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Manufacturing of seasonal and pandemic influenza vaccines–A case study
Published in Amine Kamen, Laura Cervera, Bioprocessing of Viral Vaccines, 2023
Cristina A. T. Silva, Shantoshini Dash, Amine Kamen
The influenza viral envelope is composed of a host-derived lipid bilayer that presents three different transmembrane proteins, HA (hemagglutinin), NA (neuraminidase), and M2 (matrix 2). HA, a glycosylated integral membrane protein, is the most abundant on the virus surface (around 80%), being responsible for the initial attachment of the virus to host cell receptors (bearing a terminal sialic acid) and later merging of viral envelope and host cell membrane. NA, which represents approximately 17% of viral surface proteins, cleaves the sialic acid residues in host cell receptors to release new virions, allowing for the spread of the virus [4,7]. Protective immunity against influenza viruses is mediated mainly by neutralizing antibodies against these two surface proteins, which prevents the infection and spread of the virus in host cells [11]. M2, present in minor quantities on the membrane, is an ion channel that has an important role in early phases of the infection. Inside the virus, each RNA segment is wrapped around nucleoprotein (NP) monomers, forming viral ribonucleoprotein (RNP) complexes alongside with the viral polymerases PB1, PB2 and PA. Attached to the inside of the membrane, M1 (matrix) protein interacts with RNP complexes [8].
Autoantibodies and cancer among asbestos-exposed cohorts in Western Australia
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Renee N Carey, Jean C Pfau, Marvin J Fritzler, Jenette Creaney, Nicholas de Klerk, Arthur W (Bill) Musk, Peter Franklin, Nita Sodhi-Berry, Fraser Brims, Alison Reid
Immunoassays were performed by the Mitogen Diagnostics Laboratory (Calgary, Alberta, Canada). The levels of antibodies against 13 nuclear antigens were evaluated: dsDNA, Sm, histone (H2A, H2B, H3, H4), Jo-1 (histidyl tRNA synthetase), ribonucleoprotein (RNP), ribosomal P protein, proliferating cell nuclear antigen (PCNA), SSA/Ro60, SSB/La, Ro52/TRIM21, PM-Scl, Scl-70 (topoisomerase 1), centromere B (CENP-B). This multiplexed extractable nuclear antibody (ENA) profile utilized an addressable laser bead immunoassay (ALBIA) provided by TheraDiag (FIDIS: Paris, France). Cutoffs were established using internal calibrators provided by the manufacturers and control sera included with each assay run. Results were expressed as chemiluminescence intensity units (CIU) for ALBIA.
Analysis of autoantibody profiles in two asbestiform fiber exposure cohorts
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Jean C. Pfau, Christopher Barbour, Brad Black, Kinta M. Serve, Marvin J. Fritzler
Predictive modeling demonstrated that antibodies to histone were most predictive for exposure to LAA, with high values of anti-histone predicting the LAA cohort with a high probability. Notably, Sm-RNP and PM-Scl antibodies were also predictive for the LAA cohort. Anti-histone antibodies are common in SLE, and are often associated with a syndrome called “drug-induced lupus” (DIL) which occurs in patients taking certain medications, such as procainamide or hydralazine, but which disappears after discontinuing the drug (Patel and Richardson 2013; Rubin 2015)). Interestingly, the epitopes targeted by anti-histone antibodies in DIL tend to vary from those targeted in SLE (Portanova et al. 1987), possibly due to different types of post-translational modifications, such as acetylation, that create antigenic sites. In contrast, idiopathic SLE, histone-positive patients usually express multiple autoantibodies such as dsDNA, SSA/Ro60, Ro52, Ribosome, and Sm/RNP. It is important to point out that with the more recent use of biological therapeutics, the clinical and serological spectrum of drug-induced lupus has changed, where anti-dsDNA tends to be a dominant feature (Olsen 2004). In both of the cohorts in the present study, unlike DIL where anti-histone antibodies tend to occur in isolation, the anti-histone positive patients in our study tended to express multiple autoantibodies (including PCNA, Ro52, PM/Scl and Ribosome), and none were taking drugs associated with DIL, making DIL less likely. It would be interesting to determine the specific epitopes of these patients’ anti-histone antibodies to determine whether B cell specificity varies between the two cohorts, which suggest different triggers and pathways leading to the anti-histone response.
Case series: rheumatological manifestations attributed to exposure to Libby Asbestiform Amphiboles
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Roger Diegel, Brad Black, Jean C. Pfau, Tracy McNew, Curtis Noonan, Raja Flores
The patient was first seen at CARD in 2002 and then again in late-2009 when he reported breathing trouble over the last year or two when singing, and occasional sharp pains on the side of his chest. He was diagnosed with bilateral pleural thickening and sub-pleural interstitial changes. He was most recently seen at CARD in early-2014 and reported feeling somewhat better due to weight loss but continues with respiratory symptoms including chronic cough. His pulmonary function remained stable from 2002 to 2014. His most recent PFT in 2017 showed FVC 88%, FEV1 92%, and DLCO 117%. The patient was diagnosed with CREST variant of systemic sclerosis. The symptoms began with arthralgias in 1991 and 1992. The arthralgias continued and the patient saw a rheumatologist. A work up included X-rays of his hands, which were normal, no erosive disease. ANA test of 1:640 with negative SSA, negative SSB, negative double stranded DNA antibody, negative anti-Smith antibody, negative RNP antibody, negative rheumatoid factor, negative Lyme. A right forearm nodule was biopsied and revealed a subcutaneous granuloma, most consistent with a rheumatoid nodule. Sub-acute granuloma anulare was also considered in the differential. The patient was placed on hydroxychloroquine without any relief of the arthralgias. The patient was at that time diagnosed with undifferentiated connective tissue disease (UCTD). He started developing severe fatigue in August 1996, and Raynaud’s symptoms in July 1998. In 2000 and 2001, he began developing nodules on his forearms, thighs, lower extremities, hands, and fingers. Biopsy revealed multicentric reticulohistiocytosis. The symptoms continued, the Raynaud’s worsened, and he began developing sclerodactyly in his fingers, loss of pulp in the digits of his fingers and developed sclerodermatous facial features. He was diagnosed with a CREST variant of systemic sclerosis in March 2006. An ANA test in November 2001 had a titer greater than 1:320, and in January 2002, ANA titer was greater than 1:320. No reported ENA values.