Evidence of the presence of antinuclear antibodies (ANA) in healthcare workers after mRNA based anti-SARS CoV-2 vaccines

Introduction: Evidence from clinical trials strongly supports the safety and efficacy of the different COVID-19 vaccines. Indeed, the risk to develop a severe form of the disease, possibly leading to death, it is highly decreased in fully vaccinated individuals. Nowadays, vaccines effects and their possible ability to stimulate an autoimmune reaction are still poorly understood. The aim of this study was to check the development and /or persistence of antinuclear antibodies (ANA) in healthcare workers (HCPs) after mRNA based anti-SARS CoV-2 vaccines. Method(s): In this study, 77 HCPs were considered (60 females and 17 males, age range 26-67 years, median age 48) without any history of COVID-19 infection. All the subjects were vaccinated with 2 doses of BioNtech/Pfizer BNT162b2 mRNA. Furthermore, half of them received a third dose of the same vaccine, whereas the other half of Moderna (Spikevax). Blood Samples were collected before the inoculation of the vaccine (T0), at 3 (T1) and 12 months (T2) after the first dose. Therefore, at T1 all the subjects received two doses of vaccine and at T2 three doses. ANA presence was evaluated using indirect immunofluorescence on Hep-2 cells (EUROIMMUN test kit) at dilutions: 1:80, 1:160, 1:320, 1:640. Fisher and Wilcoxon statistical tests were performed using GraphPad Prism 9 Software. Result(s): Among 77 subjects enrolled, at T0 25 were positive for ANA (23 maintained this positivity also at T1 and T2) and 52 were negative. At T1, 46/52 remained negative, whereas 6/52 became ANA positive (5 maintained this positivity also at T2). At T2, 30/46 were still negative, instead 16/46 became ANA positive. In addition, from T1 to T2, it has been observed a statistically significant increase of ANA presence. Conclusion(s): Our results suggest that mRNA based anti-SARS CoV-2 vaccines seem to induce the onset of de novo ANA in 22/77 (28,57%) of subjects and that the percentage of positivity seems to directly correlate to the number of vaccine expositions: 6/77 (7,79%) after 2 doses;and 16/77 (20,78%) after 3 doses.

Evidence of autoantibodies in hospitalized COVID-19 patients

Recent studies highlight the evidence of autoantibodies in patients affected by Corona Virus Disease-2019 (COVID-19). We evaluated whether severe acute respiratory syndrome (SARS-CoV-2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria hospital between March and April 2020 with a confirmed COVID-19 diagnosis by real-time polymerase chain reaction (RT-PCR) and no previously clinical record of autoimmune disease. 40 blood donors were analyzed for the same markers and considered as healthy controls. All hospitalized patients had high levels of common inflammatory markers, such as C Reactive Protein, Lactate Dehydrogenase, ferritin and creatinine. Interleukin-6 concentrations were also increased, supporting the major role of this interleukin during COVID-19 infection. Lymphocytes number was generally lower compared to healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of ANA (57,5%), ANCA (25%), and ASCA IgA (25%) antibodies in COVID-19 patients compared to healthy controls. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID-19 virus might break the body tolerance to itself and stimulate autoimmune responses, suggesting they were directly related to viral infection, instead of being a preexisting condition. The observed increase of autoantibodies remained stable in six-month follow-up of COVID-19 patients. Moreover, preliminary data indicate in a few patients the apparence of clinical manifestations suggestive of autoimmune disease onset. More study will be needed to find out whether these autoimmune profiles persist in COVID-19 affected patients.

Case report of COVID-19 in an elderly patient: could SARS-CoV2 trigger myositis?

Though the exact etiology of autoimmune diseases still remains not completely known, there are various factors which are known to contribute to be trigger of autoimmune diseases. Viral infection is known to be among the other. It is known as the infection from severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) can be an autoimmune trigger, so, we suppose that SARS-Coronavirus (SARS-CoV-2) could be as well. Several authors have highlighted the temporal consequence between SARS-CoV-2 and autoimmune diseases. In this case report we described a patient admitted for COVID-19 pneumonia with completely negative autoimmunity at admission who developed major pulmonary interstitial disease. During the hospitalization the weaning difficulties from oxygen led us to the repetition of autoimmunity pattern which became positive (both during hospitalization then after two months from dismission) with marked positivity for specific antibodies for myositis even after the patient's infectious healing. In the follow-up, the patient continued to have asthenia and muscle weakness despite steroid therapy. She is still in follow-up and will be further evaluated over time. Can we therefore think that in this case the development of autoimmunity can persist beyond the infectious phase and determine over time the development of a real autoimmune myositis?

Isolated immune thrombocytopenic purpura in a young adult Covid-19 patient.

OBJECTIVE: Patients with Covid-19 can have different symptoms, ranging from asymptomatic patients to various grades of respiratory failure, caused by typical interstitial pneumonia, cardiac involvement or neurological symptoms. PATIENTS AND METHODS: In April 2020, we focused our attention on a young woman with diffused purpura on her lower extremities, with no respiratory, cardiac or neurological symptoms. A complete blood analysis showed us a severe thrombocytopenia. We excluded other possible causes of thrombocytopenic purpura such as hematological (lymphocyte subsets), hepatological disease or splenomegaly. On autoimmune screening, we found Isolated immune thrombocytopenic purpura in a young adult Covid-19 patient positivity of anti-nuclear antibody (ANA) with a centrosome pattern and extractable nuclear antigens (ENA) and connective tissue disease screen resulted positive but none of the included specific antigens results positive, probably due to an aspecific antibody reaction. The wide variability of COVID disease presentation may be due to a personal different immune response to the virus. CONCLUSIONS: The immune response against the virus is crucial in the evolution and understanding of COVID-19 disease but it has still to be fully understood.

The first case of systemic lupus erythematosus (SLE) triggered by COVID-19 infection.

Coronavirus disease 2019 (COVID-19) is a respiratory tract infection caused by a newly emergent coronavirus, SARS-CoV-2. The acute phase may be followed by a second phase actually not yet completely understood but probably associated to an autoimmune activation. At the moment is not possible to clearly define an association between immunological findings and pathological symptoms, however, this case report describes the case of a patient who following COVID-19 infection development autoimmune antibodies who persist in time longer than viral phase. Those antibodies can be responsible for the multi pathological clinical picture showed from our patient that, according to EULAR 2019 criteria, could be classified as systemic lupus erythematosus (SLE). SLE is probably one of the possible chronic rheumatologic diseases triggers by COVID-19 and this is the first case of SLE with vasculitis actually described in literature.