Acute and post-acute sequelae of SARS-CoV-2 infection: a review of risk factors and social determinants
Virology Journal volume 20, Article number: 124 (2023)
SARS-CoV-2 infection leading to Coronavirus Disease 2019 (COVID-19) has caused more than 762 million infections worldwide, with 10–30% of patients suffering from post-acute sequelae of SARS-CoV-2 infections (PASC). Initially thought to primarily affect the respiratory system, it is now known that SARS-CoV-2 infection and PASC can cause dysfunction in multiple organs, both during the acute and chronic stages of infection. There are also multiple risk factors that may predispose patients to worse outcomes from acute SARS-CoV-2 infection and contribute to PASC, including genetics, sex differences, age, reactivation of chronic viruses such as Epstein Barr Virus (EBV), gut microbiome dysbiosis, and behavioral and lifestyle factors, including patients’ diet, alcohol use, smoking, exercise, and sleep patterns. In addition, there are important social determinants of health, such as race and ethnicity, barriers to health equity, differential cultural perspectives and biases that influence patients’ access to health services and disease outcomes from acute COVID-19 and PASC. Here, we review risk factors in acute SARS-CoV-2 infection and PASC and highlight social determinants of health and their impact on patients affected with acute and chronic sequelae of COVID-19.
The COVID-19 pandemic has led to over 762 million infections and 6.8 million deaths . Individuals may experience asymptomatic, mild, severe or fatal illness with symptoms ranging from fever, runny nose, cough, dyspnea, fatigue, diarrhea, headache or multi-organ failure, and lasting on average for one to four weeks .
A significant portion of COVID-19 patients, estimated at 10–30% (over 10–30 million people in the US and over 60–180 million people worldwide), may experience long-term symptoms, known as post-acute sequelae of SARS-CoV-2 infection (PASC) or “Long-COVID.“ PASC symptoms can include fatigue, dyspnea, brain fog, chest and joint pain, and multi-organ dysfunction affecting the neurological, pulmonary, digestive, and cardiac systems [3, 4].
There is currently no widely accepted definition for PASC, with the World Health Organization defining PASC as “3 months from the onset of symptoms, lasting at least 2 months,” while the Centers for Disease Control and Prevention (CDC)’s guidance suggests “a wide range of new, returning, or ongoing health problems” experienced after infection with SARS-CoV-2 [3, 4].
Given the ongoing SARS-CoV-2 infections, there is a pressing need to not only understand and treat acute COVID-19 infection but to also better characterize PASC. Inclusivity and the diversity of affected patient views must be honored, and patient experiences should be translated into standardized studies investigating PASC to identify better therapies for the prevention and treatment of PASC.
The goal of our review is to compare the risk factors for acute SARS-CoV-2 infection and PASC as well as discuss how social determinants of health impact acute COVID-19 and PASC disease outcomes.
Risk factors for acute COVID-19 and PASC
The risk factors for acute COVID-19 and PASC continue to be elucidated. Here, we will review emerging data on risk factors for acute COVID-19 and PASC, including genetics, sex differences, age, co-morbid conditions, SARS-CoV-2 vaccines, as well as environmental, behavioral and lifestyle factors (Fig. 1).
The Human Leukocyte Antigen (HLA) system facilitates immune regulation through the presentation of processed peptide antigens to T-cells . Certain HLA haplotypes have been associated with a genetic predisposition to COVID-19 and may influence disease outcomes [5, 6]. For example, the HLA-B46:01114 haplotype has fewest binding sites for SARS-CoV-2, while the HLA-B15:03 haplotype has a greater ability to present conserved SARS-CoV-2 peptides. These findings suggest that individuals with the HLA-B*46:01114 haplotype may be at higher risk for more severe disease due to lower display of SARS-CoV-2 peptides to the immune system .
Type of HLA could also determine COVID-19 and PASC outcomes because of its role in triggering autoimmune reactions. For example, DRB1*15:01–DRB5*01:01–DQA1*01:02–DQB1*06:02 are overrepresented in patients with multiple sclerosis while HLA-DRB1*03, HLA-DRB1*15, and HLA-DRB1*04 are overrepresented in systemic lupus erythematosus (SLE) and dictate type of auto-antibodies and SLE symptoms [7, 8]. Interestingly, highly activated CD38+HLA-DR+ myeloid cells are elevated at 8 months in PASC patients compared to controls (Fig. 2) . Subacute thyroiditis post-COVID has also been associated with presence of HLA-B*35 . Additionally, different SARS-CoV-2 peptides may have varied immunogenicity at different HLAs, with HLA-B*40:01-presented ligands as most immunogenic . Further research is necessary to determine which HLA haplotypes may better predict PASC in certain patients.
Studies have found that biological sex is a significant risk factor in COVID-19. This is likely due to physiological differences between males and females that can affect the severity of infection and autoimmune responses [12,13,14,15].
Studies in males
Men have a higher risk of hospitalization and death from COVID-19, with one study showing an 18-fold higher in-hospital mortality risk . In another study, over 89.8% of hospitalized males exhibited low testosterone levels . However, evidence for testosterone in acute COVID-19 susceptibility has been controversial. For example, prostate cancer patients post androgen deprivation therapy (ADT) had a significantly reduced risk of COVID-19 than patients without ADT . In contrast, elevated free testosterone was associated with higher COVID-19 severity in men .
In PASC, there has been a noted association with erectile dysfunction and decreased libido in males [20, 21]. Nevertheless, it remains unclear at this time whether male sex, hypogonadism (due to direct gonadal or hypothalamic SARS-CoV-2 damage leading to low testosterone) or other factors (e.g. depression, stress, immune dysregulation) may be responsible for the observed symptoms in men with PASC. Further research is needed to clarify male-specific risk factors such as hormones and genetic versus environmental risks for acute COVID-19 and PASC.
Studies in females
Interestingly, females may have different risk factors for acute COVID-19 and PASC depending on their hormonal status. For example, menopause has been associated with increased risk for severe acute COVID-19 illness, and estrogen augmentation was correlated with a lower risk of mortality from acute COVID-19 in postmenopausal women [24, 25]. Similarly, postmenopausal women have higher rates of acute COVID-19 infections compared to women pre- menopause, suggesting that estrogen may play a role in acute COVID-19 disease severity .
X chromosome genes have been implicated in sex differences in COVID-19 outcomes . Notably, angiotensin converting enzyme 2 (ACE2), the principle receptor for SARS-CoV-2 entry into cells, is found on the X chromosome . ACE2 expression is lower in the lungs of females compared to males, and estrogen downregulates ACE2 expression [28, 29]. Thus, lower ACE2 expression in females may potentially account for lower viral entry and lower severity of acute-COVID-19. Furthermore, Toll-like receptor 7 (TLR7), a regulator of interferon (IFN) production, is another X chromosome immune gene . A higher dose of TLR7 expression has been suggested to lead to higher IFN signaling in acute COVID-19 and better viral clearance in females, though continued IFN signaling may lead to overactive immune activation and persistent inflammation, predisposing females to a higher autoimmunity risk and PASC [9, 31]. Further research is needed to fully understand the role of hormones and sex chromosome genes and how these factors contribute to male versus female specific risks in acute COVID-19 and PASC.
Age in acute COVID-19
In acute COVID-19, the risk of mortality increases with every five years of age . Using an age-structured mathematical model, Davies et al. estimated clinical symptoms to appear in 21% of infections in 10- to 19-year-olds, increasing up to 69% of infections in adults over 70 .
Age in PASC
In PASC, the role of age has been controversial, with some studies finding age to be a significant predictor of PASC, with incidence rates from 9.9% in 18–49 year old patients to 21.9% in individuals over 70 . Among women, age appears to be a female-specific risk factor with women aged 40–60 more susceptible to PASC [37, 38]. In contrast, other studies found that PASC risk decreases with age or has no association [39, 40]. Therefore, it is uncertain if age is an independent risk factor for PASC, and further research is needed to determine if certain age groups are more susceptible to PASC.
Environmental, behavioral and lifestyle risk factors of acute SARS-CoV-2 infection and PASC
Environmental and behavioral risk factors are known to influence disease outcomes. In this section, we will focus on the reactivation of Epstein-Barr Virus (EBV), gut microbiome, and lifestyle factors in acute SARS-CoV-2 infection and PASC.
Over 90% of the global population harbors a latent EBV infection, which can stay dormant in B cells and reactivate under conditions of critical illness, stress, burns, immunocompromise, or other acute infections . Primary EBV infection may be asymptomatic or associated with symptoms of mononucleosis, such as fatigue, fever, pharyngitis, cervical lymphadenopathy, and lymphocytosis . EBV reactivation symptoms are typically experienced as a recrudescence of the primary infection symptoms, like fatigue, brain fog, sleep disturbances, arthralgias/myalgias, headaches, gastrointestinal complaints, and skin rashes .
EBV reactivation in acute COVID-19
Several studies have reported EBV reactivation in acute COVID-19. Chen et al. first reported that 55.2% of hospitalized COVID-19 patients tested positive for EBV IgM two weeks after disease onset . Similarly, in a cohort of 104 COVID-19 Italian patients, Paolucci et al. found EBV reactivation in 95.2% of ICU patients . In another study, 25% of COVID-19 patients had EBV reactivation and higher rates of mortality . Since reactivation is common in critical illness (e.g. ICU patients with sepsis, burns, or pneumonia), further research on EBV reactivation in acute COVID-19 is necessary to determine whether treating EBV reactivation during acute COVID-19 illness may benefit patients long term in preventing SARS-CoV-2-related sequelae [47, 48].
EBV reactivation in PASC (Fig. 2)
In PASC, Gold et al. first reported that 66.7% of PASC patients and only 10% of the controls were positive for EBV reactivation, with a direct correlation between the number of PASC-related symptoms and presence of early antigen-diffuse immunoglobulin G antibody titers . In analyzing the relationship of EBV viremia and SARS-CoV-2 RNAemia to PASC, Su et al. found that measurements of both EBV viremia and SARS-CoV-2 RNAemia at acute COVID-19 diagnosis were significantly correlated with later PASC-related memory problems . Interestingly, PASC symptoms of fatigue and sputum production were exclusive to EBV viremia. Furthermore, Peluso et al. have also demonstrated that EBV reactivation may be a key factor in PASC and specifically relates to fatigue and neurologic symptoms . These studies suggest that PASC symptoms may at least in part arise from EBV-induced damage and/or EBV-mediated immune dysregulation post SARS-CoV-2 infection.
Due to the noted EBV reactivation in acute SARS-CoV-2 infection and PASC, treatments used to alleviate symptoms in reactivated EBV in the absence of COVID-19 might also be useful to investigate as therapies to address EBV reactivation in acute COVID-19 and PASC. For example, reactivated EBV after hematopoietic cell transplantation has been treated with the anti-CD20 monoclonal antibody, rituximab . Other antiviral therapies such as acyclovir, ganciclovir, and vidarabine inhibit viral DNA polymerase have been used to treat chronic active EBV, though have not been found to be effective in chronic non-active EBV . Infusion of immunoglobulins (IVIG) is another promising therapy that has been successfully used in some critical patients without SARS-CoV-2 infection and may be beneficial in acute COVID-19 or PASC . Further research is needed to determine whether the treatments used for non-SARS-CoV-2-related EBV reactivation may also be beneficial in the treatment of acute COVID-19 and PASC.
Gut microbiome studies in acute COVID-19
A growing body of research suggests that the gut microbiome composition is related to the severity of acute COVID-19 . However, it is unknown whether any changes in the microbiome’s makeup occur after eradication of SARS-CoV-2.
Gut microbiome studies in PASC (Fig. 1)
A study of 106 patients found that PASC patients have significantly lower levels of Collinsella aerofaciens, F. prausnitzii, Blautia obeum, and a greater level of Ruminococcus gnavus and Bacteroides vulgatus than non-COVID-19 controls at six months . Specific PASC symptoms may be associated with gut microbiome dysbiosis. For example, pathogens including Streptococcus anginosus, Streptococcus vestibularis, Streptococcus gordonii and Clostridium disporicum were correlated with persistent respiratory symptoms. Similarly, in patients with neuropsychiatric PASC, there was an association with the abundance of Clostridium innocuum and Actinomyces naeslundii. The relative abundance of Bifidobacterium pseudocatenulatum, F. prausnitzii, R. inulinivorans, and Roseburia hominis, known to benefit host immunity, exhibited the strongest inverse relationships with PASC.
Diet in acute COVID-19
Data on specific-diet outcomes in acute SARS-CoV-2 infection is currently limited. However, general guidelines for acute COVID-19 include a diet rich in vegetables, fruit, whole grains, healthy fats, low-fat dairy, and limiting red meat . For example, a plant-based diet was linked to a decreased risk and severity of COVID-19 . Similarly, participants following “plant-based” and “plant-based or pescatarian diets” had 73% and 59% lower odds of moderate-to-severe COVID-19 compared to individuals following “low carbohydrate, high protein diets,” who had 48% greater odds of moderate-to-severe COVID-19 .
Diet in PASC
In autoimmune diseases, balanced diets composed of whole grains, polyphenol-rich vegetables, and omega-3 fatty acid-rich foods may reduce inflammation and fatigue . Whether an anti-inflammatory diet or supplements can be extended to PASC patients, thought to have immune dysregulation, is currently being studied, with over 20 trials listed on clinicaltrials.gov.
Nonetheless, one emerging diet gathering patient support is an anti-histamine diet, as overactivation of mast cells and histamine release may play a role in PASC (Fig. 1) [61, 62]. Histamine intolerance in PASC may be related to diamine oxidase decrease leading to mast cell activation syndrome . Foods high in histamine include blue fish and fermented products such as cheeses, sausages, wine, beer, sauerkraut, and fermented soy derivatives . The avoidance of such foods may constitute a low histamine diet, though current research is limited .
Increasing electrolyte, salt, and water intake may alleviate PASC-related-fatigue caused by autonomic dysfunction in PASC, notably Postural orthostatic tachycardia syndrome (POTS) . Small, more frequent meals are recommended, and diets rich in fiber and probiotics may improve GI-related POTS symptoms.
Recently, a high-quality diet (upper 40% of Alternate Healthy Eating Index–2010 score) was found to be protective against PASC; however, considering the heterogeneity of PASC clinical presentations, future studies are needed to determine if specific dietary interventions can treat different PASC symptoms .
Alcohol in acute COVID-19
Alcohol abuse has been associated with an increase in acute lung injury and acute respiratory distress syndrome . However, it is uncertain how alcohol consumption impacts COVID-19 risk, severity, and mortality.
Though Hamer et al. demonstrated no relationship between alcohol and acute COVID-19 hospitalization, Bailey et al. found that patients with alcohol use disorder had a greater risk of hospitalization and mortality [69, 70]. However, intake of spirits, beer and cider raised the risk of COVID-19 independent of consumed frequency or amount, while a low frequency of drinking wine and champaign (1–2 glasses/week) was protective against COVID-19, Although certain alcohols were related to decreased COVID-19, drinking cannot be deemed an effective mechanism for infection prevention.
Alcohol in PASC
High alcohol intake disrupts several pathophysiological pathways by increasing the levels of proinflammatory cytokines, disrupting alveolar macrophage activities in the lungs, and desensitizing respiratory ciliated cells [71,72,73]. As one of the PASC characteristics is prolonged inflammation, it is possible that chronic high-dose alcohol may further exacerbate inflammation by upregulating cytokines. However, it remains unclear how alcohol interacts with or contributes to PASC. Considering the stark increase in alcohol sales during the pandemic and dichotomy in current studies, further investigations are currently taking place, inclusive of the NIH RECOVER trial regarding alcohol and susceptibility to PASC .
Smoking in acute COVID-19
There is inconclusive evidence surrounding the impact of smoking on the risk and severity of COVID-19. In one study, current smokers (71%) had 80% reduced probability of contracting COVID-19 than former smokers and nonsmokers . Another study in 43,103 adults, found that patients reporting current smoking had a reduced incidence of hospitalization or death .
In contrast, current smokers showed greater risk of hospitalization and mortality when compared to never-smokers in a study by Clift et al. . In a meta-analysis consisting of 46 peer-reviewed articles of 22,939 COVID-19 patients, of which 23.6% had disease progression, 12.7% had a history of smoking and 33.5% of prior-smokers reported illness progression, compared to 21.9% of nonsmokers . Importantly, patients with a history of smoking or any tobacco use had an increased risk of COVID-19-related mortality .
Smoking in PASC
In comparison, emerging data suggest that smoking increases risk of PASC . Specifically, smokers were more likely to experience tachycardia and/or high-blood-pressure. However, as with alcohol, the impact of smoking on PASC patients is still an area of active research and further studies are needed to confirm a causal relationship.
Exercise in acute COVID-19
Following acute SARS-CoV-2 infection, people who exercise had improved clinical outcomes [80, 81]. With recovery from acute COVID-19, Udina et al. found small intervals of 30-min daily individualized therapeutic exercise intervention increased functional status post-ICU stay .
Exercise in PASC
The role of exercise in PASC management is controversial. Rebello et al. hypothesized that exercise mitigates the neuropsychiatric and endocrine consequences of PASC by stimulating the release of circulating factors that modulate the anti-inflammatory response, promote brain homeostasis, and enhance insulin sensitivity .
However, with symptoms such as fatigue and myalgias, PASC patients find it difficult to exercise. In a survey by Davis et al., 89.1% of PASC patients reported physical and/or mental post-exertional malaise . In another study, PASC patients showed a significant decrease in peak exercise aerobic capacity, as well as an elevated hyperventilatory response during exercise . Similarly, women with PASC exhibited an increased heart rate with exertion and heart rate recovery was delayed after a 6-minute walk test .
In a survey study, the majority of PASC patients (74.8%) claimed that physical activity worsened, 0.84% said their symptoms improved, some (20.9%) stated that it had a mixed impact, and 28.7% of participants said physical activity had no effect on their PASC symptoms , Similar to acute COVID-19 rehabilitation, current approaches to PASC recovery suggest a personalized rehabilitation approach by offering tailored exercises, starting with lower intensity, building stamina, and focusing on gradual improvements [88, 89]. To determine which forms and dose of exercise might help or exacerbate PASC, more research is necessary.
Sleep in acute COVID-19
Sleep disorders are now recognized among the mosaic of COVID-19 symptoms. With acute COVID-19, Mass et al. found that patients with obstructive sleep apnea (OSA) had an 8-fold increased incidence of COVID-19 infection . OSA was linked to an elevated risk of hospitalization and nearly doubled the likelihood of having respiratory failure in acute COVID-19. In another study, OSA was a risk factor for mortality in diabetic individuals hospitalized with COVID-19 .
Sleep in PASC
In comparison, Martimbianco et al. found between 21.7% and 53% of PASC patients to have sleep difficulties or insomnia . Restless legs syndrome (RLS) is a sleep disorder that has been linked to viral infections. Weinstock et al. found that females with PASC had a 5.7% prevalence of RLS before COVID-19 and a 14.8% prevalence after COVID-19, compared to 6.7% in control females .
Sleep disorders appear to be an overlapping symptom in both acute COVID-19 and PASC. Further research could help determine whether primary versus secondary sleep disorders may be driving COVID-19-related sleep dysregulation and what types of behavioral and pharmacological therapies may offer benefit.
Social determinants of COVID-19 outcomes
Race and ethnicity
The detrimental impacts of the COVID-19 pandemic have been disproportionately felt by people of color. Recent analysis shows that the death rate for Black and Hispanic Americans is double that of Whites, taking age into account . These racial disparities are consistent when comparing rates of hospitalization and infection for Black, Latinx, American Indian, Alaska Native, Asian, Native Hawaiian and Pacific Islander and other non-white racial groups with White Americans . Black, Latinx, and Indigenous Americans have higher prevalence of hypertension, diabetes, and obesity, which are risk factors for PASC development . Disparities are also exacerbated as racial minorities have disproportionate rates of non-COVID deaths due to lack of access to care .
Barriers to health equity
Vulnerable groups face barriers to treatment that can considerably hinder management of PASC. Rates of health insurance differ considerably for Black and Latinx people compared to white people, and these disparities are particularly notable in states that did not expand Medicaid eligibility following the passing of the Affordable Care Act [95, 98]. Management of PASC could be particularly difficult for uninsured groups because healthcare costs could act as deterrents from screening and seeking advanced care .
Additionally, vulnerable groups may face barriers in managing PASC due to occupational and geographical factors. The PASC-related symptoms of fatigue and brain fog can interfere with work, and a lack of job security and occupational health services may hinder long-term care and daily activities . Transportation barriers also prevent healthcare access, leading to missed appointments, delayed care, and poorer management of chronic illness . In a survey of cancer patients in Texas, compared to 38% of whites, 55% of African Americans, and 60% of Hispanics reported poor access to transportation as a barrier to missing cancer treatment . In another study, Velasco et al. found that non-English-speaking Hispanic patients were 75% more likely to require critical care than non-Hispanic patients, identifying late presentation and poor access to care as determinants of clinical outcomes .
Chronic illness, especially non-visible illness, remains poorly understood and acknowledged by the general public, leading to additional social barriers felt by PASC survivors. A study investigating the experience of patients with Chronic Fatigue Syndrome (CFS)/myalgic encephalomyelitis (ME) found that individuals often felt discredited by professionals and experienced trivialization of their illness socially and professionally, resulting in the internalization of negative feelings . Validation of health conditions was found to be an important component in fostering social support and counteracting existing stigma against non-visible illness.
The pressure associated with stigmatization against non-visible illness is also readily felt in the workplace. Patients may be faced with the notion of “Damned if they do, damned if they do not” when deciding to disclose illness to employers . Though laws exist to protect individuals against discrimination at work, deviant labeling and stigmatization remain deterrents for people with chronic illness. Not disclosing can lead to a lack of support and validation for the patient’s symptoms, impacting their mental and physical well-being. PASC individuals have also reported feeling invalidated by friends, family, and clinicians . It is important to address the social stigma accompanying non-visible illness, and health policy interventions and further research will be necessary for educating the public on PASC and providing employment protections for patients.
Though the cause of PASC has yet to be identified, the experiences of patients are undeniable.
A study involving 24 interviews with PASC patients in the UK found common themes such as difficulty managing symptoms, difficulty finding proper care, and feeling ignored and isolated by medical providers and the public. Some patients hesitated to seek care due to fears of their symptoms being dismissed as psychological rather than physical. The lack of consensus among medical professionals on treatment added to the confusion and frustration experienced by these patients .
PASC patients, who are predominantly women, may also face gender biases that reinforce stigma against them. Gendered norms have historically characterized men as “stoic” and women as “hysterical” while in pain, leading to health disparities such as female patients receiving sedative medication rather than analgesics for pain and waiting longer to receive treatment [105,106,107]. These discriminatory ideas may contribute to the misattribution of PASC symptoms to a psychiatric etiology and a failure to properly evaluate or treat PASC.
The disproportionate impact of COVID-19 on racial minorities raises concerns that PASC may be significantly underreported for underserved populations . Economic, geographic, and occupational barriers may prevent these vulnerable populations from accessing proper healthcare and communicating their health concerns to clinicians. Directed screening and interventions of the demographic groups most impacted by PASC are necessary to ensure that underrepresented populations are not neglected.
Conclusion and future directions
The emerging pattern from multiple studies suggests that acute COVID-19 and PASC affect patients with a multitude of symptoms. The varied presentations are likely influenced by patients’ age, environmental, behavioral and lifestyle risk factors. Sex-specific genetic, hormonal and immune risk factors may help explain why more men have severe outcomes from acute SARS-CoV-2 infection, while more women are affected with PASC . In addition, social determinants of health are emerging as important factors in patients’ access to care and long-term outcomes.
With over 762 million people worldwide experiencing acute COVID-19 and an estimated 10–30% of the population experiencing PASC, these conditions have become critical public health concerns and ongoing research is needed to understand the evolving risk factors contributing to their presentation and progression. In addition, cross-disciplinary collaborations and federal funding are vital for research and the establishment of specialized Long-COVID clinics that can offer clinical care, rehabilitation, social work assistance, peer support groups, and equitable access to services for disadvantaged populations. It is further of utmost importance that clinicians caring for patients with Long-COVID continue to actively learn about the emerging science of Long-COVID and validate patient symptoms.
Severe acute respiratory syndrome coronavirus 2
Coronavirus disease 2019
Post-acute sequelae of SARS-CoV-2 infections
Human Leukocyte Antigen
Systemic lupus erythematosus
Androgen deprivation therapy
Angiotensin converting enzyme 2
Toll-like receptor 7
Postural orthostatic tachycardia syndrome
Restless legs syndrome
Chronic Fatigue Syndrome
WHO Coronavirus (COVID-19.) Dashboard [Internet]. [cited 2023 Apr 9]. Available from: https://covid19.who.int.
CDC. COVID-19 and Your Health [Internet]. Cent. Dis. Control Prev. 2020 [cited 2022 Aug 28]. Available from: https://www.cdc.gov/coronavirus/2019-ncov/need-extra-precautions/asthma.html.
A clinical case definition of post COVID-19. condition by a Delphi consensus, 6 October 2021 [Internet]. [cited 2022 Aug 4]. Available from: https://www.who.int/publications/i/item/WHO-2019-nCoV-Post_COVID-19_condition-Clinical_case_definition-2021.1.
CDC, Post. -COVID Conditions [Internet]. Cent. Dis. Control Prev. 2022 [cited 2022 Aug 4]. Available from: https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html.
Choo SY. The HLA System: Genetics, Immunology, Clinical Testing, and clinical implications. Yonsei Med J. 2007;48:11–23.
Frontiers | HLA. Immune Response, and Susceptibility to COVID-19 [Internet]. [cited 2022 Aug 9]. Available from: https://www.frontiersin.org/articles/10.3389/fimmu.2020.601886/full.
Uncoupling the Roles of HLA-DRB1. and HLA-DRB5 Genes in Multiple Sclerosis | The Journal of Immunology [Internet]. [cited 2022 Oct 17]. Available from: https://www.jimmunol.org/content/181/8/5473.
Four Systemic Lupus Erythematosus Subgroups., Defined by Autoantibodies Status, Differ Regarding HLA-DRB1 Genotype Associations and Immunological and Clinical Manifestations - Diaz‐Gallo – 2022 - ACR Open Rheumatology - Wiley Online Library [Internet]. [cited 2022 Oct 17]. Available from: https://onlinelibrary.wiley.com/doi/https://doi.org/10.1002/acr2.11343.
Phetsouphanh C, Darley DR, Wilson DB, Howe A, Munier CML, Patel SK, et al. Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection. Nat Immunol Nature Publishing Group. 2022;23:210–6.
Viruses | Free Full-Text. | Clinical Manifestation of Subacute Thyroiditis Triggered by SARS-CoV-2 Infection Can Be HLA-Dependent [Internet]. [cited 2022 Oct 17]. Available from: https://www.mdpi.com/1999-4915/13/12/2447.
HLA-dependent variation in SARS‐CoV‐2 CD. 8 + T cell cross‐reactivity with human coronaviruses - Buckley – 2022 - Immunology - Wiley Online Library [Internet]. [cited 2022 Oct 17]. Available from: https://onlinelibrary.wiley.com/doi/https://doi.org/10.1111/imm.13451.
Verthelyi D. Sex hormones as immunomodulators in health and disease. Int Immunopharmacol. 2001;1:983–93.
Cutolo M, Brizzolara R, Atzeni F, Capellino S, Straub RH, Puttini PCS. The immunomodulatory effects of estrogens: clinical relevance in immune-mediated rheumatic diseases. Ann N Y Acad Sci. 2010;1193:36–42.
Tan IJ, Peeva E, Zandman-Goddard G. Hormonal modulation of the immune system - A spotlight on the role of progestogens. Autoimmun Rev. 2015;14:536–42.
Lipsa A, Prabhu JS. Gender disparity in COVID-19: role of sex steroid hormones. Asian Pac J Trop Med. 2021;14:5–9.
Lanser L, Burkert FR, Thommes L, Egger A, Hoermann G, Kaser S, et al. Testosterone Deficiency is a risk factor for severe COVID-19. Front Endocrinol. 2021;12:694083.
Salonia A, Pontillo M, Capogrosso P, Gregori S, Tassara M, Boeri L, et al. Severely low testosterone in males with COVID-19: a case-control study. Andrology. 2021;9:1043–52.
Montopoli M, Zumerle S, Vettor R, Rugge M, Zorzi M, Catapano CV, et al. Androgen-deprivation therapies for prostate cancer and risk of infection by SARS-CoV-2: a population-based study (N = 4532). Ann Oncol Off J Eur Soc Med Oncol. 2020;31:1040–5.
Frontiers. | The Double Edge Sword of Testosterone’s Role in the COVID-19 Pandemic [Internet]. [cited 2022 Aug 8]. Available from: https://www.frontiersin.org/articles/https://doi.org/10.3389/fendo.2021.607179/full.
Travison TG, Morley JE, Araujo AB, O’Donnell AB, McKinlay JB. The relationship between libido and testosterone levels in Aging Men. J Clin Endocrinol Metab. 2006;91:2509–13.
Barkin J. Erectile dysfunction and hypogonadism (low testosterone). Can J Urol. 2011;7.
Fernández-de-las-Peñas C, Martín-Guerrero JD, Pellicer-Valero ÓJ, Navarro-Pardo E, Gómez-Mayordomo V, Cuadrado ML et al. Female Sex Is a Risk Factor Associated with Long-Term Post-COVID Related-Symptoms but Not with COVID-19 Symptoms: The LONG-COVID-EXP-CM Multicenter Study. J Clin Med. Multidisciplinary Digital Publishing Institute; 2022;11:413.
Davido B, Seang S, Tubiana R, Truchis P. de. Post–COVID-19 chronic symptoms: a postinfectious entity? Clin Microbiol Infect. Elsevier; 2020;26:1448–9.
Potential Influence of Menstrual Status and Sex Hormones on Female Severe Acute Respiratory Syndrome Coronavirus 2 Infection. : A Cross-sectional Multicenter Study in Wuhan, China | Clinical Infectious Diseases | Oxford Academic [Internet]. [cited 2022 Aug 8]. Available from: https://academic.oup.com/cid/article/72/9/e240/5875093.
Sund M, Fonseca-Rodríguez O, Josefsson A, Welen K, Fors Connolly A-M. Association between pharmaceutical modulation of oestrogen in postmenopausal women in Sweden and death due to COVID-19: a cohort study. BMJ Open. 2022;12:e053032.
Estrogen. and COVID-19 symptoms: Associations in women from the COVID Symptom Study | PLOS ONE [Internet]. [cited 2022 Aug 8]. Available from: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0257051.
Sex differences in. immune responses | Nature Reviews Immunology [Internet]. [cited 2022 Aug 8]. Available from: https://www.nature.com/articles/nri.2016.90.
Tukiainen T, Villani A-C, Yen A, Rivas MA, Marshall JL, Satija R, et al. Landscape of X chromosome inactivation across human tissues. Nature. 2017;550:244–8.
Liu J, Ji H, Zheng W, Wu X, Zhu JJ, Arnold AP, et al. Sex differences in renal angiotensin converting enzyme 2 (ACE2) activity are 17β-oestradiol-dependent and sex chromosome-independent. Biol Sex Differ. 2010;1:6.
Matz KM, Guzman RM, Goodman AG. Chapter Two - The Role of Nucleic Acid Sensing in Controlling Microbial and Autoimmune Disorders. In: Vanpouille-Box C, Galluzzi L, editors. Int Rev Cell Mol Biol [Internet]. Academic Press; 2019 [cited 2022 Aug 8]. p. 35–136. Available from: https://www.sciencedirect.com/science/article/pii/S1937644818300868.
Souyris M, Mejía JE, Chaumeil J, Guéry J-C. Female predisposition to TLR7-driven autoimmunity: gene dosage and the escape from X chromosome inactivation. Semin Immunopathol. 2019;41:153–64.
Fk H, F P-R, Sr G, Bd J, Sv K, Cl N et al. Is older age associated with COVID-19 mortality in the absence of other risk factors? General population cohort study of 470,034 participants. PloS One [Internet]. PLoS One; 2020 [cited 2022 Sep 15];15. Available from: https://pubmed.ncbi.nlm.nih.gov/33152008/.
Chinnadurai R, Ogedengbe O, Agarwal P, Money-Coomes S, Abdurrahman AZ, Mohammed S, et al. Older age and frailty are the chief predictors of mortality in COVID-19 patients admitted to an acute medical unit in a secondary care setting- a cohort study. BMC Geriatr. 2020;20:409.
Age-specific mortality and immunity patterns of SARS-CoV-. 2 | Nature [Internet]. [cited 2022 Aug 8]. Available from: https://www.nature.com/articles/s41586-020-2918-0.
Age-dependent effects in the transmission and control of COVID-19. epidemics | Nature Medicine [Internet]. [cited 2022 Aug 8]. Available from: https://www.nature.com/articles/s41591-020-0962-9.
Attributes and predictors of long COVID. | Nature Medicine [Internet]. [cited 2022 Aug 8]. Available from: https://www.nature.com/articles/s41591-021-01292-y.
Sigfrid L, Drake TM, Pauley E, Jesudason EC, Olliaro P, Lim WS, 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;8:100186.
Evans RA, McAuley H, Harrison EM, Shikotra A, Singapuri A, Sereno M et al. Physical, cognitive, and mental health impacts of COVID-19 after hospitalisation (PHOSP-COVID): a UK multicentre, prospective cohort study. Lancet Respir Med. Elsevier; 2021;9:1275–87.
Subramanian A, Nirantharakumar K, Hughes S, Myles P, Williams T, Gokhale KM et al. Symptoms and risk factors for long COVID in non-hospitalized adults. Nat Med Nature Publishing Group; 2022;1–9.
Yoo SM, Liu TC, Motwani Y, Sim MS, Viswanathan N, Samras N, et al. Factors Associated with Post-Acute Sequelae of SARS-CoV-2 (PASC) after diagnosis of symptomatic COVID-19 in the Inpatient and Outpatient setting in a diverse cohort. J Gen Intern Med. 2022;37:1988–95.
Tzellos S, Farrell PJ. Epstein-Barr Virus sequence Variation—Biology and Disease. Pathogens. 2012;1:156–75.
Sausen DG, Bhutta MS, Gallo ES, Dahari H, Borenstein R. Stress-Induced Epstein-Barr Virus Reactivation. Biomolecules. Volume 11. Multidisciplinary Digital Publishing Institute; 2021. p. 1380.
Straus SE, Tosato G, Armstrong G, Lawley T, Preble OT, Henle W, et al. Persisting illness and fatigue in adults with evidence of Epstein-Barr Virus infection. Ann Intern Med American College of Physicians. 1985;102:7–16.
Chen T, Song J, Liu H, Zheng H, Chen C. Positive Epstein–Barr virus detection in coronavirus disease 2019 (COVID-19) patients. Sci Rep. 2021;11:10902.
Paolucci S, Cassaniti I, Novazzi F, Fiorina L, Piralla A, Comolli G, et al. EBV DNA increase in COVID-19 patients with impaired lymphocyte subpopulation count. Int J Infect Dis. 2021;104:315–9.
COVID-19 associated EBV reactivation and effects. of ganciclovir treatment - Meng – 2022 - Immunity, Inflammation and Disease - Wiley Online Library [Internet]. [cited 2022 Aug 9]. Available from: https://onlinelibrary.wiley.com/doi/https://doi.org/10.1002/iid3.597.
Goh C, Burnham KL, Ansari MA, de Cesare M, Golubchik T, Hutton P, et al. Epstein-Barr virus reactivation in sepsis due to community-acquired pneumonia is associated with increased morbidity and an immunosuppressed host transcriptomic endotype. Sci Rep Nature Publishing Group. 2020;10:9838.
Libert N, Bigaillon C, Chargari C, Bensalah M, Muller V, Merat S, et al. Epstein-Barr virus reactivation in critically ill immunocompetent patients. Biomed J. 2015;38:70–6.
Investigation of Long COVID Prevalence and Its Relationship to Epstein-. Barr Virus Reactivation - PMC [Internet]. [cited 2022 Aug 9]. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8233978/.
Multiple early factors anticipate post-acute COVID. -19 sequelae: Cell [Internet]. [cited 2022 Aug 8]. Available from: https://www.cell.com/cell/fulltext/S0092-8674(22)00072-1#secsectitle0020.
Peluso MJ, Deveau T-M, Munter SE, Ryder D, Buck A, Beck-Engeser G et al. Chronic viral coinfections differentially affect the likelihood of developing long COVID. J Clin Invest [Internet]. American Society for Clinical Investigation; 2023 [cited 2023 Apr 8];133. Available from: https://www.jci.org/articles/view/163669.
Jain T, Kosiorek HE, Grys TE, Kung ST, Shah VS, Betcher JA, et al. Single dose versus multiple doses of rituximab for preemptive therapy of Epstein–Barr virus reactivation after hematopoietic cell transplantation. Leuk Lymphoma Taylor & Francis. 2019;60:110–7.
Cohen JI. Optimal treatment for chronic active Epstein-Barr Virus Disease. Pediatr Transpl. 2009;13:393–6.
Trappe R, Riess H, Anagnostopoulos I, Neuhaus R, Gärtner BC, Pohl H, et al. Efficiency of antiviral therapy plus IVIG in a case of primary EBV infection associated PTLD refractory to rituximab, chemotherapy, and antiviral therapy alone. Ann Hematol. 2009;88:167–72.
Schult D, Reitmeier S, Koyumdzhieva P, Lahmer T, Middelhoff M, Erber J, et al. Gut bacterial dysbiosis and instability is associated with the onset of complications and mortality in COVID-19. Volume 14. Gut Microbes. Taylor & Francis; 2022. p. 2031840.
Gut microbiota dynamics in. a prospective cohort of patients with post-acute COVID-19 syndrome | Gut [Internet]. [cited 2022 Aug 9]. Available from: https://gut.bmj.com/content/71/3/544.
de Faria Coelho-Ravagnani C, Corgosinho FC, Sanches FLFZ, Prado CMM, Laviano A, Mota JF. Dietary recommendations during the COVID-19 pandemic. Nutr Rev. 2020;nuaa067.
Diet quality and risk and severity of COVID-19. : a prospective cohort study | Gut [Internet]. [cited 2022 Aug 9]. Available from: https://gut.bmj.com/content/70/11/2096.
Kim H, Rebholz CM, Hegde S, LaFiura C, Raghavan M, Lloyd JF, et al. Plant-based diets, pescatarian diets and COVID-19 severity: a population-based case–control study in six countries. BMJ Nutr Prev Health. 2021;4:257–66.
Haß U, Herpich C, Norman K. Anti-inflammatory diets and fatigue. Nutrients. 2019;11:2315.
Gebremeskel S, Schanin J, Coyle KM, Butuci M, Luu T, Brock EC, et al. Mast cell and Eosinophil Activation are Associated with COVID-19 and TLR-Mediated viral inflammation: implications for an anti-siglec-8 antibody. Front Immunol. 2021;12:650331.
Covid-19 hyperinflammation. and post-Covid-19 illness may be rooted in mast cell activation syndrome - International Journal of Infectious Diseases [Internet]. [cited 2022 Aug 9]. Available from: https://www.ijidonline.com/article/S1201-9712(20)30732-3/fulltext
Histamine and histamine intolerance | The American Journal of Clinical Nutrition. | Oxford Academic [Internet]. [cited 2022 Aug 9]. Available from: https://academic.oup.com/ajcn/article/85/5/1185/4633007.
Sánchez-Pérez S, Comas-Basté O, Rabell-González J, Veciana-Nogués MT, Latorre-Moratalla ML, Vidal-Carou MC. Biogenic Amines in Plant-Origin Foods: are they frequently underestimated in low-histamine diets? Foods. Volume 7. Multidisciplinary Digital Publishing Institute; 2018. p. 205.
Jill Schofield. Persistent Antiphospholipid Antibodies, Mast Cell Activation Syndrome, Postural Orthostatic Tachycardia Syndrome and Post-COVID Syndrome: 1 Year On. Eur J Case Rep Intern Med [Internet]. 2021 [cited 2022 Aug 9]; Available from: https://www.ejcrim.com/index.php/EJCRIM/article/view/2378.
Abed H, Ball PA, Wang L-X. Diagnosis and management of postural orthostatic tachycardia syndrome: a brief review. J Geriatr Cardiol JGC. 2012;9:61–7.
Wang S, Li Y, Yue Y, Yuan C, Kang JH, Chavarro JE, et al. Adherence to healthy Lifestyle prior to infection and risk of Post–COVID-19 Condition. JAMA Intern Med. 2023;183:232–41.
Kershaw CD, Guidot DM. Alcoholic lung disease. Alcohol Res Health. 2008;31:66–75.
Hamer M, Kivimäki M, Gale CR, Batty GD. Lifestyle risk factors, inflammatory mechanisms, and COVID-19 hospitalization: a community-based cohort study of 387,109 adults in UK. Brain Behav Immun. 2020;87:184–7.
COVID-19 patients with documented. alcohol use disorder or alcohol‐related complications are more likely to be hospitalized and have higher all‐cause mortality - Bailey – 2022 - Alcoholism: Clinical and Experimental Research - Wiley Online Library [Internet]. [cited 2022 Aug 9]. Available from: https://onlinelibrary.wiley.com/doi/full/10.1111/acer.14838?campaign=wolearlyview.
Predictive values of tumor necrosis. factor-α for depression treatment outcomes: effect modification by hazardous alcohol consumption | Translational Psychiatry [Internet]. [cited 2022 Aug 9]. Available from: https://www.nature.com/articles/s41398-021-01581-7.
Frontiers | The Impact of Alcohol Use Disorder on Tuberculosis. : A Review of the Epidemiology and Potential Immunologic Mechanisms [Internet]. [cited 2022 Aug 9]. Available from: https://www.frontiersin.org/articles/https://doi.org/10.3389/fimmu.2022.864817/full.
Yeligar SM, Chen MM, Kovacs EJ, Sisson JH, Burnham EL, Brown LAS. Alcohol and Lung Injury and Immunity. Alcohol Fayettev N. 2016;55:51–9.
Alcohol use disorder. : A pre-existing condition for COVID-19? - ScienceDirect [Internet]. [cited 2022 Aug 9]. Available from: https://www.sciencedirect.com/science/article/pii/S0741832920302913.
Impact of Tobacco Smoking on the Risk of COVID-19. : A Large Scale Retrospective Cohort Study | Nicotine & Tobacco Research | Oxford Academic [Internet]. [cited 2022 Aug 9]. Available from: https://academic.oup.com/ntr/article/23/8/1398/6073671.
Yordanov Y, Dinh A, Bleibtreu A, Mensch A, Lescure F-X, Debuc E, et al. Clinical characteristics and factors associated with hospital admission or death in 43 103 adult outpatients with coronavirus disease 2019 managed with the Covidom telesurveillance solution: a prospective cohort study. Clin Microbiol Infect Elsevier. 2021;27:1158–66.
Smoking. and COVID-19 outcomes: an observational and Mendelian randomisation study using the UK Biobank cohort | Thorax [Internet]. [cited 2022 Aug 9]. Available from: https://thorax.bmj.com/content/77/1/65.
Patanavanich R, Glantz SA. Smoking is associated with worse outcomes of COVID-19 particularly among younger adults: a systematic review and meta-analysis. BMC Public Health. 2021;21:1554.
Barthélémy H, Mougenot E, Duracinsky M, Salmon-Ceron D, Bonini J, Péretz F, et al. Smoking increases the risk of post-acute COVID-19 syndrome: results from a french community-based survey. Volume 20. Tob Induc Dis. The International Society for the Prevention of Tobacco Induced Diseases; 2022. pp. 1–10.
de Souza FR, Motta-Santos D, dos Santos Soares D, de Lima JB, Cardozo GG, Guimarães LSP, et al. Association of physical activity levels and the prevalence of COVID-19-associated hospitalization. J Sci Med Sport. 2021;24:913–8.
Sallis R, Young DR, Tartof SY, Sallis JF, Sall J, Li Q et al. Physical inactivity is associated with a higher risk for severe COVID-19 outcomes: a study in 48 440 adult patients. Br J Sports Med. BMJ Publishing Group Ltd and British Association of Sport and Exercise Medicine; 2021;55:1099–105.
Udina C, Ars J, Morandi A, Vilaró J, Cáceres C, Inzitari M. Rehabilitation in Adult Post-COVID-19 Patients in Post-Acute Care with Therapeutic Exercise. J Frailty Aging. 2021;10:297–300.
Rebello CJ, Axelrod CL, Reynolds CF, Greenway FL, Kirwan JP. Exercise as a moderator of persistent neuroendocrine symptoms of COVID-19. Exerc Sport Sci Rev. 2022;50:65–72.
Davis HE, Assaf GS, McCorkell L, Wei H, Low RJ, Re’em Y, et al. Characterizing long COVID in an international cohort: 7 months of symptoms and their impact. EClinicalMedicine. 2021;38:101019.
Singh I, Joseph P, Heerdt PM, Cullinan M, Lutchmansingh DD, Gulati M, et al. Persistent Exertional Intolerance after COVID-19: insights from Invasive Cardiopulmonary Exercise Testing. Volume 161. CHEST. Elsevier;; 2022. pp. 54–63.
Baranauskas MN, Carter SJ. Evidence for impaired chronotropic responses to and recovery from 6-minute walk test in women with post-acute COVID-19 syndrome. Exp Physiol. 2022;107:722–32.
IJERPH | Free Full-Text. | The Relationship between Physical Activity and Long COVID: A Cross-Sectional Study [Internet]. [cited 2022 Aug 9]. Available from: https://www.mdpi.com/1660-4601/19/9/5093.
Cerasola D, Argano C, Corrao S, Lessons From. COVID-19: Physical Exercise Can Improve and Optimize Health Status. Front Med [Internet]. 2022 [cited 2022 Aug 28];9. Available from: https://www.frontiersin.org/articles/https://doi.org/10.3389/fmed.2022.834844.
Maley JH, Sampsel S, Abramoff BA, Herman E, Neerukonda KV, Mikkelsen ME. Consensus methodology for the development of postacute sequelae of SARS-CoV‐2 guidance statements. PM&R. 2021;13:1021–6.
Obstructive Sleep Apnea and Risk of COVID-19. Infection, Hospitalization and Respiratory Failure | SpringerLink [Internet]. [cited 2022 Aug 9]. Available from: https://link.springer.com/article/10.1007/s11325-020-02203-0.
Cariou B, Hadjadj S, Wargny M, Pichelin M, Al-Salameh A, Allix I, et al. Phenotypic characteristics and prognosis of inpatients with COVID-19 and diabetes: the CORONADO study. Diabetologia. 2020;63:1500–15.
Cabrera Martimbianco AL, Pacheco RL, Bagattini ÂM, Riera R. Frequency, signs and symptoms, and criteria adopted for long COVID-19: a systematic review. Int J Clin Pract. 2021;75:e14357.
Weinstock LB, Brook JB, Walters AS, Goris A, Afrin LB, Molderings GJ. Restless legs syndrome is associated with long-COVID in women. J Clin Sleep Med American Academy of Sleep Medicine 18:1413–8.
Romer AMPAGelrud, Shiro A, Barr, Carl. Amid the pandemic, Black and Latino men have experienced the largest drop in life expectancy [Internet]. Brookings. 2021 [cited 2022 Aug 12]. Available from: https://www.brookings.edu/research/amid-the-pandemic-black-and-latino-men-have-experienced-the-largest-drop-in-life-expectancy/.
BERGER Z, ALTIERY DE JESUS V, ASSOUMOU SA, GREENHALGH T. Long COVID and Health Inequities: the role of primary care. Milbank Q. 2021;99:519–41.
Rossen LM, Ahmad FB, Anderson RN, Branum AM, Du C, Krumholz HM, et al. Disparities in excess Mortality Associated with COVID-19 — United States, 2020. MMWR Morb Mortal Wkly Rep. 2021;70:1114–9.
Lee D-C, Liang H, Shi L. The convergence of racial and income disparities in health insurance coverage in the United States. Int J Equity Health. 2021;20:96.
Syed ST, Gerber BS, Sharp LK. Traveling towards Disease: transportation barriers to Health Care Access. J Community Health. 2013;38:976–93.
Guidry JJ, Aday LA, Zhang D, Winn RJ. Transportation as a barrier to cancer treatment. Cancer Pract. 1997;5:361–6.
Velasco F, Yang DM, Zhang M, Nelson T, Sheffield T, Keller T, et al. Association of Healthcare Access with Intensive Care Unit utilization and mortality in patients of hispanic ethnicity hospitalized with COVID-19. J Hosp Med. 2021;16:659–66.
Pilkington K, Ridge DT, Igwesi-Chidobe CN, Chew-Graham CA, Little P, Babatunde O, et al. A relational analysis of an invisible illness: a meta-ethnography of people with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) and their support needs. Soc Sci Med. 2020;265:113369.
Vickers MH. Life at work with “invisible” chronic illness (ICI): the “unseen”, unspoken, unrecognized dilemma of disclosure. J Workplace Learn MCB UP Ltd. 1997;9:240–52.
Kingstone T, Taylor AK, O’Donnell CA, Atherton H, Blane DN, Chew-Graham CA. Finding the “right” GP: a qualitative study of the experiences of people with long-COVID. BJGP Open 4:bjgpopen20X101143.
Samulowitz A, Gremyr I, Eriksson E, Hensing G. Brave Men” and “Emotional Women”: a theory-guided literature review on gender Bias in Health Care and gendered norms towards patients with Chronic Pain. Pain Res Manag. 2018;2018:6358624.
Calderone KL. The influence of gender on the frequency of pain and sedative medication administered to postoperative patients. Sex Roles. 1990;23:713–25.
Chen EH, Shofer FS, Dean AJ, Hollander JE, Baxt WG, Robey JL, et al. Gender disparity in analgesic treatment of emergency department patients with acute abdominal pain. Acad Emerg Med Off J Soc Acad Emerg Med. 2008;15:414–8.
Liu Y, Ebinger JE, Mostafa R, Budde P, Gajewski J, Walker B, et al. Paradoxical sex-specific patterns of autoantibody response to SARS-CoV-2 infection. J Transl Med. 2021;19:524.
We are grateful to Dr. William Schwartz, Dr. Adron Harris and Diane Snell for thoughtful comments and review of the manuscript; Jennifer Ramey, RN for helpful discussions and PASC patient advocacy; Diana Zuckerman and Emma Roy at the National Center for Health Research for PASC advocacy and organizing and including the authors in the autoimmune PASC group that led to ideas for this manuscript. We also appreciate Dell Medical School Neurology Department’s administrative support, by Bethaney Watson, Tran de la Torre, Rita Pedroso, and Karen Rascon.
This work was supported by NIAAA K08 T26-1616-11 (E.M.), and institutional Dell Medical School Startup funding (E.M.).
Chumeng Wang: Nothing to disclose; Akshara Ramasamy: Nothing to disclose; Monica Verduzco-Gutierrez: has received honoraria for PASC presentations, and has served as a consultant for Merz, Ipsen, and AbbVie. W. Michael Brode: has received honoraria for PASC presentations, and served as a consultant for Intrivo Diagnostics. Esther Melamed: has received NIH funding for COVID-19 research and received honorarium from the National Center for Health Research for PASC presentation, has served on advisory boards of Genentech, Horizon, Teva and Viela Bio.
Ethics approval and consent to participate
Consent for publication
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
About this article
Cite this article
Wang, C., Ramasamy, A., Verduzco-Gutierrez, M. et al. Acute and post-acute sequelae of SARS-CoV-2 infection: a review of risk factors and social determinants. Virol J 20, 124 (2023). https://doi.org/10.1186/s12985-023-02061-8