Non-adherence to malaria prophylaxis: The influence of travel-related and psychosocial factors.

BACKGROUND: The effectiveness of malaria chemoprophylaxis is limited by a lack of compliance in travellers. This study assesses the demographic, travel-related, and psychosocial determinants of non-compliance with chemoprophylaxis. METHODS: 715 adults, who received a pre-travel malaria prophylaxis prescription, were invited to complete a post-travel digital questionnaire on non-compliance, demographics, travel-related and psychosocial variables. RESULTS: 330 travellers (53% response) reported 32% non-compliance with malaria chemoprophylaxis. Logistic regression analyses revealed that 3/11 assessed psychosocial variables uniquely predicted non-compliance: 'negative attitude towards chemoprophylaxis' (ß=0.694, OR 2.0, p<0.01), 'low perceived severity of malaria' (ß=0.277, p=0.04) and 'fatigue during travel' (ß=2.225, OR 9.3, p<0.01). Furthermore, the age and education of the traveller were uniquely predictive of non-compliance (ß=-0.023 (p=0.02) and ß=0.684 (p=0.04)). None of the travel-related variables predicted non-compliance. CONCLUSIONS: About one-third of the travellers in our study were non-compliant with malaria prophylaxis, especially young travellers and highly educated travellers. Fatigue during travel seems to lead to non-compliance. Further research should focus on addressing the psychosocial factors in pre-travel consultation, since these appear to be better predictors for intention to comply than travel-related variables.

Ultrastructural proof of polyomavirus in Merkel cell carcinoma tumour cells and its absence in small cell carcinoma of the lung.

BACKGROUND: A new virus called the Merkel Cell Polyomavirus (MCPyV) has recently been found in Merkel Cell Carcinoma (MCC). MCC is a rare aggressive small cell neuroendocrine carcinoma primarily derived from the skin, morphologically indistinguishable from small cell lung carcinoma (SCLC). So far the actual presence of the virus in MCC tumour cells on a morphological level has not been demonstrated, and the presence of MCPyV in other small cell neuroendocrine carcinomas has not been studied yet. METHODOLOGY/PRINCIPAL FINDINGS: We investigated MCC tissue samples from five patients and SCLCs from ten patients for the presence of MCPyV-DNA by PCR and sequencing. Electron microscopy was used to search ultrastructurally for morphological presence of the virus in MCPyV-DNA positive samples. MCPyV was detected in two out of five primary MCCs. In one MCC patient MCPyV-DNA was detected in the primary tumour as well as in the metastasis, strongly suggesting integration of MCPyV in the cellular DNA of the tumour in this patient. In the primary MCC of another patient viral particles in tumour cell nuclei and cytoplasm were identified by electron microscopy, indicating active viral replication in the tumour cells. In none of the SCLCs MCPyV-DNA was detected. CONCLUSIONS/SIGNIFICANCE: Our results strongly suggest that MCPyV is an oncogenic polyomavirus in humans, and is potentially causally related to the development of MCC but not to the morphological similar SCLC.

The genotypic inhibitory quotient and the (cumulative) number of mutations predict the response to lopinavir therapy.

For 95 protease inhibitor-experienced HIV-1-infected patients, the genotypic inhibitory quotient (GIQ; trough level/number of mutations) was calculated for lopinavir. Three different sets of mutations showed equal predictive value. However, the use of cumulative numbers of mutations for calculation of the GIQ showed significantly better association with the virological response. Furthermore, the predictive value of the GIQ was no different from that of the number of mutations alone.