A surprisingly large number of people infected with SARS-CoV-2 never develop a fever, and some actually run colder than their usual baseline. This pattern has real consequences: low body temperature during COVID-19 has been linked to roughly double the risk of death compared to patients who mount a normal febrile response. The relationship between body temperature and COVID-19 turns out to be more nuanced than the simple “fever equals infection” screening that defined much of the early pandemic response, and the implications touch everything from who gets missed at the door of a hospital to how the immune system fights the virus at a molecular level.
What “Normal” Body Temperature Actually Looks Like
Before understanding why low temperature matters in COVID-19, it helps to know that the standard many people grew up with is wrong. The 98.6°F figure dates back to a 19th-century German physician, and modern research has consistently found it too high. A large-scale study analyzing body temperature across times of day, days of the week, and seasons found the overall mean was about 98.1°F, with the average never reaching 98.6°F during any time period studied.1PubMed. The daily, weekly, and seasonal cycles of body temperature analyzed at large scale An earlier clinical study in the 1990s placed the mean oral temperature at 98.2°F and the upper limit of normal at 99.9°F rather than the traditional 100.4°F.2JAMA. A Critical Appraisal of 98.6°F, the Upper Limit of the Normal Body Temperature, and Other Legacies of Carl Reinhold August Wunderlich
Even more striking is how much variation exists from person to person. One study found individual mean temperatures ranging from 95.4°F all the way up to 99.3°F, with a group average of about 97.0°F. More than three-quarters of people had a mean temperature at least one degree below the old 98.6°F standard.3PLOS ONE. One size does not fit all: Assuming the same normal body temperature for everyone is not justified This matters for COVID-19 because if your everyday resting temperature sits around 97°F, a reading of 99°F represents a genuine spike for you even though it would not meet the traditional fever threshold. Conversely, a reading of 97°F might be perfectly normal for you but could signal hypothermia for someone whose baseline runs higher.
Many COVID-19 Patients Never Run a Fever
During the pandemic, temperature checks became the first line of defense at hospitals, airports, offices, and grocery stores. The assumption was straightforward: infected people get fevers, and catching the fever catches the infection. The evidence tells a different story. A study of emergency department patients diagnosed with COVID-19 found that only about one in five had a temperature at or above the CDC’s recommended cutoff of 100.4°F at the time of diagnosis, making fever just the sixth most common symptom in that group.4PubMed Central. Clinical Features of Patients with COVID-19: is Temperature Screening Useful?
That means four out of five infected people would have sailed through a temperature-only check. Many of them had perfectly normal or even low readings. Cough, shortness of breath, fatigue, and body aches were all more reliable indicators than an elevated thermometer reading. The researchers noted that combining temperature with additional symptom questions caught over 80% of active cases, but temperature alone was essentially a coin flip weighted heavily toward missing infections.4PubMed Central. Clinical Features of Patients with COVID-19: is Temperature Screening Useful?
When Low Temperature During COVID Signals Danger
While the absence of fever is common and not automatically alarming, a drop below normal into hypothermic territory is a different situation entirely. A study tracking hospitalized COVID-19 patients found that those who developed hypothermia had about twice the probability of dying compared to those who did not. Among patients on ventilators who died, three-quarters had experienced hypothermia at some point during their stay.5PubMed Central. Association of hypothermia with increased mortality rate in SARS-CoV-2 infection That is a striking association, and it held even after accounting for other risk factors.
The clinical picture here is not of someone who simply “didn’t get a fever.” It is of a body that responded to a severe systemic infection by losing heat rather than generating it. This is not unique to COVID-19. In critical care settings, hypothermia during sepsis and other overwhelming infections has long been recognized as a grave sign. But COVID brought it to wider attention because so many people were being screened by temperature and the assumption was uniformly that “hot equals sick.” The reality is more like a U-shaped curve: both very high and very low temperatures during acute COVID predict worse outcomes, with the low end carrying its own distinct set of risks.
Why the Body Goes Cold Instead of Hot
Fever is a deliberate immune strategy. When your body detects an invading pathogen, it raises its thermostat to create an environment that hampers viral replication and boosts certain immune cell functions. But generating a fever is metabolically expensive. It takes a lot of energy to push your core temperature up by even one or two degrees, and that energy has to come from somewhere.
One longstanding hypothesis frames fever and hypothermia as two complementary survival strategies during severe infection. Fever represents an active offensive, spending energy to fight the pathogen directly. Hypothermia represents a defensive retreat, conserving energy to protect the body’s vital systems when reserves are too depleted to mount an effective attack.6Medical Hypotheses. Fever and hypothermia: two adaptive thermoregulatory responses to systemic inflammation Under this framework, a patient who becomes hypothermic during COVID is not simply failing to produce a fever. Their body may be making a trade-off: conserving limited metabolic resources because the infection has overwhelmed the capacity to fight offensively. The problem is that while this energy conservation might protect organs in the short term, it also means the immune system’s temperature-dependent defenses are dialed down.
In elderly patients specifically, the situation is compounded by the fact that baseline body temperature tends to be lower to begin with. A review of clinical data from elderly COVID patients in China noted that their lower starting temperatures translated into lower maximum fevers, making it harder for clinicians to recognize the severity of infection from temperature readings alone.7PubMed Central. Risk factors for predicting mortality in elderly patients with COVID-19: A review of clinical data in China An older adult with a temperature of 99°F might be mounting a febrile response equivalent to 101°F in a younger person, but if the clinical team is looking for 100.4°F as their threshold, that response goes unrecognized.
Temperature and Antiviral Defense at the Cellular Level
Research published after the pandemic began has illuminated just how directly temperature influences the body’s ability to fight SARS-CoV-2. A study in Nucleic Acids Research showed that within a narrow window of just 1.5°C (roughly 2.7°F), between 36.5°C and 38°C, the expression of antiviral genes increased dramatically. Two key branches of immune defense were affected: the production of nitric oxide and the type I interferon response, both of which are central to how cells recognize and suppress viral replication. At lower temperatures, a protein called STAT2, which helps activate these antiviral pathways, was less abundant in cells.8Nucleic Acids Research. Body temperature variation controls pre-mRNA processing and transcription of antiviral genes and SARS-CoV-2 replication
The practical implication is that a person running a temperature at the low end of normal may have cells that are less well-armed against the virus than someone running slightly warm. This does not mean artificially raising your temperature is helpful; the relationship is about the body’s integrated thermoregulatory and immune systems working together. But it helps explain why hypothermia during COVID is so concerning: it is not just a marker of severe illness, it may actively compromise the cellular defenses that need to be working hardest.
Animal research has added another layer to this picture. A study published in Nature Communications found that higher body temperature increased resistance to both influenza A virus and SARS-CoV-2 through a pathway involving gut bacteria and bile acids. Bile acid levels in the blood were significantly lower in COVID-19 patients who developed moderate disease compared to those with mild illness, and those levels correlated with markers of disease severity like fibrinogen.9Nature Communications. High body temperature increases gut microbiota-dependent host resistance to influenza A virus and SARS-CoV-2 infection This suggests the temperature-immunity connection runs through the gut in ways that are only beginning to be mapped.
Why Workplace Temperature Screening Failed
Given how many COVID patients never develop a fever, it is no surprise that the workplace temperature screening programs rolled out during 2020 and 2021 performed poorly. A study evaluating worksite temperature screening programs found that for approximately every one case of COVID-19 caught by a temperature check, about 40 cases walked right through undetected. The researchers concluded that worksite temperature screening was ineffective and recommended against it.10PubMed Central. Worksite Temperature Screening for COVID-19
The 1-to-40 ratio is damning, and it reflects several overlapping problems. Many infected people were pre-symptomatic or asymptomatic and had not yet developed (or would never develop) a fever. Others had naturally low baselines, so their febrile response never crossed the screening threshold. And some simply took antipyretics like ibuprofen or acetaminophen before showing up, masking any temperature rise. The broader lesson is that body temperature is a poor standalone proxy for infection status. It carries useful information in context, especially when combined with other symptoms and clinical judgment, but as a binary pass/fail gate it was deeply flawed.
Who Tends to Run Colder and Why It Matters for COVID
Several factors influence where your baseline temperature sits, and all of them become relevant during a COVID-19 infection. Age is the biggest one. Body temperature declines gradually over the lifespan, and older adults tend to have both lower resting temperatures and a blunted febrile response to infection. As noted earlier, this made it harder to identify severe COVID in elderly patients based on temperature alone, and it contributed to the higher mortality seen in this group.
Sex plays a role too, though in a more complex way than commonly assumed. Women generally have more active brown fat tissue, which generates heat through a process distinct from shivering. Research suggests that women maintain larger and more efficient brown fat depots into older age, which may contribute to better metabolic and thermoregulatory function over the lifespan.11PubMed Central. Sex differences and aging: Is there a role of brown adipose tissue? Paradoxically, women often report feeling colder than men in everyday life because their skin surface temperature tends to be lower, but their core thermoregulation may actually be more robust. How this translates to COVID-19 outcomes specifically is still being studied, but the sex-based differences in thermoregulation add another dimension to why a single fever cutoff is a blunt instrument.
Body composition, medications, and chronic conditions also shift the baseline. People with hypothyroidism, diabetes, or malnutrition tend to run cooler. Beta-blockers and certain sedatives can suppress the febrile response. If you take a medication that keeps your temperature down and then contract COVID-19, your clinical team may never see the fever that would otherwise alert them to worsening infection.
Temperature Dysregulation in Long COVID
The relationship between body temperature and COVID does not end when the acute infection clears. People with long COVID frequently report feeling like their internal thermostat is broken: random chills, night sweats, intolerance to heat or cold, and fluctuating temperature readings that do not match how they feel. Research has begun to put measurable data behind these complaints.
A study using infrared thermography found that long COVID patients had peripheral temperature increases ranging from 0.1°C to 1.6°C in various body regions compared to controls. These patients also had elevated levels of pro-inflammatory signaling molecules (IL-17 and IL-2) and reduced levels of the anti-inflammatory IL-4, alongside decreased heart rate variability, a marker of autonomic nervous system dysfunction.12PubMed Central. Imbalance of Peripheral Temperature, Sympathovagal, and Cytokine Profile in Long COVID The researchers suggested that the temperature changes were not just a hypothalamic glitch but part of a broader disruption of the systems that regulate circulation, metabolism, sleep, and breathing.
This fits with the emerging understanding that long COVID involves widespread autonomic dysfunction. The hypothalamus does not just set body temperature in isolation; it coordinates temperature with blood pressure, heart rate, digestion, and circadian rhythms. When that control center is disrupted by persistent inflammation or viral damage, the downstream effects ripple through multiple systems. A recent review estimated that the cumulative global incidence of long COVID ranges from 60 to 400 million individuals depending on the definition used, and that an estimated 13% to 45% of those people meet criteria for a related condition involving similar autonomic and metabolic disruption.13Cell Reports Medicine. Mechanisms of the symptoms, behavior, and metabolic changes in long COVID and myalgic encephalomyelitis/chronic fatigue syndrome Temperature dysregulation, in other words, is not a quirky side effect. It may be a window into the core pathology of long COVID itself.
Why Individual Baselines Matter More Than Universal Cutoffs
One of the clearest lessons from the pandemic is that a single temperature number applied to everyone is a poor diagnostic tool. Research on wearable temperature monitors has demonstrated this in real time. A feasibility study using wearable devices found that participants with symptoms showed a significant average temperature increase of about 0.63°C above their own baseline, but the person-to-person variability was substantial enough that using a fixed threshold like 38°C (100.4°F) for everyone would miss many cases and falsely flag others.14Scientific Reports. Feasibility of continuous fever monitoring using wearable devices
The shift in thinking here is from absolute temperature to relative change. If a wearable device knows your normal daily pattern, including its dips in the early morning and peaks in the late afternoon, it can flag a deviation that is meaningful for you personally. A half-degree rise above your personal baseline might be clinically significant even if your absolute temperature reads 98.9°F, which no forehead scanner at a building entrance would flag. This approach requires continuous data rather than a single snapshot, which is part of why it was not practical for mass screening during the pandemic. But for clinical monitoring of high-risk individuals, especially those who tend to run cold, personalized baselines could catch deterioration earlier than traditional thresholds.
Therapeutic Hypothermia and an Unexpected Research Direction
In an interesting twist, the same pandemic that revealed the dangers of unintentional hypothermia in COVID patients also prompted researchers to ask whether deliberate, controlled cooling might have therapeutic value. Mild therapeutic hypothermia has been used for years in other clinical settings, particularly after cardiac arrest and in neonatal brain injury, where lowering body temperature protects tissue from inflammation-driven damage.
A review exploring this idea for COVID-19 noted that controlled cooling reduces the release of several inflammatory molecules that drive the cytokine storm seen in severe cases. It also improves the ratio of oxygen in the blood to the oxygen being delivered, potentially helping with the respiratory failure that kills many critically ill COVID patients. Cooling may suppress the formation of tiny blood clots that contribute to organ damage and improve oxygen diffusion into tissues.15Journal of Critical Care. Cheap and simple, could it get even cooler? Mild hypothermia and COVID-19
This creates an apparent contradiction: uncontrolled hypothermia predicts death, but carefully managed cooling might prevent it. The distinction lies in context and degree. A patient whose body drifts into hypothermia because their metabolism is collapsing under overwhelming infection is in a very different physiological state from a patient whose temperature is deliberately lowered by a few degrees in an ICU with full monitoring and support. In the first case, the cold reflects a loss of control. In the second, it is a tool wielded precisely to reduce inflammation without disabling the rest of the body’s defenses. Whether therapeutic hypothermia will become a standard part of the COVID-19 treatment toolkit remains unresolved, but the research highlights how temperature is not inherently good or bad. What matters is the body’s ability to regulate it intentionally.