The pathogenesis of HIV infection, and in particular the development of immunodeficiency, remains incompletely understood. Whichever intricate molecular mechanisms are at play between HIV and the host, it is evident that the organism is incapable of restricting and eradicating the invading pathogen. Both innate and adaptive immune responses are raised, but they appear to be insufficient or too late to eliminate the virus. Moreover, the picture is complicated by the fact that the very same cells and responses aimed at eliminating the virus seem to play deleterious roles by driving ongoing immune activation and progressive immunodeficiency. Whereas much knowledge exists on the role of adaptive immunity during HIV infection, it has only recently been appreciated that the innate immune response also plays an important part in HIV pathogenesis. In this review, we present current knowledge on innate immune recognition and activation during HIV infection based on studies in cell culture, non-human primates, and HIV-infected individuals, and discuss the implications for the understanding of HIV immunopathogenesis.

The mortality in patients with persistent low CD4 count despite several years of HAART with sustained viral suppression is poorly documented. We aimed to identify predictors for inadequate CD4 cell recovery and estimate mortality in patients with low CD4 count but otherwise successful HAART.

Human infection with parvovirus B19 may lead to a diverse spectrum of clinical manifestations, including benign erythema infectiosum in children, transient aplastic crisis in patients with haemolytic anaemia, and congenital hydrops foetalis. These different diseases represent direct consequences of the ability of parvovirus B19 to target the erythroid cell lineage. However, accumulating evidence suggests that this virus can also infect other cell types resulting in diverse clinical manifestations, of which the pathogenesis remains to be fully elucidated. This has prompted important questions regarding the tropism of the virus and its possible involvement in a broad range of infectious and autoimmune medical conditions.

Objective: To estimate annual employment rates and disability retirement rates (DRRs) among HIV-infected individuals and population controls during the period 1996–2011. Design: A population-based cohort study including all HIV-infected individuals born in Denmark and not reporting intravenous (i.v.) drug abuse as a route of HIV infection or diagnosed with hepatitis C infection (n = 2799) and 22 369 individually matched persons from the background population. Study inclusion was 1 January 1996 or HIV diagnosis, which ever came last. Methods: Data on employment status and disability pension were extracted from Danish national registries. Employment rate and DRR were estimated in each calendar year after study inclusion for the cohorts included before 1996 (pre-1996), 1996–1999 and 2000–2011. Results: Employment rate in the year of study inclusion increased from 54.8% [95% confidence interval (CI) 50.5–59.6] in the pre-1996 cohort to 74.6% (66.9–83.2) and 77.4% (72.8–82.2) in the 1996–1999 and 2000–2011 cohorts, respectively, compared with 85.9–87.2% in the comparison cohorts. Five years from study inclusion, employment rates were 56.1 (51.4–61.1), 66.2 (58.7–74.6) and 70.9% (65.0–77.3) in the pre-1996, 1996–1999 and 2000–2011 cohorts, respectively, compared with 82.5–85.6% in the comparison cohorts. Five years from study inclusion, DRRs were 32.3 (28.9–36.3) in the pre-1996 cohort and decreased to 17.8 (14.1–22.4) and 11.6% (9.4–14.4) in the 1996–1999 and 2000–2011 cohorts, respectively, compared with 5.1–7.2% in the comparison cohorts. Conclusion: After the introduction of HAART, employment rates have increased profoundly among HIV-infected individuals, but have remained lower than in the background population. During the same period, DRRs decreased among HIV-infected individuals, but still remained higher than in the background population.