In this thesis, we examined the impact of HIV infection on the epidemiology (Part I) of sepsis, and host response (Part II)
to sepsis. We studied sepsis patients in Gabon, a setting with a high prevalence of HIV, and in Dutch intensive care units
In Part I, we found that HIV positive patients are more likely to present with bacterial sepsis, compared to
HIV negative patients, in particular with pathogens like non-typhoid Salmonella and Streptococcus pneumoniae. Although sepsis
patients with HIV co-infection in Gabon had increased mortality, HIV patients admitted to the ICU with sepsis in the Netherlands
no longer had a survival disadvantage compared to HIV negative patients with sepsis.
In Part II, we examined multiple
components of the immune system, including neutrophil extracellular traps, cytokine release, coagulation, the complement system
and the genomic response to sepsis. Differences in the host response to sepsis according to HIV status were most profound
in our cohort in Gabon, while we found little impact of HIV co-infection on the host response to sepsis in Dutch ICU patients.
Although HIV is well known for its immunosuppressive effect, we found no evidence for HIV induced suppression of the pro-inflammatory
response. In contrast, our findings support the idea of HIV as a cause of chronic inflammation, which may result in a more
profound inflammatory response and increased collateral damage during sepsis. Therefore, immune-modulatory treatment strategies
may be of particular benefit to sepsis patients with HIV, which is an interesting area for further research.