Does COVID Affect Body Temperature Regulation?
Explore how COVID-19 influences body temperature regulation, from fever onset to potential post-infection changes in thermoregulation.
Explore how COVID-19 influences body temperature regulation, from fever onset to potential post-infection changes in thermoregulation.
COVID-19 affects multiple systems in the body, including temperature regulation. Many people experience fever during infection, while others report unusual fluctuations in body heat even after recovery. Understanding these effects is important for recognizing lingering symptoms and their impact on health.
Research suggests COVID-19 influences thermoregulation through inflammation, nervous system involvement, and other physiological changes. Exploring these factors clarifies why some individuals struggle with persistent temperature irregularities beyond the acute phase of illness.
The body maintains a stable internal temperature through physiological processes that balance heat production and dissipation. Thermoregulation is governed by the hypothalamus, which acts as the body’s thermostat. It monitors internal temperature through signals from thermoreceptors in the skin and deeper tissues, adjusting responses to maintain homeostasis around 37°C (98.6°F).
When temperature deviates from the optimal range, the body restores balance. In cold environments, heat production increases through shivering and non-shivering thermogenesis, where brown adipose tissue metabolizes fat for warmth. Peripheral vasoconstriction reduces blood flow to the skin, minimizing heat loss. In warm conditions, vasodilation enhances heat transfer to the skin, and sweating cools the body as moisture evaporates.
Hormones also influence temperature control. Thyroid hormones regulate metabolic rate, while cortisol modulates thermoregulatory responses under stress. Neurotransmitters like dopamine and serotonin contribute to temperature perception and autonomic adjustments.
When the body encounters SARS-CoV-2, the inflammatory response activates to contain the virus. Pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) signal the immune system to initiate defense mechanisms. These molecules also influence the hypothalamus, triggering an increase in body temperature. Fever enhances immune function by optimizing white blood cell activity and inhibiting viral replication.
The hypothalamus adjusts the body’s temperature set point in response to inflammatory signals through prostaglandin E2 (PGE2). This lipid compound binds to hypothalamic receptors, prompting thermoregulatory changes such as vasoconstriction and increased metabolic heat production. Individuals often experience chills and shivering as the body works to elevate core temperature.
As fever progresses, metabolic and cardiovascular adjustments support immune activity. Increased heart and respiratory rates facilitate oxygen delivery to tissues, while energy demands rise, leading to the breakdown of glycogen and fatty acids. While fever is beneficial within a controlled range, excessive elevations—hyperpyrexia—can lead to systemic stress, dehydration, and organ dysfunction, requiring medical intervention if temperatures exceed 40°C (104°F).
The brain regulates temperature through neuronal circuits that integrate sensory input and initiate physiological responses. The hypothalamus, particularly the preoptic area (POA), processes thermal signals from thermoreceptors in the skin, muscles, and internal organs. These receptors relay information via the spinothalamic tract and other neural pathways, allowing the POA to activate heat conservation or dissipation mechanisms.
Neurotransmitters fine-tune the hypothalamic response. Gamma-aminobutyric acid (GABA) and glutamate regulate excitatory and inhibitory signals, while serotonin and norepinephrine influence autonomic adjustments. Dopaminergic pathways also play a role, with disruptions in dopamine signaling linked to altered thermoregulation in certain neurological disorders.
Beyond the hypothalamus, other brain regions contribute to thermal regulation. The brainstem, particularly the medullary raphe nuclei, coordinates autonomic responses like vasodilation and shivering. The insular cortex integrates interoceptive signals, modulating temperature perception and behavioral adaptations. The spinal cord transmits thermal information between peripheral sensors and central control centers. This network ensures dynamic responses to temperature changes.
Fever is a common symptom of COVID-19, but temperature fluctuations vary. Some experience prolonged fever, while others have intermittent spikes influenced by viral load, physiological differences, and external factors like hydration and medication. Circadian rhythms also shape temperature patterns, with fevers often peaking in the late afternoon or evening.
In mild to moderate cases, fever typically ranges between 38°C and 39°C (100.4°F–102.2°F) and lasts several days before subsiding. Severe infections, particularly those with excessive inflammation, can push temperatures beyond 40°C (104°F), increasing the risk of dehydration and cardiovascular strain. Some individuals experience chills and night sweats, indicating temperature instability as the body alternates between heat retention and dissipation.
After recovering from COVID-19, some individuals continue to experience temperature disruptions, including low-grade fevers, unexplained chills, or intolerance to temperature extremes. While fever is common during infection, post-viral dysregulation of thermoregulatory pathways may contribute to lingering fluctuations. Many with long COVID report sudden warmth or cold intolerance, suggesting impaired temperature stability even after viral clearance.
Dysautonomia, a dysfunction of the autonomic nervous system, has been observed in post-COVID patients and may explain some temperature inconsistencies. The autonomic nervous system regulates vasodilation, sweating, and metabolic heat production, all essential for thermoregulation. If SARS-CoV-2 affects autonomic control centers, it could lead to inappropriate temperature responses, such as excessive sweating or an impaired ability to generate heat. Persistent inflammation may also influence hypothalamic function, prolonging temperature instability.