Cytomegaloviral Infections: Epidemiology, Therapy, and Prevention

1985 ◽  
Vol 7 (6) ◽  
pp. 169-175
Author(s):  
George A. Nankervis
Keyword(s):  
Giant Cells ◽  
Varicella Zoster ◽  
Barr Virus ◽  
Current Review ◽  
New Concepts ◽  
The World ◽  
The Subject ◽  
Epstein Barr ◽  
Different Strains

The role of cytomegalovirus in human disease is a still-evolving story. Hanshaw presented an excellent review article on the subject in 1981 in this publication; this current review is an update, with particular emphasis on new concepts in the epidemiology and prevention of cytomegaloviral infection and disease. Historically, evidence of infection with cytomegalovirus was first reported by pathologists in many parts of the world. They noted the presence of giant cells with intranuclear inclusions while examining a diversity of organs microscopically. Isolation of the virus and development of serologic techniques eventually enabled a definitive study of the agent, its pathogenesis and epidemiology. Biologically, it is one of the herpesviruses and, as such, is a DNA virus. Other members of the group include varicella-zoster, herpes simplex, and Epstein-Barr virus. Several different strains of cytomegalovirus exist, and they have specific characteristics which are of interest. The virus is cell associated and tends to be very labile; it has a tendency to become latent and may possibly have malignant potential. EPIDEMIOLOGY Prevalence Infection with cytomegalovirus is found throughout the world. Studies of prevalence in a number of diverse populations have indicated that cytomegaloviral infection is ubiquitous. The major differences in prevalence between populations are related to the speed of acquisition of infection in various geographic and socioeconomic settings.

HIV-associated Waldeyer's ring lymphoid hyperplasias: Characterization of multinucleated giant cells and the role of Epstein-Barr virus

1999 ◽  
Vol 30 (11) ◽  
pp. 1383-1388 ◽  
Author(s):  
Silloo B Kapadia ◽  
Clayton A Wiley ◽  
Virawudh Soontornniyomkij ◽  
Guoji Wang ◽  
Steven H Swerdlow
Keyword(s):  
Epstein Barr Virus ◽  
Giant Cells ◽  
Multinucleated Giant Cells ◽  
Barr Virus ◽  
Waldeyer’S Ring ◽  
Epstein Barr

scholarly journals Infections and Multiple Sclerosis: From the World to Sardinia, From Sardinia to the World

2021 ◽  
Vol 12 ◽  
Author(s):  
Jessica Frau ◽  
Giancarlo Coghe ◽  
Lorena Lorefice ◽  
Giuseppe Fenu ◽  
Eleonora Cocco
Keyword(s):  
Multiple Sclerosis ◽  
Mycobacterium Avium Subspecies Paratuberculosis ◽  
Strong Association ◽  
Japanese Patients ◽  
Endogenous Retroviruses ◽  
Multi Centre Study ◽  
Barr Virus ◽  
The World ◽  
Epstein Barr

Multiple Sclerosis (MS) is an inflammatory disease of the central nervous system. Sardinia, an Italian island, is one of the areas with the highest global prevalence of MS. Genetic factors have been widely explored to explain this greater prevalence among some populations; the genetic makeup of the Sardinians appears to make them more likely to develop autoimmune diseases. A strong association between MS and some infections have been reported globally. The most robust evidence indicating the role of infections is MS development concerns the Epstein-Barr virus (EBV). Anti-EBV antibodies in patients once infected by EBV are associated with the development of MS years later. These features have also been noted in Sardinian patients with MS. Many groups have found an increased expression of the Human endogenous retroviruses (HERV) family in patients with MS. A role in pathogenesis, prognosis, and prediction of treatment response has been proposed for HERV. A European multi-centre study has shown that their presence was variable among populations, ranging from 59% to 100% of patients, with higher HERV expression noted in Sardinian patients with MS. The mycobacterium avium subspecies paratuberculosis (MAP) DNA and antibodies against MAP2694 protein were found to be associated with MS in Sardinian patients. More recently, this association has also been reported in Japanese patients with MS. In this study, we analysed the role of infectious factors in Sardinian patients with MS and compared it with the findings reported in other populations.

scholarly journals EBNA-1 titer gradient in families with multiple sclerosis indicates a genetic contribution

2020 ◽  
Vol 7 (6) ◽  
pp. e872 ◽  
Author(s):  
Julia Y. Mescheriakova ◽  
Gijsbert P. van Nierop ◽  
Annemiek A. van der Eijk ◽  
Karim L. Kreft ◽  
Rogier Q. Hintzen
Keyword(s):  
Nuclear Antigen ◽  
Nucleotide Polymorphisms ◽  
Genetic Contribution ◽  
Single Nucleotide ◽  
Varicella Zoster ◽  
Humoral Immune ◽  
Barr Virus ◽  
Healthy Siblings ◽  
Epstein Barr

ObjectiveIn multiplex MS families, we determined the humoral immune response to Epstein-Barr virus nuclear antigen 1 (EBNA-1)-specific immunoglobulin γ (IgG) titers in patients with MS, their healthy siblings, and biologically unrelated healthy spouses and investigated the role of specific genetic loci on the antiviral IgG titers.MethodsIgG levels against EBNA-1 and varicella zoster virus (VZV) as control were measured. HLA-DRB1*1501 and HLA-A*02 tagging single-nucleotide polymorphisms (SNPs) were genotyped. We assessed the associations between these SNPs and antiviral IgG titers.ResultsOR for abundant EBNA-1 IgG was the highest in patients with MS and intermediate in their siblings compared with spouses. We confirmed that HLA-DRB1*1501 is associated with abundant EBNA-1 IgG. After stratification for HLA-DRB1*1501, the EBNA-1 IgG gradient was still significant in patients with MS and young siblings compared with spouses. HLA-A*02 was not explanatory for EBNA-1 IgG titer gradient. No associations for VZV IgG were found.ConclusionsIn families with MS, the EBNA-1 IgG gradient being the highest in patients with MS, intermediate in their siblings, and lowest in biologically unrelated spouses indicates a genetic contribution to EBNA-1 IgG levels that is only partially explained by HLA-DRB1*1501 carriership.

Alignment

2016 ◽  
pp. 33-50
Author(s):  
Pier Giuseppe Rossi
Keyword(s):  
Teaching And Learning ◽  
Enactive Approach ◽  
The World ◽  
Strategic Role ◽  
Education Today ◽  
Current Context ◽  
The Subject

The subject of alignment is not new to the world of education. Today however, it has come to mean different things and to have a heuristic value in education according to research in different areas, not least for neuroscience, and to attention to skills and to the alternation framework.This paper, after looking at the classic references that already attributed an important role to alignment in education processes, looks at the strategic role of alignment in the current context, outlining the shared construction processes and focusing on some of the ways in which this is put into effect.Alignment is part of a participatory, enactive approach that gives a central role to the interaction between teaching and learning, avoiding the limits of behaviourism, which has a greater bias towards teaching, and cognitivism/constructivism, which focus their attention on learning and in any case, on that which separates a teacher preparing the environment and a student working in it.

Are Viruses and Parasites Linked to Celiac Disease? A Question that Still has no Definite Answer

2019 ◽  
Vol 20 (14) ◽  
pp. 1181-1193 ◽  
Author(s):  
Aref Shariati ◽  
Hamid R. Aslani ◽  
Mohammad R.H. Shayesteh ◽  
Ali Taghipour ◽  
Ahmad Nasser ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Multiple Roles ◽  
Barr Virus ◽  
The People ◽  
Intestinal Infections ◽  
Inflammatory Bowel ◽  
Epstein Barr ◽  
Irritable Bowel ◽  
Related Proteins

Celiac Disease (CD) is a complex autoimmune enteropathy of the small intestine that commonly occurs in genetically predisposed individuals due to intake of gluten and related proteins. Gluten consumption, duration of breast-feeding, various infections, especially frequent intestinal infections, vaccinations and use of antibiotics can be linked to CD. It is predicted that it affects 1% of the global population and its incidence rate is increasing. Most of the people with the HLA-DQ2 or HLADQ8 are at a higher risk of developing this disease. The link between infections and autoimmune diseases has been very much considered in recent years. In several studies, we explained that pathogenic and non-pathogenic microorganisms might have multiple roles in initiation, exacerbation, and development of Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD). In various studies, the relationship between infections caused by viruses, such as Epstein-Barr Virus (EBV), Rotavirus, Hepatitis C (HCV), Hepatitis B virus (HBV), Cytomegalovirus (CMV), and Influenza virus, and parasites including Giardia spp. and Toxoplasma gondii with CD has been raised. However, increasing evidence proposes that some of these microorganisms, especially helminths, can also have protective and even therapeutic roles in the CD process. Therefore, in order to determine the role of microorganisms in the process of this disease, we attempted to summarize the evidence suggesting the role of viral and parasitic agents in pathogenesis of CD.

scholarly journals Molecular Genetics in Epstein–Barr Virus-Associated Malignancies

Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 593
Author(s):  
Srikanth Umakanthan ◽  
Maryann M Bukelo
Keyword(s):  
Epstein Barr Virus ◽  
Diagnostic Tools ◽  
Main Role ◽  
Genetic Changes ◽  
Barr Virus ◽  
Cancer Pathogenesis ◽  
Genomic Studies ◽  
Epstein Barr ◽  
Oncogenic Form

Global genomic studies have detected the role of genomic alterations in the pathogenesis of Epstein–Barr virus (EBV)-associated tumors. EBV oncoproteins cause a vital shift of EBV from an infectious virus to an oncogenic form during the latent and lytic phase within the lymphoid B cells and epithelial cells. This epigenetic alteration modulates the virus and host genomes and inactivates and disrupts numerous tumor suppressors and signaling pathways. Genomic profiling has played the main role in identifying EBV cancer pathogenesis and its related targeted therapies. This article reviews the role of genetic changes in EBV-associated lymphomas and carcinomas. This includes the prolific molecular genesis, key diagnostic tools, and target-specific drugs that have been in recent clinical use.

EBV load is associated with cfDNA fragmentation and renal damage in SLE patients

Lupus ◽  
2021 ◽  
pp. 096120332110103
Author(s):  
Anna Truszewska ◽  
Agnieszka Wirkowska ◽  
Kamila Gala ◽  
Piotr Truszewski ◽  
Łucja Krzemień-Ojak ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Renal Damage ◽  
Healthy Individuals ◽  
Pcr Assay ◽  
Barr Virus ◽  
Fragmentation Index ◽  
Epstein Barr

Background For long Epstein–Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. Methods Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. Results SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(–) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(–) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). Conclusions We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.

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