There is a number of antiviral medications including Paxlovid and HIV medications that are showing potential benefit for Long COVID [ 17 ]. Herbal antivirals have been found to be effective against a range of viruses , including some corona viruses that cause the common cold [ 18 ]. They might be of assistance in Long COVID but research is still lacking regarding effectiveness of herbal anti-virals specifically for Long COVID .
Autoimmunity
Presence of pre-existing autoimmune disease such as diabetes , Epstein- Barr virus viremia , and presence of latent viruses associated with specific autoantibodies , increase the risk for Long COVID [ 19 ]. Acute COVID infection can trigger the formation of self-tissue antigens that persist after initial infection , and these are thought to contribute to lingering symptoms , particularly in patients with concurrent autoimmune conditions [ 9 ].
Dysautonomia
Many post-acute COVID symptoms fit comfortably under the umbrella of dysautonomia . Given the important role played by the autonomic nervous system in homeostasis and the immune response , it ’ s not surprising that dysautonomia leads to myriad symptoms including tachycardia , circulatory disturbances and orthostatic intolerance [ 20 ].
Vagal withdrawal and sympathetic nervous system over-activation are the key features of dysautonomia . Increased sympathetic nervous system activity is part of the normal inflammatory and immune response and plays a role in helping the body to fight SARS CoV2 infection . The problem that occurs in Long COVID is that the sympathetic nervous system remains somewhat overactive and dysregulated after the initial acute infection [ 21 ]. Also , SARS COV2 appears to be neuro-invasive , bypassing the blood-brain barrier and propagating towards the CNS . It can directly damage areas of the brain such as the Nucleus of the Solitary Tract involved in regulation of the autonomic nervous system as well as directly injuring the vagus and other cranial nerves [ 21 ].
Strategies such as stress reduction , slow breathing and mindfulness that improve vagal tone can reduce the inflammation and physiological dysregulation that drive dysautonomia [ 22-24 ]. Breathing on its own and in conjunction with rhythmic movement and mind-body practices can be a key tool to address dysautonomia . Breathing modulation where the breath is slowed to 0.1 Hz or 6 cycles per minute is a foundational technique for increasing vagal tone and improving cardiorespiratory homeostasis . One can then use topdown and bottom-up techniques that amplify hemodynamic influences or respiratory influences on the vagus or that hook into the central autonomic network .
Rehabilitation Principles to aid recovery in Long COVID
People with Long COVID have functional limitations in physical and cognitive capacity as well as psychological challenges , and the WHO has called on nations to prioritise rehabilitation to improve these functional limitations . A consensus statement for post-COVID rehabilitation was constructed by seven teams of international experts . These teams of experts reviewed the evidence and made recommendations for rehabilitation programs that could reduce symptoms and educate patients about self-help strategies for managing Long COVID symptoms [ 25 ].
Rehabilitation programs that utilise various combinations of self-regulation strategies , breathing exercises , cardiopulmonary rehabilitation and autonomic conditioning are starting to be investigated [ 26-28 ]. Despite the early nature of the research some are proving to be beneficial and are starting to play an increased role in management of Long COVID [ 28 , 29 ].
Stress Reduction and Sleep
Stress management and adequate sleep are important for healing . They play a huge role in the immune and inflammatory processes that drive physiological dysregulation and neuroinflammation in Long COVID [ 22 ]. Duration and quality of sleep are also very important .
A single night of partial sleep deprivation can reduce natural killer cell activity to 72 % of its normal function [ 30 ]. The pro-inflammatory effects of sleep deprivation are also well known . Reductions by 25 % and 50 % of a normative 8 hours of sleep will increase inflammatory cytokines even in healthy , asymptomatic individuals and effects are probably greater in individuals with a propensity to inflammation [ 31 ]. Many patients have undiagnosed obstructive sleep apnea ( OSA ) or some other form of sleepdisordered breathing ( SDB ). OSA , and less obvious forms of SDB such as upper airways resistance syndrome , are important causes of sleep disruption , insomnia [ 32 , 33 ], autonomic dysregulation [ 34 ], chronic stress and systemic inflammation [ 35 , 36 ].
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