scholarly journals Epstein-Barr Virus, Cytomegalovirus, and Other Viral Infections in Children After Liver Transplantatlon

1987 ◽  
Vol 156 (2) ◽  
pp. 273-279 ◽  
Author(s):  
M. K. Breinig ◽  
B. Zitelli ◽  
T. E. Starzl ◽  
M. Ho
Keyword(s):  
Epstein Barr Virus ◽  
Viral Infections ◽  
Barr Virus ◽  
Epstein Barr

Acute Pharyngitis: Etiology and Diagnosis

PEDIATRICS ◽  
1996 ◽  
Vol 97 (6) ◽  
pp. 949-954
Author(s):  
Alan L. Bisno
Keyword(s):  
Herpes Simplex ◽  
Influenza A ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Clinical Manifestations ◽  
Acute Pharyngitis ◽  
Herpesvirus Type ◽  
Barr Virus ◽  
Epstein Barr

Acute pharyngitis may be caused by a wide variety of microbial agents (Table 1). The relative importance of each of these agents varies greatly depending on a number of epidemiologic factors, including age of the patient, season of the year, and geographic locale. Viruses Most cases of acute pharyngitis are viral in etiology and involve the pharynx as well as other portions of the respiratory tract as manifestations of the common cold, influenza, or croup. Examples include the rhinoviruses, coronaviruses, influenza A and B, and the parainfluenza viruses. Certain viral infections causing sore throat may exhibit clinical manifestations that are rather distinctive. Examples include enteroviruses (herpangina due to Coxsackie A), Epstein-Barr virus (infectious mononucleosis), cytomegalovirus (cytomegalovirus mononucleosis), adenovirus (pharyngoconjunctival fever, acute respiratory disease of military recruits), and herpes simplex virus (pharyngitis, gingivitis, and stomatitis). In many instances, however, the illnesses caused by these agents may overlap so broadly with that of streptococcal pharyngitis as to be clinically indistinguishable. Thus, Epstein-Barr virus, adenovirus, and herpes virus may all cause fever, exudative pharyngitis, and cervical adenitis. Several studies have documented the role of primary herpesvirus type 1 infection as a cause of acute pharyngitis in college students.1-4 Herpesvirus type 2 can occasionally cause a similar illness as a consequence of oral-genital sexual contact.5 Although herpesvirus infections may involve the anterior oral cavity (vesicular or ulcerative gingivostomatitis) as well as the posterior pharynx, they do not routinely do so. Only about one-fourth of students with culturally and serologically proven primary herpes simplex type 1 pharyngitis studied by Glezen et al,2 for example, had gingivostomatitis.

scholarly journals Pancytopenia Secondary to SARS-CoV 2 Infection-A Case Reprt

2021 ◽  
Author(s):  
Neeraj Sharma ◽  
Rajat Shukla ◽  
Rachna Warrier ◽  
Kunal Kumar ◽  
Nalin Singh ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Blood Cells ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Parvovirus B19 ◽  
Rare Complication ◽  
Elderly Male ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr

Abstract Pancytopenia is a condition when person has low count of all three types of blood cells causing a triage of anemia, leukopenia and thrombocytopenia. It should not be considered as a disease in itself but rather the sign of a disease that needs to be further evaluated. Among the various causes, viral infections like Human Immunodeficiency Virus, Cytomegalovirus, Epstein-Barr virus and Parvovirus B19 have been implicated. Pancytopenia is a rare complication and not commonly seen in patients with COVID 19 disease. Here, we report a case of pancytopenia in previously immunocompetent elderly male patient with SARS-CoV2 infection.

scholarly journals Profound CD4+ T lymphocytopenia in human immunodeficiency virus negative individuals, improved with anti-human herpes virus treatment

2012 ◽  
pp. 305-311 ◽  
Author(s):  
María Lilia Diaz Betancourth ◽  
Julio Cesar Klinger ◽  
Victoria Eugenia Niño
Keyword(s):  
Human Immunodeficiency Virus ◽  
Epstein Barr Virus ◽  
Herpes Virus ◽  
Viral Infections ◽  
Human Herpes ◽  
Barr Virus ◽  
Human Herpes Virus ◽  
Immunodeficiency Virus ◽  
Epstein Barr ◽  
Herpès Virus

Lymphocytopenia and CD4+ T lymphocytopenia can be associated with many bacterial, fungal, parasite and viral infections. They can also be found in autoimmune and neoplastic diseases, common variable immu­nodeficiency syndrome, physical, psychological and traumatic stress, malnutrition and immunosuppressive therapy. Besides, they can also be brought into relation, without a known cause, with idiopathic CD4+ T lym­phocytopenia. Among viral infections, the Retrovirus, specially the human immunodeficiency virus, is the most frequently cause. However, many acute viral infections, including cytomegalovirus and Epstein Barr virus can be associated with transient lymphocytopenia and CD4+ T lymphocytopenia. As is well known, transient lymphocytopenia and CD4+ T lymphocytopenia are temporary and overcome when the disease improves. Nonetheless, severe CD4+ T Lymphocytopenia associated with chronic infections by human herpes virus has not been reported. We describe 6 cases of human immunodeficiency virus negative patients, with chronic cytomegalovirus and Epstein Barr virus infections and profound lymphocytopenia with clinical symptoms of cellular immunodeficiency. These patients improved rapidly with ganciclovir or valganciclovir treatment. We claim here that it is important to consider the chronic human herpes virus infection in the differential diag­nosis of profoundly CD4+ T lymphocytopenia etiology, when human immunodeficiency virus is absent, in order to start effective treatment and to determine, in future studies, the impact of chronic human herpes virus infection in human beings’ health.

scholarly journals X-linked lymphoproliferative syndromes: brothers or distant cousins?

Blood ◽  
2010 ◽  
Vol 116 (18) ◽  
pp. 3398-3408 ◽  
Author(s):  
Alexandra H. Filipovich ◽  
Kejian Zhang ◽  
Andrew L. Snow ◽  
Rebecca A. Marsh
Keyword(s):  
Epstein Barr Virus ◽  
Hematopoietic Cell Transplantation ◽  
Viral Infections ◽  
Inflammatory Responses ◽  
Lymphoproliferative Disease ◽  
Curative Therapy ◽  
Barr Virus ◽  
Clinical Consequences ◽  
Epstein Barr ◽  
Signaling Lymphocytic Activation Molecule

AbstractX-linked lymphoproliferative disease (XLP1), described in the mid-1970s and molecularly defined in 1998, and XLP2, reported in 2006, are prematurely lethal genetic immunodeficiencies that share susceptibility to overwhelming inflammatory responses to certain infectious triggers. Signaling lymphocytic activation molecule-associated protein (SAP; encoded by SH2D1A) is mutated in XLP1, and X-linked inhibitor of apoptosis (XIAP; encoded by BIRC4) is mutated in XLP2. XLP1 is a disease with multiple and variable clinical consequences, including fatal hemophagocytic lymphohistiocytosis (HLH) triggered predominantly by Epstein-Barr virus, lymphomas, antibody deficiency, and rarer consequences of immune dysregulation. To date, XLP2 has been found to cause HLH with and without exposure to Epstein-Barr virus, and HLH is commonly recurrent in these patients. For both forms of XLP, the only curative therapy at present is allogeneic hematopoietic cell transplantation. Beyond their common X-linked locus and their requirement for normal immune responses to certain viral infections, SAP and XIAP demonstrate no obvious structural or functional similarity, are not coordinately regulated with respect to their expression, and do not appear to directly interact. In this review, we describe the genetic, clinical, and immunopathologic features of these 2 disorders and discuss current diagnostic and therapeutic strategies.

scholarly journals Epstein-Barr Virus Epitope–Major Histocompatibility Complex Interaction Combined with Convergent Recombination Drives Selection of Diverse T Cell Receptor α and β Repertoires

mBio ◽  
2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Anna Gil ◽  
Larisa Kamga ◽  
Ramakanth Chirravuri-Venkata ◽  
Nuray Aslan ◽  
Fransenio Clark ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
T Cell ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Cd8 T Cell ◽  
Barr Virus ◽  
Histocompatibility Complex ◽  
Tcr Repertoire ◽  
Epstein Barr ◽  
Selection Of

ABSTRACT Recognition modes of individual T cell receptors (TCRs) are well studied, but factors driving the selection of TCR repertoires from primary through persistent human virus infections are less well understood. Using deep sequencing, we demonstrate a high degree of diversity of Epstein-Barr virus (EBV)-specific clonotypes in acute infectious mononucleosis (AIM). Only 9% of unique clonotypes detected in AIM persisted into convalescence; the majority (91%) of unique clonotypes detected in AIM were not detected in convalescence and were seeming replaced by equally diverse “de novo” clonotypes. The persistent clonotypes had a greater probability of being generated than nonpersistent clonotypes due to convergence recombination of multiple nucleotide sequences to encode the same amino acid sequence, as well as the use of shorter complementarity-determining regions 3 (CDR3s) with fewer nucleotide additions (i.e., sequences closer to germ line). Moreover, the two most immunodominant HLA-A2-restricted EBV epitopes, BRLF1109 and BMLF1280, show highly distinct antigen-specific public (i.e., shared between individuals) features. In fact, TCRα CDR3 motifs played a dominant role, while TCRβ played a minimal role, in the selection of TCR repertoire to an immunodominant EBV epitope, BRLF1. This contrasts with the majority of previously reported repertoires, which appear to be selected either on TCRβ CDR3 interactions with peptide/major histocompatibility complex (MHC) or in combination with TCRα CDR3. Understanding of how TCR-peptide-MHC complex interactions drive repertoire selection can be used to develop optimal strategies for vaccine design or generation of appropriate adoptive immunotherapies for viral infections in transplant settings or for cancer. IMPORTANCE Several lines of evidence suggest that TCRα and TCRβ repertoires play a role in disease outcomes and treatment strategies during viral infections in transplant patients and in cancer and autoimmune disease therapy. Our data suggest that it is essential that we understand the basic principles of how to drive optimum repertoires for both TCR chains, α and β. We address this important issue by characterizing the CD8 TCR repertoire to a common persistent human viral infection (EBV), which is controlled by appropriate CD8 T cell responses. The ultimate goal would be to determine if the individuals who are infected asymptomatically develop a different TCR repertoire than those that develop the immunopathology of AIM. Here, we begin by doing an in-depth characterization of both CD8 T cell TCRα and TCRβ repertoires to two immunodominant EBV epitopes over the course of AIM, identifying potential factors that may be driving their selection.

scholarly journals Coevolution of Sites under Immune Selection Shapes Epstein–Barr Virus Population Structure

2019 ◽  
Vol 36 (11) ◽  
pp. 2512-2521 ◽  
Author(s):  
Fanny Wegner ◽  
Florent Lassalle ◽  
Daniel P Depledge ◽  
François Balloux ◽  
Judith Breuer
Keyword(s):  
Epstein Barr Virus ◽  
Viral Infections ◽  
Genetic Recombination ◽  
Adaptive Immune Response ◽  
Immune Selection ◽  
Barr Virus ◽  
Genome Wide ◽  
Epstein Barr ◽  
Globally Distributed ◽  
Genome Wide Linkage Disequilibrium

Abstract Epstein–Barr virus (EBV) is one of the most common viral infections in humans and persists within its host for life. EBV therefore represents an extremely successful virus that has evolved complex strategies to evade the host’s innate and adaptive immune response during both initial and persistent stages of infection. Here, we conducted a comparative genomics analysis on 223 whole genome sequences of worldwide EBV strains. We recover extensive genome-wide linkage disequilibrium (LD) despite pervasive genetic recombination. This pattern is explained by the global EBV population being subdivided into three main subpopulations, one primarily found in East Asia, one in Southeast Asia and Oceania, and the third including most of the other globally distributed genomes we analyzed. Additionally, sites in LD were overrepresented in immunogenic genes. Taken together, our results suggest that host immune selection and local adaptation to different human host populations has shaped the genome-wide patterns of genetic diversity in EBV.

scholarly journals Epstein-Barr virus-associated hemophagocytic syndrome: virological and immunopathological studies

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1097-1104
Author(s):  
JL Sullivan ◽  
BA Woda ◽  
HG Herrod ◽  
G Koh ◽  
FP Rivara ◽  
...  
Keyword(s):  
Lymph Node ◽  
Epstein Barr Virus ◽  
Hemophagocytic Syndrome ◽  
Viral Infections ◽  
Cytotoxic T Cells ◽  
Peripheral Circulation ◽  
Barr Virus ◽  
Ebv Infection ◽  
Node Architecture ◽  
Epstein Barr

The virus-associated hemophagocytic syndrome (VAHS) is a disorder characterized by a benign, generalized histiocytic proliferation, with marked hemophagocytosis associated with systemic viral infections. We have studied the virological and immunopathological events occurring in two children experiencing Epstein-Barr VAHS. Neither of the patients had an underlying immunodeficiency and both recovered from their disease and are completely well one year after follow-up. In each patient, evidence for primary Epstein-Barr virus (EBV) infection was documented with a typical humoral immune response, including IgM antibody directed against virus capsid antigen. EBV was demonstrated in lymphoreticular tissues by electron microscopy and molecular hybridization studies. Permissive EBV infection was suggested by the finding of mature virus particles and linear viral DNA in lymphoreticular tissues. Immunopathological studies demonstrated complete effacement of lymph node architecture by a marked proliferation of immunoblasts in patient 1 and infiltration and effacement of the lymph node architecture with benign-appearing histiocytes in patient 2. Atypical lymphocytes characteristic of acute EBV infection were notably absent in the peripheral blood of both patients and cytotoxic T cells, which normally lyse EBV-infected B cells, were also absent from the peripheral circulation. Our observations suggest that EBV-induced VAHS may be the result of an increased virus burden in the face of immunoregulatory cell imbalances.

scholarly journals Association of Epstein–Barr Virus and Cytomegalovirus Infections with Esophageal Carcinoma

2021 ◽  
Vol 14 (10) ◽  
Author(s):  
Mahin Ahangar Oskouee ◽  
Jamal Sarvari ◽  
Afagh Moattari ◽  
Ahmad Habibi ◽  
Amir Taher Eftehkar Sadat
Keyword(s):  
Esophageal Carcinoma ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Control Group ◽  
Control Groups ◽  
Barr Virus ◽  
Potential Association ◽  
Epstein Barr ◽  
And Control ◽  
Cytomegalovirus Infections

Background: Given the fact that viral infections play an important role, either directly or indirectly, in around 20 percent of human cancers, this study aimed at investigating the potential association of Epstein–Barr virus (EBV) and cytomegalovirus (CMV) infections in esophageal cancer that is the sixth most common cause of cancer-related deaths. Methods: In this case-control study, a total of 200 paraffin-embedded biopsies of cancerous and benign esophageal tissues were gathered from the biopsy bank of Imam Reza Hospital, Tabriz, Iran in 2017. All samples were first deparaffinized, and then subjected to commercial DNA extraction. The quality of extracted DNA was evaluated by amplification of the beta globulin gene. Identification of EBV and CMV DNA was performed using primers designed for the EBER region of EBV and the immediate early (IE) region of the CMV genome, respectively. Results: The mean age of the subjects in the test and control groups was 52.2 (17.1) and 59.9 (18.9), respectively. The distribution of gender (male/female) in patient and control groups was 54/46 and 53/47, respectively. Our results showed that the frequency of EBV (P < 0.001) and CMV (P < 0.001) in cancerous samples was statistically higher than control group. Moreover, in the cancerous group the rate of EBV was significantly higher in the esophageal adenocarcinomas (EAC) sample (12 out of 70) than esophageal squamous cell carcinomas (ESCC) (0 out of 30) (P = 0.016) but, in the ESCC group, 17 out of 30 subjects were positive for CMV which was significantly higher in comparison with EAC patients (1 out of 70) (P < 0.001). Conclusions: Findings indicated that EBV and CMV might be contributed to the pathogenesis of EAC and ESCC types of esophageal carcinoma, respectively, although further studies are warranted.

Sign in / Sign up

Export Citation Format

Share Document