SARS-CoV-2 disrupts the body’s ability to regulate temperature during acute illness and, for some people, for months or even years afterward. The virus triggers a fever response in most infected individuals, but it can also cause the opposite problem: dangerously low body temperature in critically ill patients. Beyond the acute phase, accumulating evidence points to damage across several systems the body relies on to maintain a stable internal temperature, from the autonomic nerves that control blood vessel dilation and sweating to the tiny blood vessels that distribute heat to the skin. Understanding how these mechanisms break down helps explain why so many people recovering from COVID report strange sensations of feeling inexplicably hot, cold, or both.
Fever Is Expected, but Hypothermia Is the Dangerous Surprise
Most people associate COVID with fever, and that response is well documented. A mild fever during viral infection serves a protective purpose: it slows viral replication and boosts immune defenses against the pathogen.1PubMed Central. Effect of a fever in viral infections – the ‘Goldilocks’ phenomenon? But a significant minority of COVID patients develop body temperatures below normal rather than above it, and this turns out to be far more alarming than a high fever.
A study examining initial body temperature as a predictor of outcomes found that patients admitted with a temperature below 36°C had roughly three times the odds of dying compared to those in the normal range. All seven patients in that study who never managed to raise their body temperature above 36°C died.2Scientific Reports. Body temperature as a predictor of mortality in COVID-19 Another study found the probability of death was about twice as high in hypothermic COVID patients, and among ventilated patients who died, three-quarters had been hypothermic.3International Journal of Infectious Diseases. Association of hypothermia with increased mortality rate in SARS-CoV-2 infection
The mechanism behind this may involve the virus’s ability to reach the central nervous system. SARS-CoV-2 can enter the brain through pathways including the olfactory bulb, and once there it can interfere with the hypothalamus, the brain region that acts as the body’s thermostat. When that control center is compromised, the body may lose its ability to generate the fever it needs to fight the infection, or worse, it may fail to maintain even a baseline temperature. If left unmanaged, hypothermia in COVID patients can lead to cardiovascular complications including dangerous heart rhythms.4PubMed Central. Acute hypothermia in a patient with COVID-19: a case report and summary of the evidence
COVID Flattens the Body’s Normal Daily Temperature Cycle
Your core body temperature is not a fixed number. It follows a reliable daily rhythm, dipping in the early morning and peaking in the late afternoon. This cycle is tied to the circadian clock that governs sleep, immune cell activity, and metabolic processes. COVID disrupts that rhythm in a way researchers can measure.
One study found that COVID-19 infection blunted the normal circadian fluctuation of core body temperature, along with disrupting the daily rhythms of resting heart rate and certain immune cell populations.5PubMed Central. Is there a diurnal variation of COVID-19 patients warranting presentation to the health centre? A chronobiological observational cross-sectional study Instead of the body temperature rising and falling in a predictable wave throughout the day, it became more static, as though the internal clock controlling it had been muted. A separate study examining continuously monitored hospitalized patients found that normal skin temperature rhythmicity was present in patients who were recovering from COVID, but absent in those who were still acutely ill or who ultimately died.6PLOS ONE. Circadian patterns of heart rate, respiratory rate and skin temperature in hospitalized COVID-19 patients
This flattening of the temperature cycle is more than a curiosity. Circadian rhythms coordinate immune function, and losing that coordination may impair the body’s ability to fight infection at the times of day when immune activity is normally highest. The return of a normal temperature rhythm during hospitalization appears to be a positive sign, while its absence tracks with worse outcomes.
Autonomic Nerve Damage and the Long COVID Connection
The autonomic nervous system is the body’s background operator. It controls processes you never consciously think about: heart rate, blood pressure, digestion, and temperature regulation. A growing body of research shows that SARS-CoV-2 can damage this system, producing a cluster of problems collectively called dysautonomia that persist well beyond the initial infection.
In one early series of post-COVID autonomic evaluations, the most common complaint was lightheadedness, reported by 93% of patients. But the list also included excessive sweating, burning pain, and symptoms that developed anywhere from the first day of infection to four months later.7PubMed Central. Autonomic dysfunction following COVID-19 infection: an early experience One of the most recognized post-COVID autonomic conditions is postural orthostatic tachycardia syndrome (POTS), a condition in which the heart rate spikes excessively upon standing. A study comparing post-COVID patients and those with chronic fatigue syndrome found POTS in roughly 14% of the post-COVID group.8PubMed Central. Dysautonomia and small fiber neuropathy in post-COVID condition and Chronic Fatigue Syndrome Documented cases of post-COVID POTS include patients reporting explicit temperature dysregulation alongside the more typical symptoms of dizziness and palpitations.9PubMed Central. Postural orthostatic tachycardia syndrome and post-acute COVID-19
The underlying cause in many of these patients appears to be small fiber neuropathy: damage to the thin nerve fibers that relay pain, temperature, and autonomic signals. A cohort study found that this type of nerve damage can develop during or shortly after SARS-CoV-2 infection, provoking sensory and autonomic symptoms that tend to persist for more than six months.10PubMed. Small Fiber Neuropathy in Long COVID: A Cohort Study with Multimodal Assessment and Follow-Up A case-control study confirmed the diagnosis via skin biopsy in post-COVID patients and found that the vast majority also experienced the kind of fatigue and exercise intolerance characteristic of chronic fatigue syndrome, along with measurable dysautonomia.11PubMed Central. Case-Control Study of Individuals With Small Fiber Neuropathy After COVID-19 These small fibers are the ones responsible for telling your sweat glands to activate or instructing the blood vessels in your skin to dilate when you’re too warm. When they stop working properly, your body’s thermal fine-tuning degrades.
Sweating That Does Not Work Right
Sweating is one of the body’s primary cooling mechanisms, and it depends on functioning autonomic nerve signals reaching the sweat glands. Research has documented measurable sweat dysfunction in people who have recovered from COVID. One study using electrochemical skin conductance testing found that about a quarter of recovered COVID patients had reduced sweat function, with 6% showing severe impairment.12PubMed Central. Sudomotor dysfunction in patients recovered from COVID-19
A study comparing post-COVID patients with chronic fatigue syndrome patients found abnormal sweat-gland readings in about a fifth of the post-COVID group using a device called a Sudoscan, which measures the ability of sweat glands in the hands and feet to respond to electrical stimulation.8PubMed Central. Dysautonomia and small fiber neuropathy in post-COVID condition and Chronic Fatigue Syndrome Paradoxically, some patients experience the opposite problem: excessive sweating rather than too little. Hyperhidrosis was reported in about 11% of patients in one post-COVID autonomic dysfunction series.7PubMed Central. Autonomic dysfunction following COVID-19 infection: an early experience Whether the sweating system under-responds or over-responds, the practical result is the same: the body loses precision in one of its main tools for cooling itself.
Microvascular Damage and Poor Blood Flow to the Skin
Temperature regulation depends heavily on blood flow. When you’re warm, blood vessels near the skin surface open up to radiate heat outward. When you’re cold, they constrict to conserve warmth in the core. COVID can impair this process at the level of the smallest blood vessels.
In critically ill COVID patients, skin microvascular blood flow was significantly lower than in comparably sick patients without COVID, and the endothelium-dependent vascular response, the blood vessels’ ability to relax when signaled by the cells lining them, was roughly threefold weaker.13Annals of Intensive Care. Impaired skin microvascular endothelial reactivity in critically ill COVID-19 patients This impairment persisted even when compared against patients with similar severity scores, suggesting the virus itself, not just being critically ill, was specifically damaging the blood vessels. Another study confirmed reduced microvascular responses in critical COVID and, importantly, found that even three months after the initial illness, surviving patients still tended to show impaired vessel relaxation compared to healthy controls.14PubMed Central. Microvascular Dysfunction in Patients with Critical Covid-19, a Pilot Study
Researchers believe this involves dysfunction of both the endothelial cells lining the vessels and the smooth muscle cells that physically constrict or relax them.15PubMed Central. Impaired Microvascular Function in Patients With Critical COVID-19 When both layers are compromised, the blood vessels lose the ability to respond quickly to signals telling them to open or close. The result can manifest as cold extremities, uneven skin temperatures, or difficulty adjusting to changes in environmental temperature. Some patients develop overt vascular problems in their fingers and toes, including patterns resembling Raynaud’s phenomenon, where blood supply to the digits shuts down in response to cold or stress. Case reports describe patients with previously mild Raynaud’s experiencing dramatic worsening during acute COVID, even during warm weather.16PubMed Central. Worsening of Primary Raynaud’s Phenomenon During Episodes of Pyrexia and Rigors in SARS-CoV-2 Infection More extreme cases involve acro-ischemia, where blood flow to the fingers or toes drops enough to cause tissue damage, with researchers identifying several distinct clinical patterns of this presentation in COVID patients.17PubMed Central. Incidence, Characteristics, Laboratory Findings and Outcomes in Acro-Ischemia in COVID-19 Patients
Measurable Peripheral Temperature Changes in Long COVID
Using infrared thermal imaging, researchers have been able to detect and quantify temperature differences in long COVID patients. One study found that people within the first four months of long COVID had higher peripheral temperatures than both healthy controls and people who had been living with long COVID for longer than four months, with increases ranging from 0.1 to 1.6°C across multiple body regions. These patients also showed elevated pro-inflammatory cytokines and reduced heart rate variability, indicating simultaneous immune activation and autonomic imbalance.18PubMed Central. Imbalance of Peripheral Temperature, Sympathovagal, and Cytokine Profile in Long COVID
The fact that the temperature elevations were more pronounced in the earlier phase of long COVID suggests an active inflammatory process that may gradually settle over time, at least partially. But the concurrent reduction in heart rate variability points to autonomic dysfunction that could outlast the inflammatory trigger, potentially leaving people with lasting thermoregulatory problems even after the visible inflammation fades.
These findings also help explain a pattern many long COVID patients recognize anecdotally: the early months feel different from the later ones. In the initial period, people may feel flushed and warm, especially in the limbs. As months pass, the sensation may shift toward feeling cold or having unpredictable swings. The science suggests this tracks with the body transitioning from active inflammation to a state where the regulatory damage persists but the inflammatory fuel diminishes.
Why So Many Patients Feel Hot and Cold for No Obvious Reason
One of the most common and frustrating symptoms reported by people with post-viral fatigue syndromes, including long COVID, is the subjective sensation of being too hot or too cold without any clear environmental trigger. A study of patients with ME/CFS, a condition that shares substantial overlap with long COVID, found that about two-thirds experienced neuroendocrine manifestations including sweaty hands, night sweats, cold extremities, shivering, and the feeling of abnormal body temperature.19Frontiers in Psychiatry. Clinical Heterogeneity in ME/CFS. A Way to Understand Long-COVID19 Fatigue
One possible contributor to these sensations is neuroinflammation. Brain imaging research in ME/CFS patients, using magnetic resonance spectroscopy to measure brain metabolites linked to inflammation, has detected elevated temperature in several brain regions along with metabolic signatures consistent with inflammation. The findings correlated with the severity of reported fatigue.20Frontiers in Neurology. Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses If the brain regions involved in processing thermal signals are themselves inflamed, the mismatch between what the body is actually experiencing and what the brain perceives could produce these phantom hot and cold sensations. The thermostat is not just miscalibrated at the output level; it may be receiving garbled input from an inflamed control center.
The endocrine system adds another layer. The hypothalamic-pituitary-adrenal axis, which governs the stress response and links hormonal output to nervous system signals, can become dysfunctional after COVID. Abnormalities in adrenal and thyroid function have been noted in post-COVID fatigue, and both of these glandular systems directly influence metabolic rate and heat production. When they falter, the body’s baseline heat generation shifts in ways that can make someone feel persistently cold or cycle between chills and overheating.
Whole-Body Hyperthermia as an Experimental Treatment
Given how central temperature dysregulation is to the long COVID experience, some clinicians have explored whether deliberately manipulating body temperature could help. Whole-body hyperthermia, a treatment that gently raises core body temperature in a controlled clinical setting, has been tested as part of a multimodal approach for post-COVID syndrome. In a case series, patients who received this treatment showed significant improvement on a standardized fatigue questionnaire, and about 63% of respondents rated the hyperthermia component as effective.21International Journal of Hyperthermia. Whole-body hyperthermia as part of a multimodal treatment for patients with post-covid syndrome – a case series
The rationale is not entirely clear-cut, and this remains an experimental approach with small numbers. One hypothesis is that controlled heating may help reset autonomic reflexes, improve blood vessel function, or modulate immune activity. The treatment also draws on older research showing benefits of hyperthermia for depression and chronic pain conditions. It is not a mainstream recommendation, and anyone interested would need to pursue it through a clinical program rather than attempting it independently, since uncontrolled overheating carries its own serious risks. But the fact that researchers are now targeting the thermoregulatory system directly reflects a growing recognition that fixing temperature control is not a side issue in long COVID recovery; for many patients, it is central to what they experience every day.