Publications

BACKGROUND

Chromosome four of Drosophila melanogaster, known as the dot chromosome, is largely heterochromatic, as shown by immunofluorescent staining with antibodies to heterochromatin protein 1 (HP1) and histone H3K9me. In contrast, the absence of HP1 and H3K9me from the dot chromosome in D. virilis suggests that this region is euchromatic. D. virilis diverged from D. melanogaster 40 to 60 million years ago.

RESULTS

Here we describe finished sequencing and analysis of 11 fosmids hybridizing to the dot chromosome of D. virilis (372,650 base-pairs) and seven fosmids from major euchromatic chromosome arms (273,110 base-pairs). Most genes from the dot chromosome of D. melanogaster remain on the dot chromosome in D. virilis, but many inversions have occurred. The dot chromosomes of both species are similar to the major chromosome arms in gene density and coding density, but the dot chromosome genes of both species have larger introns. The D. virilis dot chromosome fosmids have a high repeat density (22.8%), similar to homologous regions of D. melanogaster (26.5%). There are, however, major differences in the representation of repetitive elements. Remnants of DNA transposons make up only 6.3% of the D. virilis dot chromosome fosmids, but 18.4% of the homologous regions from D. melanogaster; DINE-1 and 1360 elements are particularly enriched in D. melanogaster. Euchromatic domains on the major chromosomes in both species have very few DNA transposons (less than 0.4 %).

CONCLUSION

Combining these results with recent findings about RNAi, we suggest that specific repetitive elements, as well as density, play a role in determining higher-order chromatin packaging.

OBJECTIVE

To investigate the association between the introduction of HAART and invasive pneumococcal disease (IPD) in HIV-infected patients.

METHODS

Incidence of IPD was determined from 1990 to 2003 in a cohort of HIV-infected individuals and a nested case-control study assessed risk factors of IPD.

RESULTS

There were 72 cases over 19,020 person-years of follow-up (overall IPD rate, 379/100,000 person-years). In the calendar periods 1990-1995, 1995-1998, and 1998-2003, the IPD incidence per 100,000 person-years was 279 [95% confidence interval (CI), 150-519], 377 (95% CI, 227-625) and 410 (95% CI, 308-545), respectively (P = 0.516). CD4 cell count < 200 cells/microl [odds ratio (OR), 3.0; 95% CI, 1.2-7.6), HIV RNA > 50,000 copies/ml (OR, 2.8; 95% CI, 1.2-6.5), hepatitis C (OR, 4.9; 95% CI, 1.7-14.9), serum albumin (OR, 0.1; 95% CI, 0.04-0.5), injection drug use in women (OR, 3.8; 95% CI, 1.6-8.8), and education beyond high school (OR, 0.2; 95% CI, 0.05-0.8) were significantly associated with IPD in multivariate analysis. No treatment factor, including HAART (OR, 0.7; 95% CI, 0.3-1.5) and pneumococcal vaccination (OR, 0.9; 95% CI, 0.5-1.6), was associated with IPD.

CONCLUSIONS

IPD incidence did not change significantly during the widespread dissemination of HAART in this cohort. IPD risk was associated with several sociodemographic and clinical factors.