Sluggish in Flu? You May Blame Your Brain, Not the Virus
Image source: internet, used for representation only.
The common flu can make one want to not get out of bed, with a loss of appetite and a sluggish feeling that go with other symptoms like body pain, sore throat, and more. Such a state during a flu infection may be due to signals received by the brain from neurons – meaning that the infection itself does not lead to the symptoms but the brain does. In research published in Nature on March 8, scientists have reported on the phenomenon of feeling sluggish. Studying mice with flu, they have found out that neurons transmit signals to the brain informing it about the infection and the brain, in reaction to those signals, gives rise to the symptoms. Scientists also think that the existence of similar other neurons connecting to other parts of the body may let the brain know about other infections.
As a quick recap of neuronal signalling and brain function, it is worth mentioning that the neurons are the brain cells and they receive signals from outside and also from other parts of the body. These signals are transmitted to the brain as impulses. Commenting on it, the corresponding author of the study, Stephen Liberles of Harvard Medical School, Boston, said in a statement: “It was not clear how the brain becomes aware that there’s an infection in the body. Scientists generally thought that messenger molecules from the site of infection move through the bloodstream to the brain, diffusing into it to directly activate the regions that kickstart the sickness-behaviour program.”
The messenger molecules Liberles mentioned in his comments are considered to be the prostaglandins as the top candidate. Widely used drugs aspirin and ibuprofen block prostaglandin production and they also suppress sickness. This is a hint that prostaglandins are key messenger molecules that trigger the sickness behaviour. However, scientists were in dark about how exactly these chemicals communicate with the brain.
Previous research provided some hints that PGE2, which is a type of prostaglandin produced in response to viral infections, can travel through the blood to the brain where it interacts with the brain cells. The researchers genetically engineered mice that lacked the receptors for PGE2 in the central nervous system and the mice behaved as if they were sick with all the symptoms of flu – with loss of appetite and less movement than normal. This finding hinted that PGE2 was detected by the peripheral nervous system (as the genetically engineered mice did not have the receptors in their central nervous system). The peripheral nervous system has neurons outside the brain and the spinal cord.
The team of researchers then moved on to find out where exactly in the body the PGE2 was detected. With the help of several genetic tools, the team zeroed down to a cluster of neurons in the back of the throat which connects the brain to the upper airways (consisting of nasal cavities, pharynx, larynx, and oral cavity). Interestingly, the researchers found that the mice who lacked receptors in these areas did not show the symptoms even when they were infected by the influenza virus.
These findings have several implications. The findings show that not only do chemicals like prostaglandins act as messenger molecules which travel down to the brain to let it know about an infection, but there are neurons as well doing the same thing via transmitting signals. This implies that even in the absence or blocking of the messengers, the signal of the infection can be transmitted by neurons.
“The discovery of this peripheral pathway redefines our understanding of how influenza virus infection affects the nervous system to cause sickness behaviour. Tiny molecules such as prostaglandins are notoriously difficult to study,” commented Elia Tait Wojno, an immunologist at the University of Washington, Seattle, praising the researchers for the findings.
There is another interesting finding that the research came out with. Even blocking the PGE2 pathway was not that effective in reducing the sickness behaviours if done in the later stage of infection. This, according to the researchers, may be due to the existence of a different pathway once the infection progresses. The team also found that blocking the PGE2 pathway also increased the survivability of the mice which bolsters previous other findings that blocking the PGE2 synthesis pathway improves the chance of survival among the flu-infected mice.
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