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 Table of Contents  
Year : 2022  |  Volume : 17  |  Issue : 3  |  Page : 792-798

Autoimmune disorders with special reference to Coronavirus Disease-2019

Department of Respiratory Care, College of Applied Medical Sciences in Jubail, Imam Abdulrahman Bin Faisal University, Dammam, Kingdom of Saudi Arabia

Date of Submission29-Dec-2020
Date of Decision30-Apr-2021
Date of Acceptance26-Nov-2021
Date of Web Publication2-Nov-2022

Correspondence Address:
Dr. Swathi Gurajala
Department of Respiratory Care, College of Applied Medical Sciences in Jubail, Imam Abdul Rahman Bin Faisal University, Dammam
Kingdom of Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jdmimsu.jdmimsu_475_20

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The COVID-19 outbreak by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, was reported in late December 2019 in Wuhan, China, and has gradually evolved into a pandemic. The number of cases is increasing enormously, so is our knowledge of possible signs and symptoms, clinical manifestations, diagnosis, and management. Few cases develop complications due to excessive cytokine release and uncontrolled immune activation. Several researchers believe that the extensive organ, tissue, and cellular damage done by the virus can be due to antigenic mimicry with the human tissues and the production of autoantibodies. Recent reports of SARS-CoV-2 preceding antiphospholipid antibody syndrome, Miller Fisher syndrome, Guillain–Barré syndrome, Kawasaki syndrome, etc., provide definite examples of this virus's capability to cause the immune system dysregulation. With the rush to mass immunization against the disease, several types of vaccine candidates are in clinical trials, and the risk of developing autoimmune reactions should be considered due to host and pathogen interactions. Hence, in this review, we aim to summarize the various immune dysregulation autoimmune syndromes concerning the SARS-CoV-2 infection published to date.

Keywords: Autoantibodies, autoimmune diseases, COVID-19, immune dysregulation, severe acute respiratory syndrome coronavirus 2

How to cite this article:
Gurajala S. Autoimmune disorders with special reference to Coronavirus Disease-2019. J Datta Meghe Inst Med Sci Univ 2022;17:792-8

How to cite this URL:
Gurajala S. Autoimmune disorders with special reference to Coronavirus Disease-2019. J Datta Meghe Inst Med Sci Univ [serial online] 2022 [cited 2023 Feb 1];17:792-8. Available from: http://www.journaldmims.com/text.asp?2022/17/3/792/360226

  Introduction Top

The Corona Virus Disease 2019 (COVID-19) pandemic caused by the virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by asymptomatic infection or with minimal flu-like symptoms, with a good prognosis in most of the cases. However, very few patients develop complications such as pneumonia and sepsis causing acute respiratory distress syndrome (ARDS) with respiratory failure and sometimes associated with multiorgan failure leading to death.[1],[2] About 20% of these cases develop ARDS through the increased release of cytokines and dysregulated immune activation.[3],[4] The disease has affected people with comorbidities than otherwise normal healthy individuals. However, infrequently there have been complications in otherwise healthy young people that made the researchers think of a possible genetic and molecular explanation. Hence, this led to a hypothetical question that this extensive damage done by the virus can be due to antigenic mimicry with the human tissues and the production of autoantibodies.

Aim of the review

This review will provide a summary of various literature published in databases from January 2020 to date about the association of SARS-CoV-2 infection and the development of autoimmune disorders.

Anti angiotensin-converting enzyme 2 antibodies

The SARS-Cov-2 virus enters into the cells by attachment of the Spike protein Receptor binding Domain with the angiotensin-converting enzyme 2 (ACE 2) receptor. This binding causes dysregulation of the Renin-Angiotensin-Aldosterone system and this can contribute to disease progression. This may result in the production of autoantibodies to ACE2, which target the cells having ACE 2 receptors (abundant in lung type II alveolar cells, enterocytes of the small intestine, arterial and venous endothelial cells, and arterial smooth muscle cells, cortical neurons, and glia) and can cause an aggravated inflammatory reaction.[5]

Spike antibodies and nucleoprotein antibodies

Vojdani and Kharrazian observed that 21/50 tissue antigens reacted with the antibodies of SARS-CoV-2; suggesting cross-reactivity between a variety of tissue antigens and SARS-CoV-2 proteins. They found that the Spike protein antibody can react with transglutaminase 2. transglutaminase 3, mitochondria, myelin basic protein (MBP), ENA, nuclear antigen (NA), collagen, α-myosin, claudin 5 + 6, thyroid peroxidase (TPO), and S100B. The nucleoprotein antibody reacted strongly with tTG6, NA, mitochondria, TPO, actin, ENA, TG, and MBP.[6]

Conduct et al. in their study observed 13/24 pentapeptides were similar between SARS-CoV-2 spike protein and lung surfactant proteins, and the immune response following infection can lead to cross-reactivity with pulmonary surfactant proteins, progressing to lung damage.[7]

Anti-ankyrin 1 antibodies

Ankyrin 1 (ANK-1) is a red blood cell (RBC) membrane protein that plays an important role in the functioning of the RBC acts as a connection between the membrane cytoskeleton and the plasma membrane. The researchers from Italy reported that ANK-1 has an epitope (amino acids LLLQY) that is 100% similar to the SARS-CoV-2 Spike protein. Thus, this molecular mimicry can stimulate antibodies for the destruction of RBCs and cause autoimmune hemolytic anemia.[8]

Anti-red blood cell antibodies

The direct Coombs test/direct antibody test (DAT) is used to detect antibodies attached to the surface of RBCs. In a blood center in Milan, Italy, the researchers observed an increased frequency of DAT positivity in COVID-19 hospitalized patients. None of them received plasma therapy. In 26% of COVID-19 patients, DAT was positive, i.e., anti-RBC antibodies were detectable. The results of DAT can have an impact on blood grouping because membrane-bound autoantibodies may mask the RBC alloantibodies and this may cause a delay in the selection of matched blood units.[9]

Anti-heparin antibodies

Heparin is one of the most widely used drugs in the management of COVID-19. Many patients who have been treated with heparin are observed to have thrombocytopenia, which is more pronounced in severe forms. The authors postulated that this can be linked to the formation of anti-PF4-heparin complex antibodies and such antibodies may have a significant impact on the clinical course and this risk must be considered in the choice of the most suitable therapy.[10]

Anti-glycoprotein antibodies

In immune thrombocytopenic purpura (ITP), there is a production of autoantibodies against glycoproteins present on the platelet surface. A case report was published, a 65-year-old female patient with autoimmune hypothyroidism presented with signs of pneumonia and was diagnosed as COVID-19 positive and was hospitalized and symptomatic treatment was started. She had all normal laboratory parameters at the time of admission. Gradually the platelet count declined and was 8000/mm3 on day 7 accompanied by bleeding diathesis followed by a severe headache in the right frontal area, and a computed tomography (CT) scan of the brain demonstrated a subarachnoid microhemorrhage. Platelets were administered along with prednisolone, 100 mg. By day 10, the symptoms decreased, and on day 13, the platelet count had gradually increased above 1 lakh/mm3. This case suggests that the COVID-19 may have triggered the ITP as this is often associated with the history of autoimmune hypothyroidism.[11] Tsao et al. reported a similar case of association of ITP with COVID-19 in a pediatric patient.[12]

Anti-platelet antibodies

In COVID-19 there can be molecular mimicry between the antiplatelet antibodies produced and the antigens on the platelets resulting in platelet destruction by the reticuloendothelial cells.[13] Similar studies by Nardi et al. for HIV-1 infection and thrombocytopenia, in which they reported cross-reactivity between anti-platelet membrane antibodies and HIV-1 glycoprotein antigen.[14]

Antiphospholipid antibodies

Vascular thrombosis and stroke have been reported in COVID-19 patients along with raised activated partial thromboplastin time (aPTT) and antiphospholipid antibodies (aPL).[15] In individuals with primary antiphospholipid syndrome (APS), aPL causes vascular and obstetric complications.[16] Infection can precipitate the “catastrophic” APS which is marked by rapid multiorgan damage due to thrombus formation and features of microangiopathy on histopathology. The aPL antibodies which bind with beta2glycoprotein I (b2GPI) molecule domain demonstrate an increased risk of thrombosis while those antibodies which bind with domain 4/5, are considered to be “innocent.”[17]

The aPL detection is performed by immunoassays which detect the anticardiolipin (aCL) and anti-beta2glycoprotein I (anti-b2GPI) and lupus anticoagulant (LA).[18] In a recent study, 3 COVID-19 positive cases with severe thrombotic events had been associated with aCL/IgA isotype and anti-b2GPI/IgG and IgA isotype. The authors hypothesized that IgA immune response is stimulated by the SARS-CoV-2 and this can lead to mucosal damage.[19] In another similar study, LA was positive in 44.6% of COVID-19 patients, while IgG/IgM aCL and/or anti-b2GPI were positive only in 8.9%.[20] In a similar study, LA was studied in COVID-19 positive cases with prolonged aPTT. It was observed that > 90% of patients with prolonged aPTT, had positive LA.[21] Another study investigated the association between COVID-19 patients with ARDS and LA from acute medical care units. About 84.7% of patients had positive LA, with elevated D-dimers and thrombosis.[22]

Few studies conducted in the past revealed that aPL was detected in patients with certain microbial infections suggesting the possible existence of antigenic similarity between the peptide regions in the b2GPI molecule and membrane proteins of several microbes.[23]

Hence, aPL testing and detection can be considered in the management of critically ill COVID-19 patients with vascular involvement, as the detection of antibodies may be an indication for treatment with anticoagulants. In the case of positive aPL, retesting is warranted as a follow-up after at least 12 weeks, to note the persistence of aPL, which could suggest the postinfectious APS occurrence.

Kawasaki like disease

Kawasaki disease (KD), a self-limiting, systemic vasculitis that is usually seen in the pediatric age group for < 5 years, may be associated with coronary artery aneurism (CAA). In developed countries, it is contemplated as the top cause of acquired heart disease in children.[24] In about 5% of children with KD, severe disease with shock (Kawasaki Shock Syndrome [KSS]) can set in. The shock is due to inflammatory myocarditis which can cause leakage of capillaries and poor tissue perfusion.[25] The disease can be treated with intravenous immunoglobulins (IVIG) and this reduces the risk of CAA.[24]

A group of researchers from Northern Italy observed that since March 2020, there was an abnormal increase in the number of critically ill COVID-19 positive children with clinical characteristics consistent with KSS. The patients had classical signs and symptoms of KSS and were treated accordingly with IVIG and/or steroids. The authors decided to launch a national registry and nationwide alert for pediatricians. Similar reports were given from all over Europe, the UK, and the USA.[26],[27],[28]

The occurrence of KD cases with the classical clinical feature in children, during the peak of SARS-CoV2 infection, establishes a causative link and two hypotheses have been postulated.

  1. A microbial cause has been a possible cause of KD. The SARS-CoV-2 virus could have been a triggering factor the KD in these children
  2. The time gap between virus infection and KD points out that it can be an immune-mediated disease.

Most of bacterial infections cause shock due to the production of exotoxins that act as superantigens. The superantigens stimulate T cell proliferation and this can cause massive production of pro-inflammatory cytokines, like interleukin-1 (IL-1), IL-6, and IFN-γ (cytokine storm). This massive pro-inflammatory cytokine storm is also observed in KSS.[29]

Verdoni et al. in their study observed that majority of the infected children had SARS-CoV-2 IgG positive and IgM and polymerase chain reaction (PCR) negative. The authors have deduced the process by which this virus could cause a hyperinflammatory syndrome are: (i) molecular mimicry and the autoantibodies formation, (ii) deposition of immune complexes leading to vascular damage, (iii) the virus interacts with suboptimal IgG antibodies and binds to the Fc receptor expressed on certain immune cells and enters the cells and replication occurs by a phenomenon is known as antibody-dependent enhancement.[30]

Lindquist and Hicar in their study hypothesized that KD can be an immune-mediated disease and the IVIG which is used to treat the KD acts as an immunomodulator and decreases the activity of superantigens.[31]

Roe in their study stated that SARS-CoV-2 virus infection can cause the formation of immune complexes which can be removed in a few patients having complement dysfunction and therefore a type III hypersensitivity reaction occurs and results in the KD. This can result in the release of protease that damages the squamous epithelial basement membranes and causes inflammatory reactions in the entire body. This can be present even after the infection end if the attack of the protease continues on the basement membranes and this can lead to the development of autoantibodies secondarily and residual immune complexes.[32]

Guillain-Barre syndrome

Guillain-Barre syndrome (GBS) is an immune-mediated disorder characterized by ascending, symmetrical flaccid paralysis usually affecting the lower limbs. Certain Infections or vaccinations may trigger the disease. The peripheral nervous system gangliosides are attacked by the immune system.[33] Two case reports of GBS associated with COVID-19 infection have been reported from Italy and Iran.[34],[35] There is still ongoing research if COVID-19 induces autoantibodies against these specific gangliosides. The patients in both these case reports had neurological symptoms after 7–10 days of respiratory symptoms. The patients received IVIG and the prognosis was good.

Miller Fisher syndrome

Miller Fisher syndrome (MFS) is a rare variant of GBS and is observed in about 5% of cases. Like GBS it can be triggered by respiratory or intestinal infections or vaccinations. The patients with MFS are reported to have Anti-GQ1b and anti-GD1b antibodies in the cranial nerves 3,4 and 6. This can be a possible explanation for the association between anti-GQ1b antibodies and ophthalmoplegia. The patients are treated with IVIG as in GBS.

A case series from Spain reported that two COVID-19 positive patients presented with MFS and were positive for anti-GD1b-IgG antibodies and received treatment with IVIG.[36]

Optic neuritis and myelitis

Zhou et al. reported the first case of a case of severe optic neuritis and myelitis in the virus-infected young patient, and on testing, he was positive for both SARS-CoV-2 and myelin oligodendrocyte glycoprotein (MOG) IgG antibody.[37]

Central nervous system inflammatory vasculopathy

In a case report from the UK, a COVID-19 positive female patient with minor respiratory symptoms had incoordination of her right hand after 7 days. Magnetic resonance imaging brain with contrast at presentation showed hyperintensity in T2 and perivascular enhancement within the lesions was found. Cerebrospinal fluid (CSF) SARS-CoV-2 PCR was negative and this supports the ideology that the central nervous system (CNS) disease was not due to infection of the brain parenchyma.

Lymphocytic endothelitis with infarction is reported in patients with COVID-19. Secondary to endothelitis, the blood-brain barrier breakdown, and facilitates the entry of anti-MOG antibodies to initiate the disease process. The patient responded to intravenous methylprednisolone and plasma exchange and this reinforces the hypothesis of an immune-mediated process.[38]

Neurological symptoms

German researchers have published a study that postulates that autoantibodies may target the brain and these may be responsible for the neurological symptoms observed in few COVID-19 patients. In most patients who develop neurological symptoms, SARS-CoV-2 is not detected in the CSF. This suggests that other cellular or humoral mechanisms may be involved, including autoimmunity.

Christiana Franke et al. recently tested whether autoantibodies were present in eleven patients with severe COVID-19 and unexplained neurological symptoms. Between March and May 2020, the team assessed a large panel of antineuronal and anti-glial autoantibodies using serum and CSF samples from intensive care patients with symptoms including delirium, epileptic seizure, dystonia, and myoclonus. The team reports that no SARS-CoV-2 was detected in any of the CSF samples inflammation was indicated in most patients, and all had increased CSF levels of neurofilament light chain (NFL, a biomarker for axonal damage). The high levels of NFL in CSF may reflect damage to the tissue due to the replication of the virus or inflammation. All patients had anti-neuronal antibodies in their serum or autoantibodies in their CSF that target surface antigens known to be involved in CNS disease. Among these antigens were well-established proteins such as the N-methyl-D-aspartate (NMDA) receptor and myelin antigens. The researchers found that one patient with a high level of serum IgG autoantibodies against NMDA receptors required cardiopulmonary resuscitation. The raised IgG level may have reflected NMDA receptor encephalitis, which often causes arrhythmia and autonomic dysfunctions.[39]

Guilmot et al. observed that 4.3% of the total 349 COVID-19 patients admitted in their hospital between March and April 2020, had neurological manifestations. These patients had lymphocytic pleocytosis, anti-contactin-associated protein 2 (anti-Caspr2) antibody, and increased anti-GD1b antibodies in CSF. The patients had different clinical presentations, including delirium, cranial neuropathy, and brainstem encephalitis. PCR for SARS-CoV-2 in CSF was negative in all patients. This raises the question of SARS-CoV-2-induced immune-mediated response.[40]

Glomerular diseases

Few studies have reported the onset of acute kidney injury in more than 20% of patients infected by SARS-CoV-2. It is observed that patients with systemic autoimmune diseases have circulating autoantibodies which may cause glomerular disease and this is more exacerbated in COVID-19 due to increased production of autoantibodies.[41]

Type 1 diabetes mellitus

Type 1 diabetes mellitus (T1DM), an autoimmune disease that is characterized by an autoimmune process that destroys pancreatic beta cells and causes insulin deficiency (autoimmune insulitis) resulting in hyperglycemia.

Reports of the association of viral infections with T1DM pathogenesis are published. The viral epitopes sharing similarity with self-antigens can lead to the production of cross-reactive antibodies against beta cells.

TEDDY study in 2017 reported that 5.8% of patients in their 87327 study population developed autoantibodies against the beta cells of the pancreas after 9 months from the respiratory infection.[42] In 2018 During the H1N1 pandemic, a two-fold increase in T1DM was observed in 76,173 patients.[43] Hence, this viral infection in individuals genetically predisposed to autoimmunity can contribute to the faster development of T1DM through the release of cytokines and activation of T cells.[44]

Autoimmune rheumatic diseases

The drugs used for the treatment of COVID-19 include hydroxychloroquine (HCQ) (one of the disease-modifying antirheumatic drugs [DMARD]) and tocilizumab (monoclonal antibody). Initial studies during the pandemic postulated that patients with rheumatic diseases can have increased susceptibility to acquiring the COVID-19 or increased severity of the infection. In contrast, few studies reported the potential benefit of drugs that have been used in the therapy of rheumatic disease.[45],[46]

A study from France reported 19 SLE patients on HCQ long-term treatment, developed the COVID-19, and these patients did not show any signs of the exacerbation of the disease, except for one case of tenosynovitis.[47]

In a report from New York, the authors reviewed a group of 86 patients with autoimmune diseases. Among them, 2/3rd of the patients were receiving treatment with immunomodulatory drugs. It was observed that the hospitalized patients had more comorbidities and were receiving the conventional DMARDs and the outpatients were often using the biologics. The authors opined that the baseline use of biologics helped the patients from the worse COVID-19 outcomes.[48]

Similarly, a report by Monti et al. suggested that autoimmune disease patients treated with DMARDs did not have an increased risk of complications from COVID-19 in comparison with the normal population.[49]

A study from Italy suggests that continuing the autoimmune disease patients on the rheumatologic therapy and adherence to infection prevention and control measures can help the patients to prevent the worsening of the rheumatic disease and the risk of COVID-19 infection.[50]

Similarly, Conticini et al. from Italy reported that the use of DMARDs is not associated with worse COVID-19 outcomes.[51]

The clinical outcome may be slightly different in patients of systemic sclerosis, in which typical interstitial lung disease (ILD) can be similar to the CT features with COVID19 associated pneumonia. A COVID-19 positive patient with scleroderma associated with ILD and on treatment with tocilizumab had a good response.[52]

In a German hospital, the authors studied the similarities between COVID-19-associated ARDS and autoimmune ILD and postulated the probable role of autoimmunity in SARS-CoV-2 associated respiratory failure.[53] A similar observation was noted in China where the authors showed a prevalence of 20%–50% of autoimmune disease-related autoantibodies, suggesting the rationale for immunosuppression in COVID-19.[54]

Fujii et al. in their study reported about two COVID-19 patients with severe respiratory failure and with no history of autoimmune disease. The chest CT had multiple ground-glass opacities and they reduced with antiviral treatment; however, new patchy opacities appeared, which were similar to those of collagen vascular associated ILD. The patients' sera were tested for autoantibodies and it was found that anti-SSA/Ro antibody was in high titers. One patient recovered with antiviral therapy alone. The other patient required antiviral therapy and corticosteroid therapy (methylprednisolone). The authors hypothesized that both patients developed severe COVID-19 pneumonia due to an autoimmune response. They postulated that a high level of anti-SSA/Ro52 antibodies can be considered as a surrogate marker of pneumonia severity and poor prognosis in patients with COVID-19.[55]

A study from Greece reported that 29 COVID-19 positive patients with no history of any autoimmune disease were tested for autoantibodies. 68.7%were positive for any type of systemic autoantibody and this suggests infectious autoimmune activation.[56]

Anti IFN antibodies

Bastard et al. in their study noted that 3.5% of the study patients with severe COVID-19, had genetic mutations in interferons which are signaling proteins released in response to the viral infections and 10% of patients with severe disease had “auto-antibodies” to these interferons. This publication provides the very first explanation of severe COVID-19 infection only in a subset of the patients. They have also raised a valid point that COVID-19 severe cases have to be tested for the auto-antibodies with proper follow-up of patients with positive tests. They also observed that 94% of patients with these antibodies were men. This gender variability was linked to mutations on the X chromosome. Women may not have any effect from such mutations as they have two X chromosomes. In men, as only one X chromosome is present, even small genetic errors can be problematic.[57],[58]

Vaccination and autoantibodies?

The Pfizer and BioNTech COVID-19 vaccine candidate's first interim analysis of the phase III trial reveal that the vaccine may be > 90% effective in preventing the disease in uninfected participants. As it is an m RNA vaccine, large-scale production of the vaccine is possible.[59] Stuart M White, an anesthetist in response to this publication has responded that careful analysis of the host-pathogen interactions should be done as there are increasing reports of autoimmune interactions between the virus and host peptides, to minimize the risks both of acute autoimmune reactions to inoculation and future chronic autoimmune pathology.

  Conclusion Top

COVID-19 is now emerging as a multisystem disease. Appropriate management of patients is mandatory to prevent future complications. Based on the extensive research done to draft this manuscript we want to emphasize a few suggestions for the clinicians involved in patient care.

  1. Autoantibody screening in COVID-19 patients may be easily performed by the techniques available in the laboratory and can serve as an alert for complications such as thrombotic or neurologic events[60]
  2. Before any vaccine formulation for COVID-19, the phenomenon of “molecular mimicry” between SARS-CoV-2 and the human tissue antigens should be carefully studied. Due to antigenic similarity, the vaccine may induce immune-mediated destruction of the host cells. The proteins specific to the virus can represent the basis for safe vaccination[61]
  3. The possible autoimmune mechanism in COVID-19 requires further investigation, in a larger population in lieu of ongoing convalescence plasma therapeutic trials and the start of vaccination.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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