Molecular Mimicry as a Mechanism of Viral Immune Evasion and Autoimmunity.

Mimicry of host protein structures ("molecular mimicry") is a common mechanism employed by viruses to evade the host's immune system. To date, studies have primarily evaluated molecular mimicry in the context of full protein structural mimics. However, recent work has demonstrated that short linear amino acid (AA) molecular mimics can elicit cross-reactive antibodies and T-cells from the host, which may contribute to development and progression of autoimmunity. Despite this, the prevalence of molecular mimics throughout the human virome has not been fully explored. In this study, we evaluate 134 human infecting viruses and find significant usage of linear mimicry across the virome, particularly those in the herpesviridae and poxviridae families. Furthermore, we identify that proteins involved in cellular replication and inflammation, those expressed from autosomes, the X chromosome, and in thymic cells are over-enriched in viral mimicry. Finally, we demonstrate that short linear mimicry from Epstein-Barr virus (EBV) is significantly higher in auto-antibodies found in multiple sclerosis patients to a greater degree than previously appreciated. Our results demonstrate that human-infecting viruses frequently leverage mimicry in the course of their infection, point to substantial evolutionary pressure for mimicry, and highlight mimicry's important role in human autoimmunity. Clinically, our findings could translate to development of novel therapeutic strategies that target viral infections linked to autoimmunity, with the goal of eliminating disease-associated latent viruses and preventing their reactivation.

Immunologic and Autoimmune-Related Sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 Infection: Clinical Symptoms and Mechanisms of Disease.

The COVID-19 pandemic has resulted in a significant number of people developing long-term health effects of postacute sequelae SARS-CoV-2 infection (PASC). Both acute COVID-19 and PASC are now recognized as multiorgan diseases with multiple symptoms and disease causes. The development of immune dysregulation during acute COVID-19 and PASC is of high epidemiologic concern. Both conditions may also be influenced by comorbid conditions such as pulmonary dysfunction, cardiovascular disease, neuropsychiatric conditions, prior autoimmune conditions and cancer. This review discusses the clinical symptoms, pathophysiology, and risk factors that affect both acute COVID-19 and PASC.

Acute and post-acute sequelae of SARS-CoV-2 infection: a review of risk factors and social determinants.

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.

Mobile health apps for systemic lupus erythematosus and lupus nephritis: a critical appraisal.

OBJECTIVES: To critically assess the quality and functionality of the available mobile apps for systemic lupus erythematosus and lupus nephritis patients. METHODS: Two reviewers independently searched the App Store and Google Play Store for eligible mobile health (mHealth) apps. Two separate searches were done: one for systemic lupus erythematosus (SLE) and the other for lupus nephritis (LN). The Mobile App Rating Scale (MARS) was used to rate the quality of all selected apps. RESULTS: From the systemic lupus erythematosus screening, our search yielded 841 apps. Within these 841 apps, 17 of them were ultimately included. From the lupus nephritis screening, our search returned 1152 apps. Of the 1152 apps, 2 were ultimately included. Our search strategy included apps specifically designed for patients with SLE and LN. The MARS average of all the systemic lupus erythematosus apps was 2.7 out of 5. The MARS average of the two lupus nephritis apps was 2.6 out of 5. CONCLUSION: Mobile health apps can serve as an effective tool for telehealth, engaging patients in self-care and for increasing the quality of life of lupus patients. While several mobile health technologies exist for patients with SLE and LN, there is still a significant need for app quality improvement and expanding the comprehensiveness of offered functions.