Extracts of salivary glands of the yellow fever mosquito Aedes aegypti inhibit tumour cell-stimulated release of tumour necrosis factor alpha (TNF alpha) from rat mast cells, but do not inhibit antigen-induced histamine secretion. This inhibitory activity for TNF alpha is found in salivary glands of female but not in male mosquitoes. This inhibition is not mediated by bacterial contamination (LPS), by calcitonin gene related peptide (CGRP), nerve growth factor (NGF), epidermal growth factor (EGF) or transforming growth factor beta (TGF beta). The factor(s) has a molecular weight > 10 kDa and is neutralized by boiling for 10 min or heating at 56 degrees C for 30 min. The modulation of this proinflammatory mediator, TNF alpha, produced by mast cells in sites of blood feeding may facilitate completion of the blood meal, and as reported for certain vector-transmitted parasites, may enhance infectivity.
Infection, dissemination, and transmission of an arbovirus in mosquitoes are enhanced by concurrent ingestion of microfilariae. Ingestion of Rift Valley fever virus alone infected only 64 percent of female Aedes taeniorhynchus. Of these, only 5 percent of refeeding mosquitoes actually transmitted virus. In contrast, ingestion of the same amount of virus from concurrently microfilaremic (Brugia malayi) gerbils resulted in 88 percent infection and 31 percent transmission. Enhanced transmission of virus may be attributed to increased transit of virus across the midgut wall. Endemic filariasis may promote arbovirus transmission in nature.
We constructed an olfactometer that differentiates and quantifies attraction, inhibition, and repellency to mosquitoes. Using this device, 22 formulations of various chemicals on gauze pads and 8 dilutions of DEET on skin were tested. Four novel formulations were discovered acting as true repellents, whereas DEET did not act as a true repellent but as an inhibitor.
Monte Carlo simulations were developed to assess the potential impact of parasite pathology on vector salivary function as well as of host haemostasis on transmission. Assuming that a proportion of desisting vectors switch host following failure to locate blood, we demonstrate three possible consequences: (1) infected vectors contact more hosts than non-infected host, (2) non-infected vectors are biased to infected hosts, independently of attraction, and (3) an exponential relationship exists between parasite load and transmission. We discuss possible epidemiological implications.
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