Fever Chills Drive Warmth-Seeking That Helps Your Body Fight Infection

• Sick mice seek out warmth — As expected, the feverish mice group chose the warmer thermal plate, which resulted in an increase in body temperature. Interestingly, the researchers noted that this group produced prostaglandin E2 — the same molecule that appears in humans during viral and bacterial illness. Prostaglandin E2 is a lipid mediator that’s released into the hypothalamus, which causes your body temperature to rise in response to the invasion of pathogens.³

• Prostaglandin E2 amplifies cold sensors — The study identified a small group of neurons inside the lateral parabrachial nucleus, a region in the brainstem that processes temperature signals. These neurons express EP3 receptors, which are the docking stations for prostaglandin E2. Once this fever molecule rises during infection, it locks onto these receptors, which increases how strongly you perceive cold.

The researchers wrote that activation of these neurons increased cold-sensitive responses to innocuous cooling stimuli, meaning temperatures that usually feel fine suddenly feel harsh and icy. This explains why you’re reaching for blankets while you’re dealing with a fever.

• Chills begin almost immediately after prostaglandin E2 levels rise — This shows that the chill circuit reacts quickly as a defense mechanism. So, the faster your brain pushes you toward warmth, the faster your core temperature rises into a useful fever range. Thus, your immune system gains its thermal advantage early, allowing it to properly fight against pathogens.

• Your thermosensory neuronal pathway influences behavior beyond perception — The researchers found that activating the same neurons also elicited warmth-seeking behavior in the absence of infection. That means if you stimulate this pathway artificially, you still move toward heat even when you are not sick. This shows the system exists for one reason: to increase body temperature when your brain believes it is required.

Again, the warmth-seeking circuit becomes active before your fever reaches its peak. This shows that chills are not the result of fever — they produce fever. Understanding this sequence helps you see chills as a constructive signal rather than something to fight.

• The warmth-seeking behavior and shivering operate through different pathways — Shivering, which are rapid muscle contractions that generate heat, comes from the preoptic area of the hypothalamus. Meanwhile, warmth-seeking, which is the conscious choice to go somewhere warmer, is driven by the parabrachial-to-amygdala circuit. The researchers summarize these two distinct processes in the image below:

• Prostaglandin E2 acts as the master switch — Once produced during infection, it binds to EP3 receptors on the parabrachial neurons and changes how they fire. This firing increases the gain on cold signals coming from the skin, similar to turning up the volume on a speaker. Thus, mild cold suddenly feels extreme. This causes your brain to interpret it as a need to preserve heat and raise your temperature, launching warmth-seeking behavior.

Another mechanism involves the amygdala. When the parabrachial neurons send amplified cold signals to this emotional hub, you experience cold not only as a feeling, but as discomfort with urgency behind it.

• Fever temperatures consistently improve outcomes, regardless of whether the organism is cold-blooded or warm-blooded — When your temperature rises during an infection, your immune cells behave differently — faster, stronger, and with greater precision. The review cited a previous study on desert iguanas, where infected animals given the chance to bask in warmer environments survive at far higher rates. When that behavior is blocked, mortality rises sharply.

In humans, the authors describe how antipyretic drugs, medications that lower fever, regularly produce worse outcomes during infection. They cite evidence showing that a simple 1 to 4 degrees C increase in core temperature strengthens immune performance, and lowering the temperature weakens your defenses.

• Increasing your body’s temperature eliminates microbes — The researchers explain that at febrile temperatures around 40 to 41 degrees C (or 104 to 105 degrees F), poliovirus replication drops more than 200-fold. That means high body heat essentially cripples the virus’s ability to reproduce. This also shows that fever temperatures do more than energize your immune system — they directly interfere with pathogen survival.

Connecting this to the previously featured study, the purpose of warmth-seeking due to chills means your body is creating an environment where pathogens struggle to proliferate.

• Fever modifies not only how immune cells attack pathogens, but where they also travel — Interleukin-6 (IL-6), an immune molecule deeply involved in fever, helps shuttle immune cells into lymphoid tissues where responses are coordinated.

The review notes that this transport step is temperature-sensitive, meaning immune cells move more efficiently when your body heats up. Thus, if you suppress your fever early, you distort the timing and coordination of this movement, slowing your innate ability to clear the infection.

• Your body starts up different pathways during a fever to protect itself — Prostaglandin E2 triggers the hypothalamus to raise the internal thermostat, but adrenergic signals tied to heat production influence the behavior of immune cells.

In other words, multiple pathways generate overlapping layers of immune enhancement. The review clarifies that immune activation at febrile temperatures works through distinct but converging mechanisms — direct thermal stress on pathogens, enhanced cell trafficking, stronger cell activation, and faster replication of certain immune cells.

This multifaceted boost explains why fever is evolutionarily conserved across so many species despite having existed for 600 million years — it’s vital for survival.

• Cellular membrane fluidity adapts in the presence of fever — Higher temperatures make cellular membranes slightly more flexible. Immune cells rely on flexible membranes to move, communicate, and engulf pathogens. Pathogens, however, often rely on rigid structures that do not tolerate heat well. This difference in heat tolerance gives your immune system a structural advantage — temperature becomes a selective pressure that favors your survival over the microbe’s survival.

• Many immune cells perform better at higher temperatures — For example, certain cytokines and signaling receptors transmit stronger or more efficient messages between immune cells when the body is warmer. Meanwhile, many viral and bacterial proteins become unstable or misfolded when exposed to the same temperatures. This dual effect creates a biochemical environment that favors rapid recovery.

• Drugs suppress your body’s natural healing mechanisms — The American Academy of Pediatrics (AAP) warns against “fever phobia” and the persistent need to bring down a fever through drugs, saying:⁵

“Appropriate counseling on the management of fever begins by helping parents understand that fever, in and of itself, is not known to endanger a generally healthy child. In contrast, fever may actually be of benefit …

When counseling a family on the management of fever in a child, pediatricians and other health care providers should minimize fever phobia and emphasize that antipyretic use does not prevent febrile seizures.”

• Adopt a more relaxed approach to treating a fever — Continuing the point made above, the AAP supports the idea of letting a fever resolve on its own, saying that, “If your child has a fever, they usually do not need to be treated for it. This is especially true if they are drinking, eating, and sleeping normally — and feeling well enough to play.”⁶

Again, the entire point of a fever is to encourage your immune system to create a hostile environment for the pathogens. Essentially, your body “cooking” them. So, anytime you take a fever-reducing drug, you’re undoing any progress your natural defenses are making.

• Fever-reducing drugs masks your symptoms — The downside of taking these drugs is that they trick your body into feeling better, which may cause you to return to your usual activities too soon. When this happens, the illness can actually be prolonged. As noted in one study involving the use of acetaminophen in children with chickenpox, the drug caused prolonged itching and time to scabbing compared to a placebo.⁷

• There are risks to taking fever-reducing drugs — This class of drugs has been associated with various side effects, such as liver damage in the case of acetaminophen. Meanwhile, Ibuprofen has been linked to stomach upset. Children under 19 years old aren’t recommended to take aspirin when they have a fever due to its like to Reye’s syndrome.

• Rest and hydration are all you need — It’s natural for fevers to increase loss of fluids in your system, so it’s important to stay hydrated throughout the entire period. In addition, it would be wise to maintain fluid intake, even if you don’t feel thirsty.

• Instances that require medical intervention — While a fever is generally harmless, note that there are some exceptions:

• What to do when your child has a febrile seizure — If you have a child younger than 5 years old, fever can cause a febrile seizure. While frightening at first, know that it won’t have lasting effects. When a febrile seizure occurs, lay your child on their side or stomach on the ground, then loosen any tight clothing. Support the child during this time to prevent injury.

Once the febrile seizure stops, I still recommend you seek medical care right away to rule out the causes of the seizure, such as meningitis or bacteria in the blood.

• Let the fever run its course — Remember that allowing your body to handle the fever naturally is still the best approach to fighting off a viral or bacterial infection. To lower your risk of getting an infection in the first place, I recommend you eat a healthy diet, get regular exercise, and practice stress relief methods.