HCoV-NL63 and SARS-CoV-2 Share Recognized Epitopes by the Humoral Response in Sera of People Collected Pre- and during CoV-2 Pandemic.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause serious illness in older adults and people with chronic underlying medical conditions; however, children and young people are often asymptomatic or with mild symptoms. We evaluated the presence of specific antibodies (Abs) response against Human coronavirus NL63 (HCoV-NL63) S protein epitopes (NL63-RBM1, NL63-RBM2_1, NL63-RBM2_2, NL63-RBM3, NL63-SPIKE, and NL63-DISC-like) and SARS-CoV-2 epitopes (COV2-SPIKE and COV2-SPIKE) in plasma samples of pre-pandemic, mid-pandemic, and COVID-19 cohorts by indirect ELISA. Moreover, a competitive assay was performed to check for cross reactivity response between COV2-SPIKE and NL63-RBM3 among patients with a definitive diagnosis of SARS-CoV-2.

PtpA and PknG Proteins Secreted by subsp. are Recognized by Sera from Patients with Rheumatoid Arthritis: A Case-Control Study.

Purpose: Rheumatoid arthritis (RA) can result from complex interactions between the affected person's genetic background and environment. Viral and bacterial infections may play a pathogenetic role in RA through different mechanisms of action. We aimed to evaluate the presence of antibodies (Abs) directed against two proteins of subsp.

Association between Lipoprotein Levels and Humoral Reactivity to subsp. in Multiple Sclerosis, Type 1 Diabetes Mellitus and Rheumatoid Arthritis.

Environmental factors such as bacterial infections may play an important role in the development of autoimmune diseases. subsp. (MAP) is an obligate pathogen of ruminants able to use the host's cholesterol for survival into macrophages and has been associated with multiple sclerosis (MS), type 1 diabetes (T1DM) and rheumatoid arthritis (RA) through a molecular mimicry mechanism.

Rheumatoid arthritis patient antibodies highly recognize IL-2 in the immune response pathway involving IRF5 and EBV antigens.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by a progressive joint damage due to largely unknown environmental factors acting in concert with risk alleles conferring genetic susceptibility. A major role has been attributed to viral infections that include past contacts with Epstein-Barr virus (EBV) and, more recently, to non-protein coding sequences of human endogenous retrovirus K (HERV-K) integrated in the human genome. Molecular mimicry between viral and self proteins is supposed to cause the loss of immune tolerance in predisposed hosts.

Screening for the beta-39 mutation in thalassemia by capillary electrophoresis in free solution in strongly acidic, isoelectric buffers.

A novel method is reported for screening for point mutations in genomic DNA: free-zone capillary electrophoresis in very acidic buffers. This method exploits the charge difference among the four different bases (C, T, A, G) in a pH window between 2.5 and 3.