COVID-19, caused by the SARS-CoV-2 virus, is widely known for symptoms like fever, suggesting a direct impact on the body’s temperature control. Thermoregulation is the process of maintaining the core body temperature within a narrow, healthy range, typically around 98.6°F (37°C). The virus’s interaction with the immune system can cause varied and sometimes contradictory effects on this system, moving beyond a simple fever response. While fever is the most common sign of the body fighting the infection, COVID-19 can also lead to abnormally low temperatures and long-term regulatory problems.
Understanding Normal Thermoregulation
The body’s ability to maintain a consistent internal temperature is overseen by the hypothalamus, a small region in the brain that acts as the primary thermostat. This area constantly monitors the temperature of the blood and compares it against a predetermined set point, which is generally stable. When the body temperature deviates from this set point, the hypothalamus triggers a series of physical responses to restore balance.
To cool the body down, the hypothalamus signals for vasodilation, which widens blood vessels near the skin’s surface, allowing heat to radiate away. The body also initiates sweating, where the evaporation of moisture from the skin provides a powerful cooling effect. Conversely, if the body needs to generate heat, the hypothalamus triggers vasoconstriction, narrowing blood vessels to conserve warmth near the core. Shivering, which is rapid, involuntary muscle contraction, is also initiated to produce heat through increased metabolic activity.
The Immune Pathway Driving Acute Fever
A typical fever response during a COVID-19 infection begins when the immune system detects the SARS-CoV-2 virus. Immune cells, such as macrophages and monocytes, respond by releasing signaling proteins called cytokines and other inflammatory mediators known as endogenous pyrogens. These chemical messengers, including Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α), travel through the bloodstream.
When these pyrogens reach the hypothalamus, they trigger the local production of prostaglandin E2 (PGE2) in the brain. The PGE2 acts directly on the hypothalamic thermostat, effectively raising the body’s temperature set point. This raised setting then causes the body to initiate heat-generating and heat-conserving mechanisms, such as vasoconstriction and shivering, resulting in chills despite the rising temperature. This elevated temperature is a controlled response, distinct from hyperthermia. The intensity of the fever often correlates with the level of cytokine activity, reflecting the severity of the inflammatory response.
Atypical Temperature Responses During Infection
While fever is the expected response, some patients with severe COVID-19 exhibit an abnormal drop in core body temperature, a condition known as hypothermia, defined as a temperature below 95°F (35°C). This response is particularly observed in vulnerable groups, including the elderly or those with underlying conditions. Hypothermia in the context of severe infection can signal a profound failure of the body’s homeostatic mechanisms.
In critically ill patients, hypothermia can be a manifestation of an overwhelming systemic inflammatory response syndrome (SIRS) or sepsis. Even with elevated levels of inflammatory cytokines, which usually cause fever, a small percentage of patients with sepsis will present with a low temperature. This unexpected drop suggests a failure of the body to mount a coordinated febrile response or a direct disruption of the hypothalamic function due to severe systemic stress. In rare instances, the SARS-CoV-2 virus may directly affect the brainstem or the hypothalamus, potentially causing the temperature regulation center to malfunction and promote a hypothermic state.
Persistent Dysregulation and Post-Infection Syndrome
Long after the acute infection has resolved, some individuals experience “Long COVID,” which includes persistent issues with temperature regulation. Patients frequently report extreme intolerance to hot or cold environments, profuse sweating, or intermittent low-grade fevers and chills. These symptoms indicate a lingering dysfunction within the autonomic nervous system (ANS), which controls involuntary functions like heart rate, blood pressure, and thermoregulation.
This persistent issue is broadly classified as dysautonomia, where the sympathetic and parasympathetic branches of the ANS are imbalanced. The dysregulation can lead to inappropriate signaling to the blood vessels and sweat glands, manifesting as sudden flushing or feeling intensely cold. Research suggests that chronic inflammation or an autoimmune response triggered by the initial viral infection may cause damage to the small nerve fibers that regulate these processes.