Attorney Reference No.: A2169-7048WO (ESS-135.WO) BIOMARKERS OF AMINO ACID COMPOSITION TREATMENT RESPONSE IN LONG COVID RELATED APPLICATIONS This application claims priority to U.S. Serial No. 63/394,205 filed August 1, 2022, the contents of which are incorporated herein by reference in their entirety. BACKGROUND Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for coronavirus disease 2019 (COVID-19). Research to determine the full long-term sequelae of COVID-19 is on-going. Efforts to study and treat long-term sequelae of COVID-19 are hindered by a paucity of biomarkers and clinical tests to reliably ascertain the efficacy of therapies for long COVID. New objective methods for assessing response to long COVID therapies are needed. SUMMARY Disclosed herein, at least in part, are methods of assessing a response to post-acute sequelae of COVID-19 (PASC), also known as long COVID. In some embodiments, the method of assessing a response further comprises administration of a composition including at least four different amino acid entities. In some embodiments, the subject has one or more symptoms or signs selected from the group consisting of anorexia, anxiety, arrythmias, confusion (“brain fog”), dementia, depression, dyspnea, fatigue, hair loss, headache, heart failure, cardiomyopathy, angina, hepatic dysfunction, hyperglycemia, type 2 diabetes, increased heart rate, inflammation, loss of appetite, loss of memory, loss of smell, mood disorder, muscle weakness, myocardial ischemia, post-exertional malaise, diminished neurocognition, diminished sensory function, pulmonary infiltrates or fibrosis, postural orthostatic hypotension, renal dysfunction, and respiratory distress. In certain embodiments, the subject has one or more symptoms or signs selected from the group consisting of myalgia, fibromyalgia, idiopathic pulmonary fibrosis, fatigue, muscle 1 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) fatigue, mitochondrial dysfunction, dyspnea after exertion, postural orthostatic tachycardia syndrome, tachycardia, mood disorders, and depression. In certain embodiments, the subject has one or more of the following characteristics: i. impaired or delayed immune response; ii. increased oxidative stress and/or proinflammatory state; or iii. dysregulated endothelial function (e.g., hypercoagulation or perfusion). In certain embodiments, after administration, the subject exhibits one or more of the following: i. increased mitochondrial biogenesis; ii. restored (e.g., partially or fully restored) mitochondrial oxidative capacity; iii. restored (e.g., partially or fully restored) cellular respiration and/or cellular energetics; iv. improved cellular response under higher metabolic demand conditions (e.g., exertion), e.g., in muscle; v. improved mitochondrial respiration (e.g., comprising increased substrate mobilization, increased nitric oxide (NO) signaling, enhanced microvascular or tissue perfusion, enhanced vascular conduction, or increased micro- vascular perfusion) vi. reduced inflammation (e.g., reduce liver inflammation), protein breakdown, and muscle fatigue post-exercise; vii. normalized (e.g., partially or fully normalized) coagulation function; viii. improved mitochondrial energetics and/or redox balance, ix. decreased oxidative stress; x. improved cellular respiration, antioxidant and/or anti-inflammatory effects, xi. increased nucleotide pool availability; xii. increased preferential fatty acid oxidation relative to glycolysis; xiii. increased level of ketone bodies; xiv. decreased FGF-21 xv. decreased vascular permeability 2 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) xvi. decreased fatigue, e.g., from moderate or severe fatigue to mild fatigue; e.g. from mild fatigue to absence of fatigue; from moderate or severe fatigue to absence of fatigue; xvii. improved sleep, e.g., improved sleep/wake cycle; xviii. improved mobility; xix. improved exercise capacity; xx. improved epithelial cell survival; xxi. improved T-cell response; xxii. reduced mitochondrial ROS production; xxiii. reduced HIF1a signaling; xxiv. improved oxidative phosphorylation; xxv. improved executive function; and xxvi. increased ability to concentrate. In certain embodiments, the fatigue comprises one or both of persistent fatigue and exertional fatigue. In some embodiments, the fatigue comprises one or both of mental fatigue and physical fatigue. In certain embodiments, the subject had a COVID-19 infection and is experiencing fatigue. In certain embodiments, the subject experiences fatigue at at least 4, 8, 12, or 16 weeks after infection with SARS-Cov-2. In certain embodiments, the subject experiences fatigue at less than 4 weeks (e.g., at less than 3 weeks, 2 weeks, or 1 week) after infection with SARS-Cov-2. In some embodioments, the amino acid entities administered further comprises a glycine (G)-amino acid entity. In certain embodiments, the amino acid entities administered further comprise one, two, three or more (e.g., all) of a histidine (H)-amino acid entity, a lysine (K)- amino acid entity, a phenylalanine (F)-amino acid entity, and a threonine (T)-amino acid entity. In some embodiments, the subject was infected with an alpha strain of SARS-CoV-2 (e.g., a B.1.1.7 or Q lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with a beta strain of SARS-CoV-2 (e.g., a B.1.351 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with a gamma strain of SARS-CoV-2 (e.g., a P.1 lineage or a lineage descendent therefrom). In some embodiments, the 3 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) subject was infected with a delta strain of SARS-CoV-2 (e.g., a B.1.617.2 or AY lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with an epsilon strain of SARS-CoV-2 (e.g., a B.1.427 or B.1.429 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with an eta strain of SARS-CoV-2 (e.g., a B.1.525 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with an iota strain of SARS-CoV-2 (e.g., a B.1.526 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with a kappa strain of SARS-CoV-2 (e.g., a B.1.617.1 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with a 1.617.3 strain of SARS-CoV-2 or a lineage descendent therefrom. In some embodiments, the subject was infected with a Mu strain of SARS-CoV-2 (e.g., a B.1.621 or B.1.621.1 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with a zeta strain of SARS-CoV-2 (e.g., a P.2 lineage or a lineage descendent therefrom). In some embodiments, the subject was infected with an Omicron strain of SARS- CoV-2 (e.g., a B.1.1.529, BA.1, BA.1.1, BA.2, BA.3, BA.4 or BA.5 lineage or a lineage descendent therefrom). In some embodiments, the subject is an adult. In some embodiments, the subject is between 18 and 65 years of age (e.g., between 18 and 30, 30 and 40, 40 and 50, 50 and 60, or 60 and 65 years of age). In some embodiments, the subject is an adolescent or a child. In some embodiments, the subject is 17 years of age or younger. In some embodiments, the subject is between 1 and 17 years of age (e.g., between 1 and 5, 5 and 10, 10 and 15, or 15 and 17). In some embodiments, the subject has fatigue-predominant PASC. Another aspect of the invention further provides a method for treating a subject diagnosed with post-viral fatigue, particularly post-acute sequelae of COVID-19 comprising administering to a subject in need thereof an effective amount of the composition of any one of aspects or embodiments disclosed herein. In some embodiments, a subject has one or more symptoms or signs selected from the group consisting of anorexia, anxiety, arrhythmias, confusion (“brain fog”), dementia, depression, dyspnea, fatigue, hair loss, headache, heart failure, cardiomyopathy, angina, hepatic dysfunction, hyperglycemia, type 2 diabetes, increased heart rate, inflammation, loss of appetite, loss of memory, loss of smell, mood disorder, muscle weakness, myocardial ischemia, post-exertional malaise, diminished neurocognition, diminished sensory function, pulmonary infiltrates or fibrosis, postural orthostatic hypotension, renal 4 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) dysfunction, and respiratory distress. In some embodiments, a subject has one or more symptoms or signs selected from the group consisting of myalgia, fibromyalgia, idiopathic pulmonary fibrosis, fatigue, muscle fatigue, mitochondrial dysfunction (e.g., increase lactic acid production), dyspnea after exertion, postural orthostatic tachycardia syndrome, tachycardia, mood disorders, and depression. In some embodiments of the methods disclosed herein, e.g., of any of the methods described herein, the subject has immunologic symptoms or signs, metabolic symptoms or signs, and/or neurologic symptoms or signs. In some embodiments, an immunologic symptom or sign is selected from the group consisting of increased markers of inflammation (e.g., erythrocyte sedimentation rate, c reactive protein), increased proinflammatory cytokines (e.g., CRP, IL-1A, IL-17a, TNF-alpha), decreased cytotoxicity of natural killer cells, expression of cytolytic proteins, and production of cytokines, increased CD8+ cytotoxic T cells with CD38 activation antigen, T cell exhaustion, and increased autoantibodies, especially against targets in CNS and autonomic nervous system. In some embodiments, a metabolic symptom or sign is selected from the group consisting of increased lactic acid, reduced ATP generation from glucose by the tricarboxylic acid (TCA) cycle, reduced levels of fatty acids and of acyl-carnitine, reduced levels of amino acids via the urea cycle, impaired oxidative phosphorylation, redox imbalance (e.g., increased levels of oxidants, e.g., peroxides and superoxides, isoprostanes, at rest and/or after exercise or exertion; decreased levels of antioxidants, e.g., decreased levels of alpha-tocopherol, e.g., thiobarbituric acid reactive substances), increased inducible nitric oxide synthase (iNOS), increased NFκB, increased nitric oxide (NO), peroxynitrite, and/or nitrate (e.g., after exercise or exertion), elevated levels of brain ventricular lactic acid, and increased blood glucose (e.g., new onset diabetes). In some embodiments, a neurologic symptom or sign is selected from the group consisting of cognitive deficits (e.g., in attention and reaction time), impaired response to cognitive, motor, visual, and auditory challenges, abnormal nerve conduction studies, abnormal imaging of the brain, hypoperfusion and/or metabolic dysfunction of glial cells, neuroinflammation characterized by widespread activation of both astrocytes and microglia, downregulation of the hypothalamic–pituitary–adrenal (HPA) axis, impaired response of one region of the brain to signals from another region (impaired connectivity), disordered sympathetic and parasympathetic activity, increased levels of tissue repair-indicative proteins (e.g., alpha-2-macroglobulin, keratin 16, orosomucoid), autoantibodies targeting cholinergic, 5 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) adrenergic, and muscarinic receptors, reduced anaerobic threshold and/or reduced peak work (e.g., after exercise or exertion), and increased lactic acid in muscle and the need to recruit additional brain regions to respond to cognitive challenges (by functional MRI) (e.g., following exertion). In some embodiments of any of the methods described herein, the subject has increased levels of inflammatory cytokines relative to a normal subject, e.g., the subject has increased levels of CRP or TNFα relative to a normal subject e.g., without the one or more symptoms or without post-acute sequelae of COVID-19. In some embodiments, e.g., of any of the methods described herein, the subject exhibits muscle atrophy or has a decreased ratio of muscle tissue to adipose tissue relative to a normal subject, e.g., without the one or more symptoms or without post-acute sequelae of COVID-19. In some embodiments, e.g., of any of the methods described herein, the subject exhibits brain fog or has a decreased neurocognitive function relative to a normal subject, e.g., without the one or more symptoms or without post-acute sequelae of COVID-19. In some embodiments, e.g., of any of the methods described herein, the subject exhibits dyspnea or has a decreased pulmonary function relative to a normal subject, e.g., without the one or more symptoms or without post-acute sequelae of COVID-19. In some embodiments, e.g., of any of the methods described herein, the subject exhibits decreased metabolic function relative to a normal subject, e.g., without the one or more symptoms or without post-acute sequelae of COVID-19. In some embodiments, e.g., of any of the methods described herein, the subject exhibits abnormal (e.g., increased) immunologic function relative to a normal subject, e.g., without the one or more symptoms or without post-acute sequelae of COVID-19. BRIEF DESCRIPTION OF THE DRAWINGS The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee. FIG. 1 is a schematic of the timeline for the study as described in Example 1. FIG. 2 is a graph depicting the change in level of FGF21 from baseline at Week 4 in LIVRQNac-treated subjects versus placebo. Wilcoxon test p-value = 0.083. 6 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) FIG. 3A and 3B are graphs depicting the change in level of INHBA (FIG. 3A; Wilcoxon test p-value = 0.00016) and level of INHBC (FIG. 3B; Wilcoxon test p-value = 1.2e-0.6) from baseline at Week 4 in LIVRQNac-treated subjects versus placebo. FIG. 4 is a graph depicting the change in level of NEFL (NfL) from baseline at Week 4 in LIVRQNac-treated subjects versus placebo. Wilcoxon test p-value = 0.002. FIG. 5 is a graph depicting the change in level of IL-26 from baseline at Week 4 in LIVRQNac-treated subjects versus placebo. Wilcoxon test p-value = 0.00044. FIG. 6 is a graph depicting the change in level of GPX3 from baseline at Week 4 in LIVRQNac-treated subjects versus placebo. Wilcoxon test p-value = 0.0025. FIG. 7A and 7B are graphs depicting the correlation between the change in level of GPX3 and physical fatigue (FIG. 7A) and total fatigue (FIG. 7B) scores. FIG. 7A: Spearman’s rank correlation tests, 95% CIs shaded; Treatment arm: p = 0.0287, coef = 0.245; Placebo arm: p = 0.737, coef = 0.15. FIG. 7B: Spearman’s rank correlation tests, 95% CIs shaded; Treatment arm: p = 0.045, coef = 0.442; Placebo arm: p = 0.611, coef = -0.125. FIG. 8 is a graph depicting the change in level of GSR from baseline at Week 4 in LIVRQNac-treated subjects versus placebo. Wilcoxon test p-value = 0.014. DETAILED DESCRIPTION Definitions Terms used in the claims and specification are defined as set forth below unless otherwise specified. It must be noted that, as used in the specification and the appended claims, the singular forms “a,” “an” and “the” include plural referents unless the context clearly dictates otherwise. As used herein, the term “amino acid entity” refers to a (L)-amino acid in free form or salt form (or both), the L-amino acid residue in a peptide smaller than 20 amino acid residues (e.g., oligopeptide, e.g., a dipeptide or a tripeptide), a derivative of the amino acid, a precursor of the amino acid, or a metabolite of the amino acid. An amino acid entity includes a derivative of the amino acid, a precursor of the amino acid, a metabolite of the amino acid, or a salt form of the amino acid that is capable of effecting biological functionality of the free L-amino acid. An 7 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) amino acid entity does not include a naturally occurring polypeptide or protein of greater than 20 amino acid residues, either in whole or modified form, e.g., hydrolyzed form. As used herein the term “XXX amino acid entity” refers to an amino acid entity that if a free amino acid, comprises free XXX or XXX in salt form; if a peptide, refers to a peptide (e.g., a dipeptide or a tripeptide) comprising an XXX residue; if a derivative, refers to a derivative of XXX; if a precursor, refers to a precursor of XXX; and if a metabolite, refers to a XXX metabolite. For example, where XXX is leucine (L), then L-amino acid entity refers to free L or L in salt form, a peptide (e.g., a dipeptide or a tripeptide) comprising a L residue, a L derivative, a L precursor, or a metabolite of L; where XXX is arginine (R), then R-amino acid entity refers to free R or R in salt form, a peptide (e.g., a dipeptide or a tripeptide) comprising a R residue, a R derivative, a R precursor, or a metabolite of R; where XXX is glutamine (Q), then Q-amino acid entity refers to free Q or Q in salt form, a peptide (e.g., a dipeptide or a tripeptide) comprising a Q residue, a Q derivative, a Q precursor, or a metabolite of Q; and where XXX is N- acetylcysteine (NAC), then NAC entity refers to free NAC or NAC in salt form, a peptide (e.g., a dipeptide or a tripeptide) comprising a NAC residue, a NAC derivative, a NAC precursor, or a metabolite of NAC. “About” and “approximately” shall generally mean an acceptable degree of error for the quantity measured given the nature or precision of the measurements. Exemplary degrees of error are within 20 percent (%), typically, within 15%, more typically, within 10%, and more typically, within 5% of a given value or range of values. An “amino acid” refers to an organic compound having an amino group (-NH2), a carboxylic acid group (-C(=O)OH), and a side chain bonded through a central carbon atom, and includes essential and non-essential amino acids, as well as natural and unnatural amino acids. The term “effective amount” as used herein means an amount of an amino acid, or pharmaceutical composition which is sufficient enough to significantly and positively modify the symptoms and/or conditions to be treated (e.g., to positively modify one, two, or more of a subject’s symptoms, e.g., provide a positive clinical response). The effective amount of an active ingredient for use in a pharmaceutical composition will vary with the particular condition being treated, the severity of the condition, the duration of treatment, the nature of concurrent therapy, the particular active ingredient(s) being employed, the particular pharmaceutically- 8 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) acceptable excipient(s) and/or carrier(s) utilized, and like factors with the knowledge and expertise of the attending physician. A “pharmaceutical composition” described herein comprises at least one amino acid and a pharmaceutically acceptable carrier or excipient. In some embodiments, the pharmaceutical composition is used as a therapeutic, a nutraceutical, a medical food, or as a supplement. The term “pharmaceutically acceptable” as used herein, refers to amino acids, materials, excipients, compositions and/or dosage forms which are, within the scope of sound medical judgment, suitable for use in contact with the tissues of human beings and animals without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit/risk ratio. This may be a standard used by the pharmaceutical industry or by agencies or entities (e.g., government or trade agencies or entities) regulating the pharmaceutical industry to ensure one or more product quality parameters are within acceptable ranges for a medicine, pharmaceutical composition, treatment, or other therapeutic. A product quality parameter can be any parameter regulated by the pharmaceutical industry or by agencies or entities, e.g., government or trade agencies or entities, including but not limited to composition; composition uniformity; dosage; dosage uniformity; presence, absence, and/or level of contaminants or impurities; and level of sterility (e.g., the presence, absence and/or level of microbes). Exemplary government regulatory agencies include: Federal Drug Administration (FDA), European Medicines Agency (EMA), SwissMedic, China Food and Drug Administration (CFDA), or Japanese Pharmaceuticals and Medical Devices Agency (PMDA). The term “post acute sequelae of COVID-19” or “PASC” as used herein, refers to symptoms experienced by a subject four or more weeks after initial infection with SARS-CoV-2. Other terms used to describe PASC include long COVID, long haul COVID, post-acute COVID, post-acute COVID syndrome (PACS) and/or chronic COVID. A composition, formulation or product is “therapeutic” if it provides a beneficial clinical effect. A beneficial clinical effect can be shown by lessening the progression of a disease and/or alleviating one or more symptoms of the disease. As used herein, the terms “treat,” “treating,” or “treatment” of PASC refer in one embodiment, to ameliorating PASC, (i.e., slowing or arresting or reducing the development of the disease or at least one of the clinical symptoms thereof). In another embodiment, “treat,” “treating,” or “treatment” refers to alleviating or ameliorating at least one physical parameter 9 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) including those which may not be discernible by the patient. In yet another embodiment, “treat,” “treating,” or “treatment” refers to modulating a symptom of PASC, either physically, (e.g., stabilization of a discernible symptom), physiologically, (e.g., stabilization of a physical parameter), or both. In yet another embodiment, “treat,” “treating,” or “treatment” refers to preventing or delaying the onset or development or progression of PASC. Determination of amino acid weight percent and amino acid ratios in a composition The weight ratio of a particular amino acid or particular amino acids in a composition or mixture of amino acids is the ratio of the weight of the particular amino acid or amino acids in the composition or mixture compared to the total weight of amino acids present in the composition or mixture. This value is calculated by dividing the weight of the particular amino acid or of the particular amino acids in the composition or mixture by the weight of all amino acids present in the composition or mixture. It is understood that NAC is considered to be an amino acid for the purpose of this calculation. Methods of Treatment Based on a diagnosis or confirmation of a diagnosis of PASC, various therapeutic products can be administered to a subject to improve mitochondrial, metabolic, immunologic, musculoskeletal, neurocognitive, and/or pulmonary function. They can be administered to treat (e.g., reverse, reduce, ameliorate, or prevent) a disorder, e.g., post-acute sequelae of COVID-19 in a subject. The composition as described herein can also be administered to treat (e.g., reverse, reduce, ameliorate, or prevent) a disorder, e.g., myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), post-infectious fatigue syndrome, post-critical illness syndrome, or post- intensive care unit syndrome, following illness or infection, e.g., related to post-acute sequelae of COVID-19 in a subject. The present disclosure provides methods of treating post-acute sequelae of COVID-19 selected from myalgia, fibromyalgia, idiopathic pulmonary fibrosis, fatigue, muscle fatigue, mitochondrial dysfunction, dyspnea after exertion, postural orthostatic tachycardia syndrome, and tachycardia in subject diagnosed or in whom diagnosis is confirmed in accordance with the invention. In particular, an effective amount of the composition can be administered (e.g., according to a dosage regimen described herein) to treat a subject with post- acute sequelae of COVID-19. 10 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) In some embodiments, a method described herein comprises administering a composition as described in International Applications WO/2018/118941 or WO/2018/118957, each of which is herein incorporated by reference in its entirety. In some embodiments, a method described herein comprises a treatment as described in International Application PCT/US22/38200, which is herein incorporated by reference in its entirety. In some embodiments, a method described herein comprises administering one or more of, e.g., all of, a histidine (H)-amino acid entity, a lysine (K)-amino acid entity, a phenylalanine (F)-amino acid entity, and a threonine (T)-amino acid entity. In some embodiments, the H-amino acid entity is selected from the group consisting of L-histidine, histidinol, histidinal, ribose-5- phosphate, carnosine, histamine, urocanate, and N-acetyl histidine, or a salt of any of the forgoing. In some embodiments, the H-amino acid entity is L-histidine or a salt thereof. In some embodiments, the K-amino acid entity is selected from the group consisting of L-lysine, diaminopimelate, trimethyllysine, carnitine, saccharopine, and N-acetyl lysine, or a salt of any of the forgoing. In some embodiments, the K-amino acid entity is L-lysine or a salt thereof. In some embodiments, the F-amino acid entity is selected from the group consisting of from L-phenylalanine, phenylpyruvate, tyrosine, and N-acetyl-phenylalanine, or a salt of any of the forgoing. In some embodiment, the F-amino acid entity is L-phenylalanine or a salt thereof. In some embodiments, the T-amino acid entity is selected from the group consisting of L-threonine, homoserine, O-phosphohomoserine, oxobutyrate, and N-acetyl-threonine, or a salt of any of the forgoing. In some embodiments the T-amino acid entity is L-threonine or a salt thereof. Subjects with Post-Acute Sequelae of COVID-19 (PASC) In some embodiments, a subject has post-acute sequelae of COVID-19. In some embodiments, a subject has one or more symptoms selected from the group consisting of anorexia, anxiety, arrhythmias, confusion (“brain fog”), dementia, depression, dyspnea, fatigue, hair loss, headache, heart failure, cardiomyopathy, angina, hepatic dysfunction, hyperglycemia, type 2 diabetes, increased heart rate, inflammation, loss of appetite, loss of memory, loss of 11 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) smell, mood disorder, muscle weakness, myocardial ischemia, post-exertional malaise, diminished neurocognition, diminished sensory function, pulmonary fibrosis, postural orthostatic hypotension, renal dysfunction, and respiratory distress. In some embodiments, a subject has one or more symptoms selected from the group consisting of myalgia, muscle fatigue, fatigue, dyspnea after exertion, postural orthostatic tachycardia syndrome, tachycardia, mood disorders, and depression. In some embodiments, a subject has been hospitalized for acute COVID-19. In some embodiments, a subject has been hospitalized for one or more symptoms of post-acute sequelae of COVID-19. In some embodiments, a subject had not been vaccinated for COVID-19 prior to contracting COVID-19. In some embodiments, a subject had not been vaccinated (e.g., partially vaccinated or fully vaccinated) for COVID-19 prior to contracting COVID-19. In some embodiments, a subject had been vaccinated for COVID-19 after contracting COVID-19. In some embodiments, the subject tested positive for SARS-CoV-2 and developed symptoms consistent with infection. In some embodiments, the subject tested positive for SARS-CoV-2 and was asymptomatic, but later developed symptoms consistent with PASC. In some embodiments, the subject tested positive for SARS-COV-2, had symptoms of infection, became antibody negative or asymptomatic, and then was re-infected with another variant of SARS- CoV-2. In some embodiments, the subject has tested positive for SARS-CoV-2 more than once. In certain embodiments, the subject has tested positive for SARS-CoV-21, 2, 3, 4, or more times. In some embodiments, the subject has been diagnosed with more than one infection of SARS-CoV-2 (e.g., 1, 2, 3, 4, or more separate SARS-CoV-2 infections). In some embodiments, a subject tested positive for COVID-19, e.g., about 1, 2, 3, or 4 weeks before administration. In some embodiments, a subject tested positive for COVID-19 at least twice over a period of time, e.g., at least 3 or 4 weeks, before administering a composition described herein. In some embodiments, a subject had acute COVID-19 for about 3, 4, 5, 6, 8, 10, or 12 weeks, before administering a composition described herein. In some embodiments, a subject had one or more symptoms of acute COVID-19 for at least 3 or 4 weeks, before administration of a composition described herein. In some embodiments, a subject is (e.g., is determined to be) negative for SARS-CoV-2 at the time of administration of a composition described herein. In some embodiments, at the time of administration of a composition described herein, the subject is (e.g., is determined to be) positive for SARS-CoV-2. In some embodiments, 12 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) at the time of administration, the subject no longer has detectable SARS-CoV-2 in a nasal sample at the time they are administered the composition. Biomarkers Without wishing to be bound by theory, FGF21 levels are elevated in skeletal muscle stress, in CFS, and in acute COVID-19 infection. Without wishing to be bound by theory, IL-26 is a chronic inflammation cytokine and implicated in autoimmune disease. Without wishing to be bound by theory, Activin A/B are inflammatory cytokines implicated in inflammatory bowel disease (IBD), sepsis, and other immune diseases. Without wishing to be bound by theory, Activin A/B levels are elevated following COVID-19 infection. Without wishing to be bound by theory, NfL (also called NEFL) is a neuron-specific cytoskeleton protein and a marker of neuro- axonal injury in neuroinflammatory and neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS), multiple sclerosis (MS) and post-concussion. Without wishing to be bound by theory, circulating levels of NfL are increased in severe COVID-19 and higher levels are associated with worse clinical outcomes. GPX3 is involved in antioxidant response. Without wishing to be bound by theory, GPX3 levels are correlated with physical and total fatigue scores in an assay for fatigue (e.g., CFQ-11). In some embodiments, methods herein comprise acquiring the level of a protein, e.g., from an assay or from a third party. In some embodiments, the level of a protein comprises a numerical value. In some embodiments, the level of a protein is a a boolean value, e.g., above or below a given threshold. Vascular Cell Adhesion Molecule 1 (VCAM-1) Vascular cell adhesion molecule 1 (VCAM-1) is expressed on the surface of endothelial cells and facilitates adhesion of inflammatory cells through interaction with leukocyte integrins (Smadja et al., ("COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects." Angiogenesis 24(4): 755-788, 2021). Constitutive expression of VCAM-1 is low in healthy individuals but upregulated on the cell surface in response to inflammatory conditions, including COVID-19 (Ambrosino et al., ("Endothelial Dysfunction in COVID-19: A Unifying Mechanism and a Potential Therapeutic Target." Biomedicines 10(4), 2022)). Increases in circulating VCAM-1 (soluble VCAM-1; sVCAM-1) is a marker of vascular inflammation and endothelial activation. In COVID-19 patients, elevated sVCAM-1 levels are associated with 13 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) higher viral load, greater disease severity and increased mortality (Bermejo-Martin et al., ("Viral RNA load in plasma is associated with critical illness and a dysregulated host response in COVID-19." Crit Care 24(1): 691, 2020); Tong et al., ("Elevated Expression of Serum Endothelial Cell Adhesion Molecules in COVID-19 Patients." J Infect Dis 222(6): 894-898, 2020); Birnhuber et al., ("Between inflammation and thrombosis: endothelial cells in COVID- 19." Eur Respir J 58(3), 2021); Spadaro et al., ("Markers of endothelial and epithelial pulmonary injury in mechanically ventilated COVID-19 ICU patients." Crit Care 25(1): 74, 2021); Vieceli Dalla Sega et al., ("Time course of endothelial dysfunction markers and mortality in COVID-19 patients: A pilot study." Clin Transl Med 11(3): e283, 2021)). Recently, platelet-derived and endothelial-cell-derived microparticles from intubated COVID-19 patients have been shown to induce VCAM-1 expression and apoptosis in in vitro cultured endothelial cells (Garnier et al., ("Plasma microparticles of intubated COVID-19 patients cause endothelial cell death, neutrophil adhesion and netosis, in a phosphatidylserine-dependent manner." Br J Haematol 196(5): 1159- 1169, 2021)). In some embodiments, the biomarker is Vascular cell adhesion molecule 1 (VCAM- 1). Without wishing to be bound by theory, VCAM-1 is expressed on the surface of endothelial cells and facilitates adhesion of inflammatory cells through interaction with leukocyte integrins. Without wishing to be bound by theory, increases in circulating VCAM-1 (soluble VCAM-1; sVCAM-1) is a marker of vascular inflammation and endothelial activation. In some embodiments, a test for VCAM-1 levels comprises measuring the amount of VCAM-1 in the blood (e.g., serum). In some embodiments, VCAM-1 is measured by electrochemiluminescence immunoassay (ECLIA). Measuring VCAM-1 as part of an ECLIA may help diagnose an inflammatory condition. Constitutive expression of VCAM-1 is low in healthy individuals but upregulated on the cell surface in response to inflammatory conditions, including COVID-19. In COVID-19 patients, elevated sVCAM-1 levels are associated with higher viral load, greater disease severity and increased mortality (Bermejo-Martin et al., 2020, supra; Tong et al., 2020, supra; Birnhuber et al., 2021, supra; Spadaro et al., 2021, supra; Vieceli Dalla Sega et al., 2021, supra). Recently, platelet-derived and endothelial-cell-derived microparticles from intubated COVID-19 patients have been shown to induce VCAM-1 expression and apoptosis in in vitro cultured endothelial cells (Garnier et al., 2021, supra). In some embodiments, VCAM-1 (e.g., sVCAM-1) levels in the serum are decreased in a subject treated with a composition described 14 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) herein. In some embodiments, VCAM-1 (e.g., sVCAM-1) levels in the serum are decreased in a subject treated with a composition described herein compared to a control (e.g., a subject not treated with a composition described herein). EXAMPLES The Example below is set forth to aid in the understanding of the inventions, but is not intended to, and should not be construed to, limit its scope in any way. Example 1 – Evaluation of LIVRQNac in Subjects with Long COVID Fatigue Long COVID-19 with fatigue is a serious condition with urgent unmet medical need: Long COVID-19 is a chronic, multi-organ disease predominantly characterized by fatigue and muscle weakness (Lopez Leon et al (More than 50 long-term effects of COVID-19: a systematic review and meta-analysis. Sci Rep. 2021 Aug 9;11(1):16144. doi: 10.1038/s41598- 021-95565-8.). Although many patients recover from COVID-19 within several weeks, a substantial proportion of patients exhibit persistent or new symptoms more than 4 weeks after being diagnosed (Sigfrid et al (Long Covid in adults discharged from UK hospitals after Covid- 19: A prospective, multicentre cohort study using the ISARIC WHO Clinical Characterisation Protocol. Lancet Reg Health Eur. 2021 Sep;8:100186. doi: 10.1016/j.lanepe.2021.100186. Epub 2021 Aug 6.). These patients with persistent post-acute COVID (PASC) symptoms are often referred to as suffering from long COVID. It is estimated that long COVID affects 20% to 70% of the survivors of acute infection. Many cross-sectional and cohort studies report that chronic fatigue is the most frequently reported symptom following recovery from acute COVID-19 (Evans, et al. (Physical, cognitive, and mental health impacts of COVID-19 after hospitalisation (PHOSP-COVID): a UK multicentre, prospective cohort study. Lancet Respir Med. 2021 Nov;9(11):1275-1287. doi: 10.1016/S2213-2600(21)00383-0. Epub 2021 Oct 7. Erratum in: Lancet Respir Med. 2022 Jan;10(1):e9. PMID: 34627560; PMCID: PMC8497028); Crook, et al. (Long covid-mechanisms, risk factors, and management. BMJ. 2021 Jul 26;374:n1648. doi: 10.1136/bmj.n1648. Erratum in: BMJ. 2021 Aug 3;374:n1944.). A recent large database of nearly 2 million individuals diagnosed with COVID-19 estimated that 23.2% of patients report at least 1 post-COVID-19 condition, and fatigue is among the 3 most common complaints, typically reported in more than half of subjects with persistent symptoms. Reports of fatigue are 15 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) independent of the severity of initial illness (Townsend, et al. (Persistent poor health after COVID-19 is not associated with respiratory complications or initial disease severity. Ann Am Thorac Soc. 2021;18(6):997-1003); Augustin, et al. (Post-COVID syndrome in non-hospitalised patients with COVID-19: a longitudinal prospective cohort study. Lancet Reg Health Eur. 2021 Jul;6:100122. doi: 10.1016/j.lanepe.2021.100122. Epub 2021 May 18.). There is evidence of substantial negative impact on quality of life (QoL) (Halpin et al. (Postdischarge symptoms and rehabilitation needs in survivors of COVID-19 infection: a cross-sectional evaluation. J Med Virol. 2020)), and given the large number of survivors with long COVID, it is reasonable to assume that there will be substantial long-term effects not only on individuals but also on the health care system. In a study that examined 1-year outcomes in hospital survivors with COVID-19, only 76% had returned to a pre-COVID-19 level of employment, with 32% of individuals attributing this to decreased physical function (Huang, et al. (1-year outcomes in hospital survivors with COVID-19: a longitudinal cohort study. Lancet. 2021;398(10302):747- 758)). Thus, long COVID-19 with fatigue is a serious disease, with the potential to substantially impair QoL and lead to increased health risks and costs and impairment of the ability to work. Clinical STUDY for long COVID-19 A randomized, double-blind, placebo-controlled Phase 2a trial was conducted to evaluate the efficacy and safety of a LIVRQNac Test Article in patients with moderate to severe fatigue related to long COVID (>12 weeks after initial infection). Enrollment in the study has been completed, with 41 patients randomized evenly to receive either 67.8 grams per day of LIVRQNac or a matched placebo in two divided doses for 28 days, with a one-week safety follow-up period. The total study duration for each subject is approximately 9 weeks and comprising of a Screening Period of up to 4 weeks, a Treatment Period of up to 4 weeks, and a Follow-up Period of 1 week (FIG. 1). The primary efficacy endpoint is the mean change from baseline at Week 4 in the phosphocreatine (PCr) recovery rate following moderate exercise, as assessed by phosphorus magnetic resonance spectroscopy ( ³¹ P-MRS), which is evaluated at Screening and End of Trial (EOT) (visit 4). To assess fatigue, 6-minute walk test (6MWT) and Chalder Fatigue scale, which 16 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) have been successfully validated and used in previous studies on chronic fatigue syndrome (Mantha 2020) were utilized. An analysis of the results from the first 20 subjects has been conducted, with the results presented here. Top line results with the 41 subjects enrolled in the study are expected to be available in the near future. Description of study test article The LIVRQNac Test Article is an orally active mixture of 5 specific AAs (leucine, isoleucine, valine, arginine, glutamine), and N-acetylcysteine (Nac) as presented in Table 1. Table 1. Amino Acid and Excipient Composition Within LIVRQNac Test Article Unit Dosage Percent (%) in Total Maximal Amino Acid Composition Dry Weight (g) Unit Dosage Daily Dose (g) y u u g ^a Arginine is sourced as arginine monohydrochloride The Test Article is supplied in a dry powder form that is dissolved in approximately 6 oz (approximately 180 mL) of water to form a uniform suspension and is administered orally, twice daily, as an orange-flavored drink. 17 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) STUDY ENDPOINTS Rationale for choosing PCr recovery as the primary endpoint: The primary objective of this study was to assess the impact of LIVRQNac on muscle function (metabolism) following exercise. A change in the time constant of phosphocreatine (PCr) recovery from baseline after 4 weeks treatment as measured by ³¹ P-MRS was chosen as the primary endpoint as it is objective and sensitive to changes in mitochondrial function. In brief, ³¹ P-MRS is used to estimate the concentration of high-energy phosphate compounds; thus, the bioenergetic state of a tissue can be characterized in vivo as it may reflect changes in mitochondrial function (Prompers 2006; Kemp 2015; Valkovič 2016). ³¹ P-MRS has been used to assess mitochondrial function in a variety of conditions, including heart failure patients (Menon 2021), diabetes (Ripley 2018), and mitochondrial abnormalities following drug administration (Fleischman 2007). If, as expected, a composition comprising LIVRQNac improves mitochondrial oxidative capacity, then a decrease, relative to subject baseline, in the phosphocreatine recovery time is predicted. The assumption at the beginning of the trial was that individuals with prolonged fatigue after COVID-19 would have a baseline PCr of 50 seconds, which would be comparable to aged individuals or those with heart failure. Rationale for choosing CFQ-11 and 6MWT to assess fatigue: The Chalder Fatigue Scale (CFQ-11) and the 6MWT have been utilized in multiple therapeutic areas and several indications and have been paramount in characterizing the patient's condition and overall quality of life. Both these tests are suitable in evaluating scientifically supported and logical combination of symptoms that are common in patients with long COVID- 19 with fatigue and inform the design of a subsequent study with appropriate power to detect differences in these key endpoints. While many instruments are available to assess fatigue, the CFQ-11 has been validated in a number of different patient population including those with myalgic encephalomyelitis/chronic fatigue syndrome (Whitehead 2009; Morriss 1998; Crawley 2013) which has parallels to the clinical presentation of patients with long COVID-19 experiencing fatigue (Paul 2021). There has also been use of the CFQ-11 in patients with long COVID-19 (Staven 2021, Tuzon 2021, Townsend 2021). Given the reliability of this instrument in a wide range of conditions, ongoing 18 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) public health emergency and the serious unmet medical need for patients with long COVID with fatigue, the use of such existing, reliable functional assessment and PROs to assess clinical benefit outweighed the risks of not performing additional validation in the target patient population. The fatigue scale developed by Chalder et al. is an 11-item scale intended to measure the severity of fatigue-related symptoms, both mental and physical, experienced by individuals with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS). The scale has two scoring systems: bimodal and Likert. In the bimodal system, respondents answer each question with a 1 or a 0 to indicate the questions apply to them or not. In the Likert system, respondents can give a score of 0 to 3 to indicate how each statement applies to them, from “less than usual” to “much more than usual”. The scores are then summed, and a higher score indicates more severe fatigue- related symptomatology. The “Physical Fatigue” items include questions such as “Do you have problems with tiredness?” or “Do you lack energy?” The remaining items constitute a “Mental Fatigue” factor with questions such as “Do you have difficulty concentrating?” or “Do you make slips of the tongue when speaking?” The total scale demonstrated sufficient internal consistency with alpha coefficients of 0.89 (Chalder 1993). At the 90% sensitivity level for the CFQ-11 Scale (with a score ≥ 14.50) a specificity of 0.61 was detected, and these scales were able to identify 90% of those individuals with CFS (Jason 2011). As an example of a measure of fatigue intensity alone, Chalder et al.’s Fatigue Scale is a verbal rating measure that has strong internal consistency. Using an ROC curve analysis, (Jason 1997), this scale was able to discriminate a CFS sample from a healthy control sample. Near-maximal scoring on six physical fatigue scale items from the total of 14 items constituting the Chalder fatigue scale supports the validity of scoring the physical fatigue scale on a two-point scale (presence or absence) rather than the four- point scoring. As noted in the paragraph above, the CFQ-11 has been applied to the study of outcomes in COVID-19 (Steven 2021, Tuzon 2021, Townsend 2021). Additionally, the 6-minute walk test (6MWT) is a validated clinical test to assess the cardiopulmonary reserve and fundamentally designed for use in adults with chronic respiratory disease (Holland 2014) and therefore may be an appropriate test to evaluate functional status of COVID-19 patients. Results from this Analysis of this Study An analysis was conducted after 20 subjects (10 subjects taking Test Article and 10 19 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) taking Placebo) in the study completed 4 weeks of treatment. The analysis was focused on the study endpoint of phosphocreatine (PCr) recover time along with secondary endpoints including; CFQ-11, 6-MWT, MRS, and safety and tolerability. Subjects who received LIVRQNac Test Article, relative to placebo, achieved statistically significant improvements in the CFQ-11. A major entry criterion for the study was the presence of moderate to severe fatigue (score of > 8, with a score of 4 or more indictive of fatigue using bimodal score, with scores ranging from 0-11). Relative to placebo, subjects who received LIVRQNac Test Article had a 4 point improvement in the CFQ-11 score. The results for the 6MWT showed that there was no significant change from Baseline in the LIVRQNac Test Article Group versus the Placebo Group in the distance walked at Week 4 whether calculated as absolute change in distance or percent predicted. The mean 6MWT was 533 M ± 106 M, or approximately 85% predicted with approximately one quarter of subjects below the 75% of the predicted distance based on age or gender; these results are consistent with the literature. These results may be due to the relatively short duration of the study (4 weeks) and the unexpected severity and magnitude of fatigue encountered by this patient population. Magnetic resonance spectroscopy PCr results, measured as described above, indicated an unexpectedly large variation in both Baseline and deviation from the mean (mean 84.56 sec ± 30.816). There was no difference in the change from Baseline in PCr between the LIVRQNac Test Article Group and the Placebo Group at Week 4 as examined by both absolute and percent change, whether unadjusted or adjusted statistical models were used. There was no correlation with either Fatigue score or 6- MWT. Additional MRS assessments showed positive trending changes in the LIVRQNac Test Article Group from Baseline as compared to the Placebo Group at Week 4 including; Intramyocellular Lipid Content: LIVRQNac Test Article Group (Baseline mean= 0.42, Week 4 change= -0.17) versus Placebo Group (Baseline mean= 0.36, Week 4 change= 0.16), Peak Lactate: LIVRQNac Test Article Group (Baseline mean= 1.74, Week 4 change= - 0.53) versus Placebo Group (baseline mean= 2.11, Week 4 change= -0.20), and Carnosine: LIVRQNac Test Article Group (Baseline mean= 4.43, Week 4 change= 0.78) versus Placebo Group (Baseline mean= 4.38, Week 4 change= -0.56). 20 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) The safety results in this analysis of the first 20 subjects showed no safety issues in the LIVRQNac Test Article Group: two subjects had the adverse events of abdominal pain, and headache which were mild and resolved. There were two adverse events of diarrhea (one in subject with upper respiratory infection), and the other one in subject with nasal congestion, nausea post MRI. One subject had COVID. In the Placebo Group, there was an increase in liver function tests which was most likely related to concomitant medications. These results proved a benign safety and tolerability profile for LIVRQNac which is consistent with the published literature on LIVRQNac constituent AAs and safety data gathered from other clinical studies conducted with LIVRQNac in NASH. Example 2 - Effects of Amino Acid Compositions on Biomarkers in Long COVID LIVRQNac Decreases Serum Levels of FGF21 Background: Fibroblast growth factor 21 (FGF21) is an important hormone in metabolism and energy homeostasis. The regulation and biological activity of FGF21 is highly complex and dependent on the physiological context including tissue of origin, systemic concentration, age and synergism with other signaling molecules (Tezze et al., 2019). Metabolic activities encompass effects on insulin sensitivity and glucose homeostasis, ketogenesis and lipid metabolism. While the liver is the primary site of FGF21 synthesis, secretion from other organs including skeletal and cardiac muscle, kidney and adipose tissue is well-documented (Sun et al., 2021). A wide range of serum FGF21 concentrations has been reported in healthy humans, ranging from 5 pg/mL to 5 ng/mL (Tezze et al., 2019). FGF21 secretion is induced in conditions such as aging, obesity and nutritional imbalance by a variety of stress-responsive pathways, and acts in an autocrine, paracrine and endocrine fashion to restore homeostasis (Sun et al., 2021). Effector pathways downstream of FGF21 include AMPK-Sirt1-PGC1a, ERK/MAPK, PI3K/AKT, IGF-1 and mTOR signaling pathways (Chau et al., 2010; Tezze et al., 2019) and numerous tissues such as central nervous system, skeletal muscle, adipose tissue and others are targets of FGF21 signaling (Sun et al., 2021). FGF21 expression and activity is also regulated in a variety of disease conditions (Tezze et al., 21 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) 2019; Sun et al., 2021) and has been proposed as a biomarker of mitochondrial dysfunction (Lehtonen et al., 2016; Morovat et al., 2017; Scholle et al., 2018; Riley et al., 2022). In line with accumulated evidence supporting dysregulated metabolism in COVID-19, elevated FGF21 levels were detected in COVID-19 patients aged 54-80 and were correlated with disease severity and mortality (Ajaz et al., 2020). In contrast, a study of young adults with COVID-19 found that FGF-21 concentrations were higher in asymptomatic individuals versus study participants with symptomatic disease (Soares-Schanoski et al., 2022). FGF21 was also found to be enriched in circulating extracellular vesicles (EVs) from hospitalized COVID-19 patients (Krishnamachary et al., 2021), convalescent COVID-19 patients (Sun et al., 2021) and in the serum of insulin resistant, hyperglycemic COVID-19 patients (He et al., 2021). Given its prominent role in metabolism and associations with SARS-CoV-2 infection, FGF21 concentrations were measured in plasma samples from the study described in Example 1 above. Methods: Plasma concentrations of FGF21 were analyzed by ELISA (MRL-US). The data presented below reflect analyses conducted on samples available at the End of Trial (EOT), with samples from 41 subjects from the study described in Example 1 above. Data are expressed as change from Baseline at EOT to correct for potential intrinsic (treatment unrelated) differences between treatment and placebo groups. The statistical test applied is Wilcoxon (Mann-Whitney), a nonparametric test based on ranks. This approach has less statistical power than a parametric test but is more conservative, as it avoids spurious conclusions based on inadequacy of a distribution model. Results: Significant downregulation (p = 0.083) of serum FGF21 was observed (FIG. 2) in LIVRQNac treated subjects vs. placebo from the study described in Example 1 above. The reduction in FGF21 may reflect improvements in metabolism and mitochondrial function with LIVRQNac treatment. LIVRQNac Decreases Plasma Levels of Activins and Activin Beta Subunits Background: 22 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) Activins are multifunctional members of the TGFβ superfamily that regulate a broad array of biological processes including biosynthesis and secretion of reproductive regulatory hormones, embryonic development, wound repair, hematopoiesis, cell proliferation and differentiation, and immune regulation. Activins exist as dimers of two activin beta (β) subunits (also referred to as inhibin β subunits), of which the best characterized are βA, βB and βC. The β subunits combine as homodimers or heterodimers to form different activin proteins. The role of activins in immune regulation are well-established. Activins induce both pro- and anti-inflammatory responses in numerous leukocyte types depending on the activation and maturation status of the cells as well as the spatiotemporal context (Morianos et al., 2019). Activin A has been implicated in a variety of pathologies including autoimmune diseases, allergic disorders and viral infection. Viral infection typically leads to elevated blood levels of activin A, which might correlate with IL-6, TNFα or viral load, depending on the virus (Morianos et al., 2019). Increased levels of activin A have also been reported in bronchial alveolar lavage fluid from patients with acute respiratory disease syndrome (ARDS) (Apostolou et al., 2012). In hospitalized COVID-19 patients, elevated blood levels of activin A and activin B were found to be associated with and/or predictive of more severe disease and mortality (Synolaki et al., 2021; McAleavy et al., 2021; McAleavy et al., 2022), whereas lower levels of activin A and activin B were associated with reduced mortality and improvements in clinical scores (McAleavy et al., 2022). Cells implicated in pulmonary diseases, including lung fibroblasts and smooth muscle cells, secrete activin A in vitro in response to the inflammatory cytokines IL-1α and TNFα and IKK/NF-kB signaling (McAleavy et al., 2022). Activin A is overexpressed in lung microvascular endothelial cells of patients with idiopathic pulmonary arterial hypertension, and acts as an angiocrine factor promoting endothelial dyfunction by inducing degradation of bone morphogenetic protein receptor type 2 (Ryanto et al., 2021). Activin subunit beta A mRNA and Activin A protein are expressed at higher levels in the lung microvascular endothelium of these patients versus other vascular beds (Ryanto et al., 2021). Due to its multifactorial effects and broad tissue distribution, elevation of activins including activin A and activin B in COVID-19 could be attributable to numerous tissue and cell types. Nonetheless, the studies summarized above suggest that activins might be contributing to COVID-19 disease pathophysiology via effects on the pulmonary microvascular endothelium and other vascular tissues. 23 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) Methods: Proteomics analysis was performed on 41 study subjects from the study described in Example 1 above, via a multiplexed proteomics assay that uses aptamer reagents to detect and measure the presence, absence, or relative abundance in a biological sample of approximately 7000 proteins (Somalogic; Boulder, Colorado). Data are expressed as change from BL at Week 4 (EOT) to correct for potential intrinsic (treatment unrelated) differences between treatment and placebo groups. The statistical test applied is Wilcoxon (Mann-Whitney), a nonparametric test based on ranks. This approach has less statistical power than a parametric test but is more conservative, as it avoids spurious conclusions based on inadequacy of a distribution model. Results: Significant downregulation of plasma Activin βC was observed, along with strong trends toward downregulation of Activin βB, βA, and βC, as well as activin A and Activin AC dimers (See FIG. 3A, FIG. 3B, and Table 2), in LIVRQNac treated subjects vs. placebo from the study described in Example 1 above. These data suggest an overall decrease in activin signaling with LIVRQNac treatment. LIVRQNac could contribute to the observed improvement in PROs from the study described in Example 1 above by reducing activin-mediated dysfunction of pulmonary tissue and endothelium. Table 2. Levels of activin proteins in LIVRQNac treated subjects vs. placebo. Name Symbol Subunit Composition UniProt ID Log2Ratio p value FDR A ti in A A ti in A β β h m dim r P08476 053943 000018 0068 3 LIVRQNac Treatment Significantly Reduces Plasma Neurofilament Light Chain, a Biomarker of Neuro-Axonal Injury 24 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) Background: Neurofilaments are cytoskeleton proteins of the central and peripheral axons specific to neurons. Because of its low molecular weight, Neurofilament light chain (NfL) can easily diffuse from parenchyma to CSF and blood (Fuchs and Cleveland, 1998; Scherling 2014; Alirezaei 2020) and serve as a key noninvasive biomarker of neuro-axonal injury in diverse neuropathological conditions (Barro 2020). Neuro-axonal injury can affect both the central and peripheral nervous systems and occur in a variety of neurodegenerative and neuroinflammatory diseases. With the ability to quantify neuronal damage in blood and to overcome the invasiveness of CSF sampling that previously restricted NfL clinical application, NfL is now being applied to a wide range of neurologic conditions to investigate and monitor disease including assessment of treatment efficacy. NfL was measured in many clinical trials and translational studies in multiple sclerosis (MS), traumatic brain injury (TBI), stroke, ALS, Alzheimer’s and other diseases. NfL shows the strongest diagnostic value in ALS. NfL levels in ALS are higher than in most diseases due to severe neurodegeneration and the fact that the degeneration affects large myelinated axons that have a high expression of NfL, which could be further amplified by the long length of the axons (Yuan 2017). Two longitudinal studies reported that patients that converted to the symptomatic stage had blood NfL levels higher than healthy controls up to 1 year prior to symptom onset (Benatar 2018, Benatar 2019). Blood NfL has also been investigated as a prognostic biomarker once the disease has been diagnosed. Several studies found that NfL levels at symptom onset were prognostic of the disease progression rate (Lu 2015, Gille 2019, Thouvenot 2020, Weydt 2016, Verde 2019). In MS, serum NfL showed an association with brain atrophy over 2 years and number of MRI lesions (Kuhle 2017). In 2020, Thebault et al demonstrated that serum NfL was predictive of long-term outcomes in MS (Thebault 2020). In the 2018 MS study by Chitnis, averaged annual serum NfL levels showed statistically significant associations with fatigue score worsening between years 1 and 10 using Modified Fatigue Impact Scale, MFIS (Chitnis 2018). The 2017 Shahim study investigated serum NfL as a biomarker for mild TBI in contact sports and showed that NfL is able to separate players with rapidly resolving post-concussion symptoms (PCS) from those with prolonged PCS (Shahim 2017). 25 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) Interestingly, increased levels of circulating NfL have been observed in patients with severe COVID-19. Prudencio et al 2021 reported that COVID patients with increased NfL have worse clinical outcomes and may experience neuro-axonal injury that can put them at risk for long-term neurological sequelae (Prudencio 2021). Higher NfL levels were predictive of mortality in critically ill COVID-19 patients, and addition of NfL to age and gender significantly improved the accuracy of 48 mortality prediction (Masvekar 2022). Methods: Proteomic profiling was performed on plasma samples collected at baseline and at 4 weeks post-treatment from 41 study subjects in the study described in Example 1 above (total 82 samples). A multiplexed proteomics assay using aptamer reagents to detect and measure the presence, absence, or relative abundance in a biological sample of approximately 7000 proteins (Somalogic; Boulder, Colorado) was used. Data are expressed as change from baseline at Week 4 (EOT) to correct for potential intrinsic (treatment unrelated) differences between treatment and placebo groups. The statistical test applied is Wilcoxon (Mann-Whitney), a nonparametric test based on ranks. This approach has less statistical power than a parametric test but is more conservative, as it avoids spurious conclusions based on inadequacy of a distribution model. Results: In the study described in Example 1 above, patients treated with LIVRQNac for 4 weeks demonstrated significant reduction in plasma NfL compared to placebo (FIG. 4). These results suggest that long COVID patients may still have residual neuro-axonal damage and the treatment has a neuroprotective effect. Previously reported associations between circulating NfL and fatigue (Chitnis 2018) may explain improvement in the CFQ-11 scores. LIVRQNac Treatment Significantly Decreases IL-26, a Biomarker of Chronic Inflammation Background: Interleukin 26 (IL-26) is a proinflammatory cytokine that also possesses antimicrobial properties and can be categorized as a kinocidin. 26 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) IL-26 is expressed on activated T cells, fibroblasts and epithelial cells and stimulates the production of other proinflammatory cytokines in various cell types. Additionally, IL-26 is a driver of chronic inflammation due its ability to act as a carrier of extracellular DNA released from damaged cells. The dysregulated expression of IL-26 may lead to the amplification of inflammatory responses and sustained inflammation. Elevated IL-26 levels were found in inflamed tissues and in plasma of patients with rheumatoid arthritis (Corvaisier 2012), IBD (Fuji 2017), hepatitis C virus (HCV) (Miot 2014), and systemic Lupus erythematosus (Brillant 2021). In several diseases, the highest expression of IL-26 was detected in pro-inflammatory IL- 17 producing T cells in chronically inflamed tissues. The roles of IL-26 in normal physiology remain unknown. As an antimicrobial, IL-26 has a direct role in viral infections. It was shown to inhibit cytomegalovirus and HCV replication and to promote the replication of vesicular stomatitis virus (Braum 2013, Miot 2014). Elevated serum levels of IL-26 were detected in patients with chronic HCV infection. To date, no reports are available on the role of IL-26 or IL-26 levels in SARS-CoV-2 infections. Methods: Proteomic profiling was performed on plasma samples collected at baseline and at 4 weeks post-treatment from 41 study subjects in the study described in Example 1 above (total 82 samples). A multiplexed proteomics assay using aptamer reagents to detect and measure the presence, absence, or relative abundance in a biological sample of approximately 7000 proteins (Somalogic; Boulder, Colorado) was used. Data are expressed as change from baseline at Week 4 (EOT) to correct for potential intrinsic (treatment unrelated) differences between treatment and placebo groups. The statistical test applied is Wilcoxon (Mann-Whitney), a nonparametric test based on ranks. This approach has less statistical power than a parametric test but is more conservative, as it avoids spurious conclusions based on inadequacy of a distribution model. Results: In the study described in Example 1 above, patients treated with LIVRQNac for 4 weeks demonstrated a statistically significant reduction in plasma IL-26 compared to placebo, 27 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) Wilcoxon test p-value = 0.00044 (FIG. 5). This effect on IL-26 suggests that the treatment may decrease cellular damage with release of DNA and reduce chronic inflammation associated with long COVID. LIVRQNac Treatment Significantly Increases Levels of an Antioxidant, GPX3 Background: Members of the glutathione peroxidase (GPx) family are antioxidants that reduce hydrogen peroxide to water. Glutathione peroxidase 3 (GPX3) belongs to the glutathione peroxidase family and protects cells and enzymes from oxidative damage, by catalyzing the reduction of hydrogen peroxide, lipid peroxides and organic hydroperoxide, by glutathione. GPX3 is the only extracellular GPx. It has been shown that aging is accompanied by decrease in GPX3 activity (Razygraev 2019). GPX3 is markedly downregulated in breast cancer, possesses significant diagnostic and prognostic values, and attenuated in vitro growth and metastasis of breast cancer (Lu 2020). The 2020 Chang study demonstrated that GPx3 has a dichotomous role in different tumor types, acting as both a tumor suppressor and pro-survival protein (Chang 2020). GPX3 deficiency has been associated with cardiovascular disease and stroke. Serum GPx3 activity was shown to be inversely associated with mean carotid intima-media thickness and carotid plaque, suggesting that lower GPx3 activity may be an independent predictor for carotid atherosclerosis in T2DM (Ling 2020). GPX3 deficiency promotes vascular dysfunction and platelet-dependent arterial thrombosis and increases cerebral infarct size in mice with permanent MCAO (Forrester 2018). Reactive oxygen species (ROS) have long been known to contribute to the development and severity of IBD. In the mouse model of IBD, GPx3 was required to mediate the antioxidant effects of GPx1 that was previously shown to protect against dextran sodium sulfate (DSS)- induced colitis and augment intestinal proliferation (Blunt 2022). Human myoblast in vitro studies showed that oxidative stress induced apoptosis and pre- treatment with retinoic acid rescued cell viability. The anti-cytotoxic effects of retinoic acid were impaired in GPx3 inactivated myoblasts, which indicates that GPx3 regulates the antioxidative effects of retinoic acid and is important for the viability of human muscle stem cells (Haddad 2012). 28 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) GPX3 was identified as a factor that might be involved in the regulation of myocardial fibrosis under cardiac pressure overload in the single cell transcriptomic analysis used to characterize the dynamic changes associated with fibroblast differentiation. These findings suggested that GPX3 may represent a potential intervention target in myocardial fibrosis (Li 2022). No previous reports are available on the levels of circulating GPX3 in SARS-CoV-2 infections, in COVID or PASC. Methods: Proteomic profiling was performed on plasma samples collected at baseline and at 4 weeks post-treatment from 41 study subjects in the study described in Example 1 above (total 82 samples). A multiplexed proteomics assay using aptamer reagents to detect and measure the presence, absence, or relative abundance in a biological sample of approximately 7000 proteins (Somalogic; Boulder, Colorado) was used. Data are expressed as change from baseline at Week 4 (EOT) to correct for potential intrinsic (treatment unrelated) differences between treatment and placebo groups. The statistical test applied is Wilcoxon (Mann-Whitney), a nonparametric test based on ranks. This approach has less statistical power than a parametric test but is more conservative, as it avoids spurious conclusions based on inadequacy of a distribution model. Results: In the study described in Example 1 above, patients treated with LIVRQNac for 4 weeks demonstrated a statistically significant increase in plasma GPX3 compared to placebo, Wilcoxon test p-value = 0.00025 (FIG. 6). Higher levels of GPX3 suggest that the treatment has an antioxidant effect, reduces ROS and promotes healthy environments for successful healing in many tissues and organs. Notably, the non-treated placebo group had reduced GPX3, suggestive of lower antioxidant activities and potentially higher oxidative stress. Improvements in GPX3 correlated with improvement in total and physical fatigue scores (FIG. 7A and FIG. 7B). LIVRQNac Treatment Significantly Increases Levels of an Antioxidant, GSR Background: 29 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) Glutathione-disulfide reductase (GSR) encodes a member of the class-I pyridine nucleotide-disulfide oxidoreductase family that is located in the cytosol and in mitochondria. It is a central enzyme of cellular antioxidant defense that maintains high levels of reduced glutathione in the cytosol. Exercise leads to sustainable cardioprotection through a mechanism involving improved glutathione replenishment. Adaptive cardioprotective signaling is triggered by reactive oxygen species from NADPH oxidase and leads to improved glutathione replenishment through increased GSR activity and redox-dependent modifications in GSR (Frazier 2013). Klotho is an aging-suppressor gene which leads to accelerated aging when disrupted. Klotho haplodeficiency impaired kidney function as evidenced by significant increase in plasma urea and creatinine and a decrease in urinary creatinine in KL ^+/– mice. The expression and activity of GSR was decreased significantly in renal tubular epithelial cells of KL ^+/– mice, suggesting that Klotho deficiency downregulated GSR. In vivo AAV-GSR delivery significantly improved Klotho deficiency-induced renal functional impairment and structural remodeling. Furthermore, in vivo expression of GSR rescued the downregulation of the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, which subsequently diminished oxidative damage in kidneys, as evidenced by significant decrease in renal 4-HNE expression and urinary 8-isoprostane levels in KL mice. It is proposed that GSR may be a promising therapeutic approach for aging-related kidney damage (Gao 2020). The 2021 Nadhashpour study assessed comorbidities, clinical symptoms and serum GSR levels in the PCR-negative and PCR-positive COVID-19 outpatients. In the PCR-positive group, follow-ups on clinical symptoms were carried out for 28 days at 7-day intervals and identified hypertension, diabetes, liver disease, chronic heart disease, and chronic kidney disease as the most common comorbidities. There was a significant difference in neurologic symptoms, except for ear pain, between PCR-negative and PCR-positive groups. Significantly lower levels of serum GSR in PCR-positive outpatients were detected suggesting that the antioxidant defense systems are repressed following SARS-CoV-2 infection (Nadhashpour 2019). Methods: Proteomic profiling was performed on plasma samples collected at baseline and at 4 weeks post-treatment from 41 study subjects in the study described in Example 1 above (total 82 30 316100602.1 Attorney Reference No.: A2169-7048WO (ESS-135.WO) samples). A multiplexed proteomics assay using aptamer reagents to detect and measure the presence, absence, or relative abundance in a biological sample of approximately 7000 proteins (Somalogic; Boulder, Colorado) was used. Data are expressed as change from baseline at Week 4 (EOT) to correct for potential intrinsic (treatment unrelated) differences between treatment and placebo groups. The statistical test applied is Wilcoxon (Mann-Whitney), a nonparametric test based on ranks. This approach has less statistical power than a parametric test but is more conservative, as it avoids spurious conclusions based on inadequacy of a distribution model. Results: In the study described in Example 1 above, patients treated with LIVRQNac for 4 weeks demonstrated a small but statistically significant increase in plasma GSR compared to placebo, Wilcoxon test p-value = 0.014 (FIG. 8). The increase in GSR levels suggest that the treatment has an antioxidant effect and may promote recovery. The non-treated placebo group had reduced GSR that may indicate that the antioxidant defense system is still repressed following the SARS- CoV-2 infection. While the invention has been particularly shown and described with reference to a preferred embodiment and various alternate embodiments, it will be understood by persons skilled in the relevant art that various changes in form and details can be made therein without departing from the spirit and scope of the invention. All references, issued patents and patent applications cited within the body of the instant specification are hereby incorporated by reference in their entirety, for all purposes. 31 316100602.1