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Battling the Bite: Tradeoffs in Immunity
to Insect-Borne Pathogens
David Samuel Schneider1,*
1Stanford Microbiology and Immunology, Stanford, CA 94305-5124, USA
*Correspondence: dschneid@stanford.edu
http://dx.doi.org/10.1016/j.immuni.2016.06.008
Effective pathogens are successful, by definition, because they can defeat our immune response. Pingen
et al. (2016) in this issue of Immunity demonstrate that some mosquito-transmitted viruses depend upon a
strong host immune response triggered by the innate immune response to the bite to promote dissemination
through the body.
Insect bites are complicated; a bloodfeeding arthropod doesnt simply slice
open our skin and feed on the pooling
blood or dip a proboscis into a capillary
for a drink. If they tried that, they would
surely get slapped or if we failed to notice
the bite, our rapid ability to clot would
prevent the pest from feeding. Mosquito,
sandfly, blackfly, bug, and tick salivas
contain a pharmacopeia of compounds
that manipulate the bite to provide anesthesia, modulate inflammation, reduce
clotting, and even physically glue the
blood sucker to the host (Schneider and
Higgs, 2008). Vector-mediated disease
transmission of viruses, bacteria, worms,
and protozoa occurs in the middle of this
battlefield where the host is mounting
a response to a small wound while
the arthropod interferes with the host
response. Pingen et al. (2016) wanted to
understand how these non-viral factors
affect pathogen proliferation.
Diseases transmitted through arthropod
bites are peculiar in that they must initiate
an infection with the tiny inoculum contained in an insect bite, but to be transmitted from a vertebrate host back to an
insect, the virus must reach high titers in
the blood so that it can be picked up in
a miniscule blood meal. Typically, this
means that the pathogens need to spread
systemically and replicate spectacularly;
their growth burst and the accompanying
immune reaction are responsible for the
symptoms we experience. The balance
between how hard the host tries to clear
the pathogen and the intensity of the
resulting symptoms defines our disease
tolerance to the pathogen (Ayres and
Schneider, 2012). In the case of viral transmission from an Aedes mosquito, this
balance seems set too much toward killing
Immunity 44, June 21, 2016 2016 Published by Elsevier Inc. 1251
Immunity
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