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S clustered within the CRF02_AG clade, reinforcing the notion that this viral clade is a major contributor of genetic material to new recombinants [20]; an alternative explanation, however, could be that the gag and nef genes were amplified from different viruses co-infecting the same patients. Ongoing molecular and clinical surveillance will reveal whether new recombinants will begin to circulate
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Ormation were obtained. RNA was extracted from plasma samples, reverse transcribed and PCR amplified as described previously [12] using subtype non-specific HIV-1 primers for HIV-1 full length gag [12] and nef [13] genes, and sequenced. Sequenced fragments were assembled using ChromasPro. Full length gag and nef sequences were generated and aligned using MUSCLE with manual editing in MEGA5, togeth
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Eshly isolated AMs from MS-/- mice, the cell lines exhibit decreased phagocytosis of unopsonized titanium dioxide (TiO2), fluorescent latex beads and bacteria (Staphylococcus aureus) compared with the primary AMs from wild type (WT) C57BL/6 mice. Conclusion: Our results indicated that three contiguous murine alveolar macrophage cell lines with MS-/- (ZK1, ZK2 and ZK6) were established successfully
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Ibution of HIV-1 in CameroonSample ID BS01 BS02 BS03 BS04 BS05 BS06 BS09 BS10 BS11 BS12 BS13 BS14 BS16 BS18 BS19 BS20 BS21 BS22 BS23 BS24 BS25 BS26 BS27 BS29 BS30 BS31 BS32 BS35 BS38 BS39 BS40 BS42 BS43 BS44 BS45 BS46 BS47 BS48 BS49 BS50 BS51 BS53 BS54 BS55 gag gene CRF02_AG A-like G G CRF02_AG CRF02_AG CRF02_AG A1 CRF02_AG G CRF02_AG CRF02_AG CRF02_AG NDc CRF02_AG NDc CRF02_AG CRF02_AG CRF02_AG C
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S clustered within the CRF02_AG clade, reinforcing the notion that this viral clade is a major contributor of genetic material to new recombinants [20]; an alternative explanation, however, could be that the gag and nef genes were amplified from different viruses co-infecting the same patients. Ongoing molecular and clinical surveillance will reveal whether new recombinants will begin to circulate
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Allele primers, amplifies a 434 bp DNA fragment from SRA-deficient ZK1, ZK2 and ZK6 cells. With primers for MARCO wild-type allele, amplifies a 500 bp DNA fragment from WT mice; with primers for MARCO mutant allele, amplifies a 850 bp DNA fragment from ZK cells. ZK1, ZK2 and ZK6 clones exhibited both MARCO and SRA-I/II-deficient. PCR products, ca.10 l/each was resolved on a 1.5 agarose gel by gel
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Allele primers, amplifies a 434 bp DNA fragment from SRA-deficient ZK1, ZK2 and ZK6 cells. With primers for MARCO wild-type allele, amplifies a 500 bp DNA fragment from WT mice; with primers for MARCO mutant allele, amplifies a 850 bp DNA fragment from ZK cells. ZK1, ZK2 and ZK6 clones exhibited both MARCO and SRA-I/II-deficient. PCR products, ca.10 l/each was resolved on a 1.5 agarose gel by gel
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Cell lines from primary alveolar macrophages from MS-/- mice. Results: We used in vitro infection of the primary AMs with the J2 retrovirus carrying the v-raf and v-myc oncogenes. Following initial isolation in media supplemented with murine macrophage colony-stimulating factor (M-CSF), we subcloned three AM cell lines, designated ZK-1, ZK-2 and ZK-6. These cell lines grow well in RPMI-1640-10 FB