Comorbid insomnia and sleep apnea (COMISA) as an additional risk factor for reduced response to the COVID-19 vaccination?

First, we would like to congratulate all the authors involved in producing the published article “Undiagnosed sleep disorder breathing as a risk factor for critical COVID-19 and pulmonary consequences at the midterm follow-up.” [1]. Then, share some of our ideas about the theme, make suggestions and raise hypotheses.

Inflammation is a core feature of obstructive sleep apnea (OSA). Elevated pro inflammatory cytokines, such as IL-6 are often observed in OSA patients and participate in autonomic related pathophysiological challenges [2]. Insomnia patients may present with a compromised immunity and therefore may experience suboptimal vaccine-induced antibody response. In this context, Taylor et al. have found an immune dysregulation in insomniacs [3]. On the other hand, Vgontzas et al. pointed out that insomnia is characterized by a state of hyperarousal with 24-hr increases in ACTH and cortisol secretion. Hence, the relationship between the effects of cortisol and immune suppression are well defined [4] and the interaction between both factors seems to predispose to an increased severity of COVID-19.

Insomnia and obstructive sleep apnea (OSA) are the most common sleep disorders and frequently co-occur as in COMISA patients. For example, 30–40% of insomnia patients meet the diagnostic criteria for OSA when evaluated with overnight polysomnography and 30–50% of OSA patients inform clinically relevant symptoms of insomnia [5]. Interaction between sleep disorders are common and this deleterious “cross talk” can have an impact on cytokine balance; also this process can contribute to changes in the profile of immune responses [6]. Accordingly, Mello et al. also suggested that just one night of disturbed sleep can reduce immunologic response to vaccination to influenza A and hepatitis A [6]. It is plausible the same could be true for COVID-19 vaccination and that COMISA could be an important player.

Funding

Research was funded by (CNPq), granting number: 126739/2020-0.