org/10.11588/diglit.48120#0129
Abstracts
111
0 2 4 6 8 10 kb
I gag |
pol | | env
* * * * * *
2106 GATCTGCCTTCCTACAAGGGAAGGCCAG GGACTTTTCTTCAGAGCAGACCAGAG 2159
I GATCTGCCTTCCTGCAAGGGAAGC CAGTGGACTTTTCT CAGAGCAGCCAAGAG 53
2231 GGTAGA GACAACAACTCCCCCTCAGAA GCAGGA6CCGATAGACAAGGAACT6T
74 GGTAGAAGACAACAACTCC6TCTCAGAACGCAGGA CCGATAGA A CTGT
ATCC TTTAACTTCCCTCAGATCACTC 2309
ATC TT AACTTCCATCAGATCATTC 145
Fig. 1. The homology of E 6 (152-297) to the proviral genome of HIV 1 (2106 — 2309).
Mismatches are indicated by asterisks
nested deletions made with Exonuclease III and Nuclease S 1 from the single
stranded templates induced by a helper phage.
Since it was not possible to detect integrated, nuclear DNA in the transfected
cells by Southern blotting, possibly due to the low percentage of infected cells,
we applied the polymerase chain reaction (PCR) technique for DNA amplifica-
tion using oligonucleotide primers derived from the E 6 sequence. In both
B 62/cells and 7 put of 30 B cell lines from 10 different SLE patients, amplifica-
tion products of 150 to 500 bp were found; a similar pattern was observed in
peripheral blood lymphycte (PBL) samples from AIDS patients, who served as
positive controls, and PBL samples of an SLE patient, as well as one patient with
clinical signs of rheumatoid arthritis. No DNA amplification products were
found in samples of healthy individuals so far (n = 5); therefore, PCR proved to
be useful for rapid detection of E 6 homologous DNA and supported the hypoth-
esis of a retroviral participation in the pathogenesis of SLE.
111
0 2 4 6 8 10 kb
I gag |
pol | | env
* * * * * *
2106 GATCTGCCTTCCTACAAGGGAAGGCCAG GGACTTTTCTTCAGAGCAGACCAGAG 2159
I GATCTGCCTTCCTGCAAGGGAAGC CAGTGGACTTTTCT CAGAGCAGCCAAGAG 53
2231 GGTAGA GACAACAACTCCCCCTCAGAA GCAGGA6CCGATAGACAAGGAACT6T
74 GGTAGAAGACAACAACTCC6TCTCAGAACGCAGGA CCGATAGA A CTGT
ATCC TTTAACTTCCCTCAGATCACTC 2309
ATC TT AACTTCCATCAGATCATTC 145
Fig. 1. The homology of E 6 (152-297) to the proviral genome of HIV 1 (2106 — 2309).
Mismatches are indicated by asterisks
nested deletions made with Exonuclease III and Nuclease S 1 from the single
stranded templates induced by a helper phage.
Since it was not possible to detect integrated, nuclear DNA in the transfected
cells by Southern blotting, possibly due to the low percentage of infected cells,
we applied the polymerase chain reaction (PCR) technique for DNA amplifica-
tion using oligonucleotide primers derived from the E 6 sequence. In both
B 62/cells and 7 put of 30 B cell lines from 10 different SLE patients, amplifica-
tion products of 150 to 500 bp were found; a similar pattern was observed in
peripheral blood lymphycte (PBL) samples from AIDS patients, who served as
positive controls, and PBL samples of an SLE patient, as well as one patient with
clinical signs of rheumatoid arthritis. No DNA amplification products were
found in samples of healthy individuals so far (n = 5); therefore, PCR proved to
be useful for rapid detection of E 6 homologous DNA and supported the hypoth-
esis of a retroviral participation in the pathogenesis of SLE.