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Trending Science: Mosquito saliva hijacks immune cells to spread viruses

A European study has revealed that when immune cells travel to the site of a mosquito bite, they may inadvertently be infected with a mosquito-borne virus then help spread the virus to the rest of the body.

When responding to mosquito-carried pathogens, such as dengue, Zika or West Nile, the body’s immune response acts as a free ride for them to spread throughout the body, according to the research published in the journal ‘Immunity’. When mosquitoes bite, they inject a tiny amount of their saliva (less than a microlitre) that contains a specialised, potent cocktail of molecules that numbs the pain and stops the blood clotting, which benefits any pathogen that’s present in the saliva. It has been observed that mice develop more severe infections when infected with a virus via a mosquito than by a researcher using a needle, but until now, it has been unclear why. The European research team, led from the University of Leeds in the UK conducted an experiment where they infected mice with a relatively harmless variety of the Semliki Forest virus (SFV). When the virus was injected into the skin by hand, none of the mice got very sick and all of them survived. But when they were injected into a mosquito bite on the skin, the virus spread faster and more easily to the rest of the body, with 4 of eleven mice dying from the infection. One theory as to why mosquito saliva is so much more potent is transmitting a virus through the body is that compounds in the saliva suppresses the natural immune response, but this study found that this was not the case. Instead, saliva causes an inflammation, in essence a warning that the body’s natural defences have been breached. A class of cells known as neutrophils, that act as the body’s first responders, rush to the bite site. They are then followed by macrophages, cells whose role is to eat up any alien microbes that do not belong in the body. Using SFV labelled with a fluorescent dye, the research team discovered that the macrophages are themselves infected by the viruses and then begin spreading the disease further. When the researchers infected a strain of mice lacking macrophages with SFV, the mice fared similarly well whether they had been infected at a bite site or not. This shows that the virus actually uses the macrophages to replicate and disseminate quickly in the body. The new findings are particularly alluring as they may point to one target - the bite site -for fighting disease formation more effectively. ‘If you can inhibit bite inflammation, you could have a way of stopping viruses before they establish infection. Moreover, it could be useful for many such infections, since bite inflammation is common to all of them,’ commented Clive McKimmie, the immunologist who led the study. If their rodent findings hold true for humans and with multiple mosquito-borne viruses, his hope is that researchers could inhibit immune system responses at bite sites regardless of the pathogen. One possible way to reduce severe infections as a result of mosquito bites could be the simple act of applying an anti-inflammatory cream, which would also prevent the suppression of the immune system as a whole. Although these findings are highly promising for preventing the outbreak of mosquito viruses that impact millions of people worldwide, McKimmie has emphasised the need for further research before any solid public health recommendations could be made.

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