ABSTRACT
PURPOSE: To report two cases; bilateral arteritic anterior ischemic optic neuropathy (AAION) and bilateral acute zonal occult outer retinopathy (AZOOR) after COVID-19 mRNA vaccination. CASE REPORT: The first patient was a 79-year-old female was presented to us 35 days after a sudden bilateral loss of vision, which occurred two days after receiving the second recombinant mRNA vaccine (Pfizer) injection. Temporal artery biopsy was compatible with AAION. At presentation, the best-corrected visual acuity was 20/1250 and 20/40 in the right and left eyes on the Snellen acuity chart, respectively. There was 3+ afferent pupillary defect in the right eye. The anterior segment and posterior segment exams were normal except for pallor of the optic nerve head in both eyes. Intraocular pressure was normal in both eyes. She was diagnosed with bilateral AAION and Subcutaneous tocilizumab 162 mg weekly was recommended with monitoring her ESR, CRP, and IL-6.The second patient was a 33-year-old healthy female who was referred to us for a progressive nasal field defect in her left eye, and for flashes in both eyes. Her symptoms started 10 days after receiving the second recombinant mRNA vaccine (Moderna) injection. Complete bloodwork performed by a uveitis specialist demonstrated high ESR (25) and CRP (19) levels. As a result, she was diagnosed with unilateral AZOOR in her left eye and was subsequently treated with an intravitreal dexamethasone implant in the same eye. At presentation, vision was20/20 in both eyes. The anterior segment and posterior segment exams were completely normal except for the presence of abnormal white reflex in the temporal macula of her left eye. We diagnosed her with bilateral AZOOR. Since she was nursing, intravitreal dexamethasone implant was recommended for the right eye. CONCLUSION: There may be a correlation between ocular inflammatory diseases with autoimmune mechanism and the mRNA COVID-19 vaccination.
ABSTRACT
There is very little knowledge about the immune responses, particularly cellular immunity to coronavirus disease 2019 (COVID-19). The main objective of this study was to evaluate the frequency of T helper (Th) cell subtypes, including Th1, Th17, and Treg cells, in moderate-to-severe and critical COVID-19 patients compared to healthy controls. Twenty-nine moderate-to-severe and 13 critical patients confirmed for COVID-19, and 15 healthy subjects were included in this study. Interferon-γ (IFN-γ)-producing Th1 and interleukin-17A-producing Th17 and Treg cells in peripheral blood were measured with flow cytometry. The frequency of Th1 and Th17 was significantly decreased in critical patients compared to healthy subjects (aMD: -2.76 and - 2.34) and moderate-to-severe patients (aMD: -1.89 and - 1.89), respectively (p < 0.05). Differences were not significant between moderate-to-severe patients and healthy subjects for both Th1 (p = 0.358) and Th17 (p = 0.535), respectively. In contrast, significant difference was not observed between study subjects regarding the frequency of Treg cells. Patients with critical COVID-19 had a markedly lower Th1/Treg and Th17/Treg ratios compared with the controls and moderate-to-severe cases. Our study showed a dysregulated balance of Th1 and Th17 cells and its relation to the severity of COVID-19.
Subject(s)
COVID-19/immunology , SARS-CoV-2/immunology , T-Lymphocytes, Regulatory/immunology , Th1 Cells/immunology , Th17 Cells/immunology , Adolescent , Adult , Aged , Aged, 80 and over , CD4 Lymphocyte Count , COVID-19/pathology , Critical Illness , Female , Flow Cytometry , Humans , Interferon-gamma/biosynthesis , Interleukin-17/biosynthesis , Male , Middle Aged , Severity of Illness Index , Young AdultABSTRACT
Today, Coronavirus Disease 2019 (COVID-19) is a global public health emergency and vaccination measures to counter its diffusion are deemed necessary. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiological agent of the disease, unleashes a T-helper 2 immune response in those patients requiring intensive care. Here, we illustrate the immunological mechanism to train the immune system towards a more effective and less symptomatic T-helper 1 immune response, to be exploited against SARS-CoV-2.