Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus behind the coronavirus disease 2019 (COVID-19) pandemic, is a type of RNA virus that is nonsegmented. Cardiovascular diseases (CVDs) increase the mortality risk of patients. In this review article, we overview the existing evidence regarding the potential mechanisms of myocardial damage in coronavirus disease 2019 (COVID-19) patients. Having a comprehensive knowledge of the cardiovascular damage caused by SARS-CoV-2 and its underlying mechanisms is essential for providing prompt and efficient treatment, ultimately leading to a reduction in mortality rates. Severe COVID-19 causes acute respiratory distress syndrome and shock in patients. In addition, awareness regarding COVID-19 cardiovascular manifestations has increased, including the adverse impact on prognosis with cardiovascular involvement. Angiotensin-converting enzyme 2 receptor may play a role in acute myocardial injury caused by SARS-CoV-2 infection. COVID-19 patients experiencing heart failure may have their condition exacerbated by various contributing factors and mechanisms. Increased oxygen demand, myocarditis, stress cardiomyopathy, elevated pulmonary pressures, and venous thrombosis are potential health issues. The combination of these factors may lead to COVID-19-related cardiogenic shock, resulting in acute systolic heart failure. Extracorporeal membrane oxygenation (ECMO) and left ventricular assist devices (LVADs) are treatment options when inotropic support fails for effective circulatory support. To ensure effective COVID-19-related cardiovascular disease (CVD) surveillance, it is crucial to closely monitor the future host adaptation, viral evolution, and transmissibility of SARS-CoV-2, given the virus's pandemic potential.

To date, over 250 million people have been reportedly infected by COVID‐19 disease, which has spread across the globe and led to approximately 5.1 million fatalities. To prevent both COVID‐19 and viral transmission, DNA‐based/RNA‐based vaccines, non‐replicating viral vector vaccines, and inactivated vaccines have been recently developed. However, a precise clinical and histological characterization of SARS‐CoV‐2 vaccine‐related dermatological manifestations is still lacking. A systematic review of 229 articles was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines, in order to provide an extensive overview of SARS‐CoV‐2 vaccine‐related skin manifestations. Data on demographics, number of reported cases with cutaneous involvement, vaccine, and rash type (morphology) were extracted from articles and summarized. A total of 5941 SARS‐CoV‐2 vaccine‐related dermatological manifestations were gathered. Local injection‐site reactions were the most frequently observed, followed by rash/unspecified cutaneous eruption, urticarial rashes, angioedema, herpes zoster, morbilliform/maculopapular/erythematous macular eruption, pityriasis rosea and pityriasis rosea‐like eruptions, and other less common dermatological manifestations. Flares of pre‐existing dermatological conditions were also reported. Cutaneous adverse reactions following SARS‐CoV‐2 vaccine administration seem to be heterogeneous, rather infrequent, and not life‐threatening. Vaccinated patients should be monitored for skin manifestations, and dermatological evaluation should be offered, when needed.

Immunization with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines has greatly reduced coronavirus disease 2019 (COVID-19)-related deaths and hospitalizations, but waning immunity and the emergence of variants capable of immune escape indicate the need for novel SARS-CoV-2 vaccines. An intranasal parainfluenza virus 5 (PIV5)-vectored COVID-19 vaccine CVXGA1 has been proven efficacious in animal models and blocks contact transmission of SARS-CoV-2 in ferrets. CVXGA1 vaccine is currently in human clinical trials in the United States. This work investigates the immunogenicity and efficacy of CVXGA1 and other PIV5-vectored vaccines expressing additional antigen SARS-CoV-2 nucleoprotein (N) or SARS-CoV-2 variant spike (S) proteins of beta, delta, gamma, and omicron variants against homologous and heterologous challenges in hamsters. A single intranasal dose of CVXGA1 induces neutralizing antibodies against SARS-CoV-2 WA1 (ancestral), delta variant, and omicron variant and protects against both homologous and heterologous virus challenges. Compared to mRNA COVID-19 vaccine, neutralizing antibody titers induced by CVXGA1 were well-maintained over time. When administered as a boost following two doses of a mRNA COVID-19 vaccine, PIV5-vectored vaccines expressing the S protein from WA1 (CVXGA1), delta, or omicron variants generate higher levels of cross-reactive neutralizing antibodies compared to three doses of a mRNA vaccine. In addition to the S protein, the N protein provides added protection as assessed by the highest body weight gain post-challenge infection. Our data indicates that PIV5-vectored COVID-19 vaccines, such as CVXGA1, can serve as booster vaccines against emerging variants.

Although there is a great demand for increased coronavirus disease 2019 (COVID-19) vaccination worldwide, rare side effects of the vaccine in susceptible individuals are attracting attention. We recently treated a patient with type 1 diabetes who had HLA-A*240201/A*020101, B*5401/B*5601, DRB1*0405/DRB1*0405, DPB1*0501/DPB1*0501 and DQB1*0401/DQB1*040 and developed Graves' disease soon after the administration of a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine. While causal relationships between vaccinations and adverse events are difficult to discern due to both confounding and masking factors, our findings suggest that attention to possible adjuvant-related endocrinological diseases in certain individuals receiving SARS-CoV-2 vaccines is appropriate.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic is a public health emergency of global concern. Besides the profound severe pulmonary damage, SARS-CoV-2 infection also causes a series of cardiovascular abnormalities, including myocardial injury, myocarditis and pericarditis, arrhythmia and cardiac arrest, cardiomyopathy, heart failure, cardiogenic shock, and coagulation abnormalities. COVID-19 patients with preexisting cardiovascular diseases are often at a much higher risk of increased morbidity and mortality. Number of mechanisms have been postulated for SARS CoV-2-associated cardiovascular damage including direct myocardial injury, systemic inflammation, hypoxemia, coronary thrombosis and drug-induced cardiac damage. Special attention should be given towards patients of SARS CoV-2 with concurrent cardiovascular diseases. Knowledge of the injury caused by SARS CoV-2 to the cardiovascular system and the mechanisms behind it is of the utmost importance to reduce the morbidity and mortality of these patients by treating them in time.

The current coronavirus disease 2019 (COVID-19) pandemic has urged the scientific community internationally to find answers in terms of therapeutics and vaccines to control SARS-CoV-2. SARS-CoV-2 is the 7th member of the human coronavirus (CoV) family to be implicated in this zoonotic outbreak. With the global popularity of immunization against COVID-19, reports of vaccine-related adverse events are rapidly growing. Local pain at the injection site is the most prevalent occurrence, as are unusual symptoms such as fever, headache, myalgia, and overall discomfort. Those with COVID-19 and pre-existing cardiovascular disorders (CVDs) are at an increased likelihood of severe morbidity and fatality, and the condition has been related to a number of both direct and indirect CVDs outcomes. As a result of acute coronary syndrome, COVID-19 produces CVDs such as arrhythmias, cardiac arrest, cardiogenic shock, myocarditis, stress-cardiomyopathy, and acute myocardial damage (AMD). Because of underlying chronic comorbidities or impaired immune systems, older persons and adolescents should be particularly cautious about vaccine-related CVDs.

Abstract Background Coronavirus disease 2019 (COVID-19) is a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that resulted in a pandemic in 2019, causing systemic complications including endocrine system diseases. Subacute thyroiditis (SAT) of COVID-19 infection is believed to be due to direct virus entry into cells and cell destruction, cellular dysfunction due to inflammation and immune/antibody-mediated hormonal dysfunction. Here we present a case of SAT after the SARS-CoV-2 vaccine (Pfizer-BioNTech). Clinical Case A 39-year-old male healthcare worker presented with four weeks history of symptoms: fullness of the anterior neck, odynophagia, enlarged cervical lymph nodes, palpitations, anxiety and weight loss. Onset of symptoms was two days the second dose of Pfizer-BioNTech vaccine. There was no recent history of upper respiratory system infection or COVID-19 infection. Vital signs and physical exam findings were unavailable, as it was a telephone encounter. Initial workup was significant for a TSH of 0. 020 uIU/mL (n 0.45-5.330 uIU/mL), free T4 of 2.42 ng/mL (n 0.45-1.80 ng/mL) and total T3 225.4 pg/mL (n 87-179 pg/mL). There was no evidence of leukocytosis. Ultrasound of the thyroid gland was unremarkable for nodules or hyperemia. Autoimmune thyroid disease was ruled out with negative levels of thyroid stimulating immunoglobulin, thyroid receptor antibody and anti-microsomal antibody. Thyroid scintigraphy was significant for abnormally low uptake, consistent with SAT. Clinical and biochemical improvements (TSH 4.193 uIU/mL; free T4 0.98 ng/dL) were seen after 5 months. Conclusion Subacute thyroiditis (SAT) is an acute inflammatory disorder of the thyroid usually related to a viral infection. It was described in total of 27 patients of COVID-19 infection (3) . There are only a handful of cases related to COVID-19 vaccine and most of them are due to the inactivated vaccine (1,2) . To our knowledge, there are only three documented cases of subacute thyroiditis after receiving the Pfizer mRNA vaccine (1) . The pathophysiology in generating an autoimmune response is believed to be due to molecular mimicry and cross recognition between the coronavirus spike protein targeted with the mRNA vaccine and healthy thyroid cell antigens (1,2) . Clinicians should be alert and consider the possibility of SARS-CoV-2 vaccine as an etiology when evaluating patients for subacute thyroiditis.

Coronavirus Disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), a newly emerged coronavirus, and has been pandemic since March 2020 and led to many fatalities. Vaccines represent the most efficient means to control and stop the pandemic of COVID-19. However, currently there is no effective COVID-19 vaccine approved to use worldwide except for two human adenovirus vector vaccines, three inactivated vaccines, and one peptide vaccine for early or limited use in China and Russia. Safe and effective vaccines against COVID-19 are in urgent need. Researchers around the world are developing 213 COVID-19 candidate vaccines, among which 44 are in human trials. In this review, we summarize and analyze vaccine progress against SARS-CoV, Middle-East respiratory syndrome Coronavirus (MERS-CoV), and SARS-CoV-2, including inactivated vaccines, live attenuated vaccines, subunit vaccines, virus like particles, nucleic acid vaccines, and viral vector vaccines. As SARS-CoV-2, SARS-CoV, and MERS-CoV share the common genus, Betacoronavirus, this review of the major research progress will provide a reference and new insights into the COVID-19 vaccine design and development.

Vaccination strongly reduces the risk of hospitalization and death due to coronavirus disease 2019 (COVID-19). However, the severity of the acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and the degree of protection exerted over time by vaccination remains to be fully elucidated among hospitalized comorbid and vulnerable patients with SARS-CoV-2 infection. We report a case series of nine hospitalized vulnerable patients who developed a SARS-CoV-2 infection during a cardiac rehabilitation inpatient program. Age ranged from 50 to 81years. All but one patient had received at least three doses of anti-COVID-19 vaccine more than 4months before the cardiac event. Indications for cardiac rehabilitation included acute coronary syndromes, congestive heart failure, heart valve surgery, and coronary artery bypass graft. After the confirmed diagnosis of SARS-CoV-2 infection, all patients developed symptoms. Eight patients developed at least one SARS-CoV-2-related complication, including a significant increase in high-sensitivity troponin I levels, new-onset hypoxemia, persistent atrial fibrillation, non-sustained ventricular tachycardia and recurrent sinus arrest, pericardial effusion, and a persistent increase in blood pressure. Almost all patients developed complications which, however, did not evolve towards more severe expressions of the disease. These data suggest that even in this new phase of the pandemic, vaccination may exert a potential role to reduce the risk of progression towards more severe disease of SARS-CoV-2 infection in vulnerable patients with cardiovascular comorbidities.

Vaccines have been considered the most promising solution for ending the coronavirus disease 2019 (COVID-19) pandemic. Information regarding neutralizing antibodies (NAbs) and T-cell immune response in inactivated SARS-CoV-2 vaccine-immunized COVID-19 convalescent patients were either only available for a short time after illness recovered or not available at all (T-cell immunity). We evaluated SARS-CoV-2 NAbs and cellular immune responses to the SARS-CoV-2 inactivated vaccine in convalescent patients who recovered from infection for about one and a half years. We found that compared to before vaccination, SARS-CoV-2 NAbs and specific T-cell responses were significantly boosted by the inactivated vaccine in convalescent patients, which confirmed the pre-existing adaptive immunity in SARS-CoV-2 infected people. We observed that NAbs and IFN-γ-secreting T-cell response elicited by a single vaccine dose in subjects with prior COVID-19 infection were higher than after two doses of vaccine in SARS-CoV-2 naïve subjects. Both humoral and cellular immune responses elicited by one and two doses of inactivated vaccine were comparable in COVID-19-recovered persons. In conclusion, inactivated COVID-19 vaccine induced robust NAbs and T-cell responses to SARS-CoV-2 in COVID-19 convalescent patients and immune responses after one dose were equal to that after receiving two doses, which highlighted that robust humoral and cellular immune response can be reactivated by the inactivated vaccine in SARS-CoV-2 convalescent patients.