A warm slice of toast dripping with honey is one of life's guilty pleasures, but the fate of the humble workers that produce this golden treat hangs in the balance. Ryan Kuster, Humberto Bonicristiani and Olav Rueppell from the University of North Carolina at Greensboro, USA, explain that European honey bee populations are in rapid and dramatic decline and that more than just the honey harvest is at stake: ‘Honey bees (Apis mellifera L.) are the most important commercial pollinators worldwide’, they explain. One of the most pernicious threats to honey bee health is the parasitic Varroa destructor mite. The mites not only harm their victims directly, but they also transmit other life-threatening diseases to the unwitting hosts. The team says, ‘Vector-borne diseases and their vectors often share the common interest to attenuate the host's immune response to facilitate feeding and reproduction.’ However, whether the V. destructor mite supresses the honey bee's immune system was unclear. Rueppell and his team embarked on a comprehensive survey of the parasite's impact on honey bees to lay the question to rest (p. 1710).
After deliberately infecting some honey bee larvae with one, two, or three or more V. destructor mites, or simulating the wound inflicted by a feeding mite on other larvae, the team then resealed the youngsters back into their cells to develop. Then, over a period of 10 days, they monitored the insect's immune response by measuring the expression of various genes related to the larvae's immune response. They also analysed the infection levels in the larvae of a virus (deformed wing virus) that is transmitted by the mites and is harmful to the developing insects.
However, when the team examined the larvae's immune response to the mite infection, they were surprised to see that it was unsuppressed. Only two of the immune response proteins that they monitored showed a drop in expression over the course of the infection: a pattern recognition receptor (PGRP-S2) 10 days after the mites were introduced and the encapsulation response effector (PPOAct) after 5 days. And the team was surprised to see that three immune effector genes (defensin, hymenoptaecin and abaecin) increased their expression levels, as did the intermediary protein, relish, in response to the V. destructor mites. The scientists add that the degree of V. destructor infection (one or more than three mites) did not alter the larvae's immune response, although they say, ‘Our findings do not exclude the possibility that V. destructor parasitism has a delayed effect on adult honey bees’.
Next the team investigated how the presence of the mite affected the degree to which the larvae were infected by deformed wing virus, and this time there was a clear correlation: the greater the number of introduced mites in a larva's cell, the higher the level of deformed wing virus. ‘This pattern seems to be established at 72 h post capping [of the cell]’, the team says. In addition, the larvae that had been wounded – to simulate a mite feeding without introducing infection – were more vulnerable to the harmful virus, which they carry naturally and is usually asymptomatic.
Summing the data up, the team says, ‘These results suggest that mite feeding activity itself and not immunosuppression may contribute to the synergy between viruses and mites.’ They conclude by offering a possible strategy for combating the mites, saying, ‘Increased expression of honey bee immune genes decreases mite reproductive success, which may be explored to enhance mite control strategies.’
