Vaccination against human cytomegalovirus (CMV) infection remains high priority. A recombinant form of a protein essential for CMV entry, glycoprotein B (gB), demonstrated partial protection in a clinical trial (NCT00299260) when delivered with the MF59 adjuvant. Although the antibody titre against gB correlated with protection poor neutralising responses against the 5 known antigenic domains (AD) of gB were evident. Here, we show that vaccination of CMV seronegative patients induces an antibody response against a region of gB we term AD-6. Responses to the polypeptide AD-6 are detected in >70% of vaccine recipients yet in <5% of naturally infected people. An AD-6 antibody binds to gB and to infected cells but not the virion directly. Consistent with this, the AD-6 antibody is non-neutralising but, instead, prevents cell-cell spread of CMV in vitro. The discovery of AD-6 responses has the potential to explain part of the protection mediated by gB vaccines against CMV following transplantation.
CD8+ T cells are cytotoxic lymphocytes that destroy pathogen infected and malignant cells through release of cytolytic molecules and proinflammatory cytokines. Although the role of CD8+ T cells in connective tissue diseases (CTDs) has not been explored as thoroughly as that of other immune cells, research focusing on this key component of the immune system has recently gained momentum. Aberrations in cytotoxic cell function may have implications in triggering autoimmunity and may promote tissue damage leading to exacerbation of disease. In this comprehensive review of current literature, we examine the role of CD8+ T cells in systemic lupus erythematosus, Sjögren’s syndrome, systemic sclerosis, polymyositis, and dermatomyositis with specific focus on comparing what is known about CD8+ T cell peripheral blood phenotypes, CD8+ T cell function, and CD8+ T cell organ-specific profiles in adult and juvenile forms of these disorders. Although, the precise role of CD8+ T cells in the initiation of autoimmunity and disease progression remains to be elucidated, increasing evidence indicates that CD8+ T cells are emerging as an attractive target for therapy in CTDs.
AIMS Patients with gliomas often present with generalised seizures, but subsequently develop focal seizures on treatment. The occurrence of a single generalised seizure at onset precludes the return of a driving licence, even if a patient continues to have only focal aware seizures. We investigated seizure semiology over time, to determine how many patients with ongoing seizures may be safe to drive. METHOD We analysed clinical data of patients with histologically-confirmed IDH-mutant diffuse gliomas, diagnosed between 2004-2015. Seizures were classified as: 1 – focal / 2 - generalised; A – aware / B – unaware; M – motor / N – non-motor. Seizure type at diagnosis and last follow-up was recorded. RESULTS 189 patients were identified, of whom 140 presented with seizures (74%). 115 of these patients had a full data set. 59 (51%) presented with generalised seizures. 10% had only a single seizure at presentation, 55 % had further seizures then became seizure-free and 35% continued to have seizures at last follow-up. Of the 40 patients who continued to have seizures, 7 (17.5%) had 1AN, 16 (40%) had 1AM, 1 (2.5%) had 1BN and 5 (12.5%) had 1BM. 11 (27.5%) had generalised seizures. Of the 7 patients with 1AN seizures at last follow-up, 4 initially presented with a generalised seizure, 1 with 1AN, 1 with 1AM and 1 with 1BM. CONCLUSION Almost two thirds of patients became seizure-free and, of those that continued to have seizures, 57.5% developed only focal aware seizures. Current driving regulations may be unduly restrictive for patients with gliomas.
A 36-year-old diabetic woman presented to hospital with a seizure that started with shaking of the right hand which sequentially progressed to the entire right side of the body with associated loss of consciousness. Capillary Blood Glucose was 29 mmol/L. HbA1c was 133 mmol/L. Non-contrast computerised tomography (CT) scan of the brain was normal suggesting that the cause of her seizure was hyperglycaemia. However, Magnetic Resonance Imaging (MRI) of the brain showed infarcts in the left paracentral lobule and caudate nucleus. It also identified loss of signal flow void in the intracranial segment of the left internal carotid artery (ICA) raising the suspicion for thrombosis secondary to dissection. This was later confirmed on CT angiogram. This case demonstrates how the initial CT Head was non-diagnostic. We stress the importance of taking a careful seizure history and subsequently obtaining an MRI scan to fully exclude structural pathology.
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