Insomnia, the persistent inability to fall asleep or stay asleep, is a frequently reported symptom during and after a COVID-19 infection, hindering recovery and reducing overall quality of life. Understanding the relationship between the SARS-CoV-2 infection and sleep involves looking at the body’s physiological response to the virus and the psychological effects of the illness and the pandemic itself. A complex interplay of inflammatory signals, direct neurological effects, and profound psychological stress contributes to COVID-related insomnia.
The Acute Role of Systemic Inflammation and Cytokines
The body’s immediate defense against the SARS-CoV-2 virus involves a powerful immune response marked by systemic inflammation. During this acute phase, the immune system releases chemical messengers known as pro-inflammatory cytokines, such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-\(\alpha\)). While these molecules are necessary to fight the infection, their heightened presence can disrupt the body’s normal sleep regulation processes.
These cytokines are known to be “somnogenic,” meaning they can induce sleep, but an excessive or dysregulated release actually leads to fragmented sleep architecture. The brain structures that regulate sleep, including the hypothalamus, are highly sensitive to these inflammatory signals. Instead of deep, restorative sleep, the inflammation promotes a state of hyperarousal and changes the balance of sleep stages, often reducing the amount of rapid eye movement (REM) and slow-wave sleep. The resulting poor sleep quality then creates a cycle, as sleep deprivation itself can further increase the levels of these pro-inflammatory cytokines, amplifying the overall inflammatory state.
Direct Neurological Impact and Post-Infection Sleep Changes
For many people, sleep issues persist long after the initial infection has cleared, becoming a symptom of post-COVID conditions, often called Long COVID. This lingering insomnia is often tied to the virus’s impact on the nervous system itself, rather than the acute inflammatory battle. The virus or the resulting chronic inflammation can affect parts of the brain that regulate the sleep-wake cycle, such as the hypothalamus and brainstem.
One significant factor is the development of autonomic nervous system (ANS) dysfunction. This dysregulation can manifest as Postural Orthostatic Tachycardia Syndrome (POTS), where poorly controlled heart rate and blood pressure make it difficult to lie down comfortably and maintain sleep. Persistent fatigue and “brain fog,” other common symptoms of Long COVID, are also linked to poor sleep quality and chronic immune activation. These persistent changes in the nervous system and ongoing low-grade inflammation contribute to chronic insomnia.
Psychological Stress and Disruption of Circadian Rhythms
Non-physiological factors contributing to COVID-related insomnia stem from the psychological toll of the pandemic, the illness, and isolation. Illness itself is a stressor, and health anxiety about the virus’s progression or lasting effects can trigger a state of hyperarousal. This state keeps the mind and body highly alert, making it nearly impossible to initiate or maintain sleep.
The disruption of daily routines due to quarantine, working from home, or hospitalization also affects the body’s internal clock, the circadian rhythm. Irregular schedules and altered light exposure—such as reduced daylight and increased screen time at night—can desynchronize the production of melatonin, the hormone that signals the body to sleep. This disruption leads to a delayed sleep phase, causing individuals to feel wide awake late into the night and struggle to wake up in the morning. The resulting lack of sleep then increases anxiety and stress, creating a vicious cycle where psychological distress feeds the insomnia.