scholarly journals Cytomegalovirus Cholangiopathy in an Immunocompetent Patient: A Case Report and Literature Review

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Ervin Alibegovic ◽  
Admir Kurtcehajic ◽  
Boris Ilic ◽  
Ahmed Hujdurovic ◽  
Edinka Smajic ◽  
...  

A 37-year-old man presented with jaundice, upper right quadrant pain, and intermittent fever with chills. Laboratory assessment showed biliary stasis, with total bilirubin of 203 µmol/L (2–20), conjugated bilirubin of 105 µmol/L, and alkaline phosphatase of 556 U/L (30–120). Markers for hepatitis A–E viruses were negative. Serology assessment for rubeola, herpes simplex virus, Epstein-Barr virus, and Toxoplasma gondii showed negative IgM antibodies. HIV serology status was negative. For cytomegalovirus, both types of antibodies (IgM and IgG) were positive, with an IgM level >300 U/mL. pp65 antigen was also detected as well as CMV DNA. Diagnostic imaging of the abdomen except the dilated common bile duct showed a normal appearance of the gallbladder, liver, pancreas, spleen, and both kidneys. To our knowledge, cytomegalovirus cholangiopathy in the absence of any other underlying disease has not been reported. Therefore, the presence of cholangiopathy in our patient is interesting from an imaging, laboratory, and clinical point of view.

2021 ◽  
Vol 9 (2) ◽  
pp. 292
Author(s):  
Miroslava Šudomová ◽  
Sherif T. S. Hassan

Herpesviruses are DNA viruses that infect humans and animals with the ability to induce latent and lytic infections in their hosts, causing critical health complications. The enrolment of nutraceutical anti-herpesvirus drugs in clinical investigations with promising levels of reduced resistance, free or minimal cellular toxicity, and diverse mechanisms of action might be an effective way to defeat challenges that hurdle the progress of anti-herpesvirus drug development, including the problems with drug resistance and recurrent infections. Therefore, in this review, we aim to hunt down all investigations that feature the curative properties of curcumin, a principal bioactive phenolic compound of the spice turmeric, in regard to various human and animal herpesvirus infections and inflammation connected with these diseases. Curcumin was explored with potent antiherpetic actions against herpes simplex virus type 1 and type 2, human cytomegalovirus, Kaposi’s sarcoma-associated herpesvirus, Epstein–Barr virus, bovine herpesvirus 1, and pseudorabies virus. The mechanisms and pathways by which curcumin inhibits anti-herpesvirus activities by targeting multiple steps in herpesvirus life/infectious cycle are emphasized. Improved strategies to overcome bioavailability challenges that limit its use in clinical practice, along with approaches and new directions to enhance the anti-herpesvirus efficacy of this compound, are also reviewed. According to the reviewed studies, this paper presents curcumin as a promising natural drug for the prevention and treatment of herpesvirus infections and their associated inflammatory diseases.


2016 ◽  
Vol 90 (11) ◽  
pp. 5353-5367 ◽  
Author(s):  
Jayaraju Dheekollu ◽  
Andreas Wiedmer ◽  
Daniel Sentana-Lledo ◽  
Joel Cassel ◽  
Troy Messick ◽  
...  

ABSTRACTEpstein-Barr virus (EBV) establishes latent infections as multicopy episomes with complex patterns of viral gene transcription and chromatin structure. The EBV origin of plasmid replication (OriP) has been implicated as a critical control element for viral transcription, as well as viral DNA replication and episome maintenance. Here, we examine cellular factors that bind OriP and regulate histone modification, transcription regulation, and episome maintenance. We found that OriP is enriched for histone H3 lysine 4 (H3K4) methylation in multiple cell types and latency types. Host cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase complex, and transcription factor OCT2 (octamer-binding transcription factor 2) bound cooperatively with EBNA1 (Epstein-Barr virus nuclear antigen 1) at OriP. Depletion of OCT2 or HCF1 deregulated latency transcription and histone modifications at OriP, as well as the OriP-regulated latency type-dependent C promoter (Cp) and Q promoter (Qp). HCF1 depletion led to a loss of histone H3K4me3 (trimethylation of histone H3 at lysine 4) and H3 acetylation at Cp in type III latency and Qp in type I latency, as well as an increase in heterochromatic H3K9me3 at these sites. HCF1 depletion resulted in the loss of EBV episomes from Burkitt's lymphoma cells with type I latency and reactivation from lymphoblastoid cells (LCLs) with type III latency. These findings indicate that HCF1 and OCT2 function at OriP to regulate viral transcription, histone modifications, and episome maintenance. As HCF1 is best known for its function in herpes simplex virus 1 (HSV-1) immediate early gene transcription, our findings suggest that EBV latency transcription shares unexpected features with HSV gene regulation.IMPORTANCEEBV latency is associated with several human cancers. Viral latent cycle gene expression is regulated by the epigenetic control of the OriP enhancer region. Here, we show that cellular factors OCT2 and HCF1 bind OriP in association with EBNA1 to maintain elevated histone H3K4me3 and transcriptional enhancer function. HCF1 is known as a transcriptional coactivator of herpes simplex virus (HSV) immediate early (IE) transcription, suggesting that OriP enhancer shares aspects of HSV IE transcription control.


2017 ◽  
Vol 214 (2) ◽  
pp. 269-283 ◽  
Author(s):  
Stuart G. Tangye ◽  
Umaimainthan Palendira ◽  
Emily S.J. Edwards

The mammalian immune system has evolved over many millennia to be best equipped to protect the host from pathogen infection. In many cases, host and pathogen have coevolved, each acquiring sophisticated ways of inducing or protecting from disease. Epstein-Barr virus (EBV) is a human herpes virus that infects >90% of individuals. Despite its ubiquity, infection by EBV is often subclinical; this invariably reflects the necessity of the virus to preserve its host, balanced with sophisticated host immune mechanisms that maintain viral latency. However, EBV infection can result in various, and often fatal, clinical sequelae, including fulminant infectious mononucleosis, hemophagocytic lymphohistiocytosis, lymphoproliferative disease, organomegaly, and/or malignancy. Such clinical outcomes are typically observed in immunosuppressed individuals, with the most extreme cases being Mendelian primary immunodeficiencies (PIDs). Although these conditions are rare, they have provided critical insight into the cellular, biochemical, and molecular requirements for robust and long-lasting immunity against EBV infection. Here, we review the virology of EBV, mechanisms underlying disease pathogenesis in PIDs, and developments in immune cell–mediated therapy to treat disorders associated with or induced by EBV infection.


2021 ◽  
Vol 9 (4) ◽  
pp. 778
Author(s):  
Takayuki Murata

The immune system has evolved as a complex and efficient means of coping with extrinsic materials, such as pathogens and toxins, as well as intrinsic abnormalities, such as cancers. Although rapid and timely activation of the immune system is obviously important, regulated downregulation of the system is almost as significant as activation to prevent runaway immunity, such as allergies and hypercytokinemia. Therefore, the immune checkpoint programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is beneficial for the host. On the other hand, pathogens have evolved to evade host immunity by taking advantage of the PD-1/PD-L1 pathway. This review is focused on human herpesviruses, such as herpes simplex virus (HSV), cytomegalovirus (CMV), and Epstein–Barr virus (EBV), which cause various types of disorders, and their relationships with the PD-1/PD-L1 pathway. Understanding such relationships will be useful for developing preventative and therapeutic methods for disorders caused by herpesviruses.


PEDIATRICS ◽  
1985 ◽  
Vol 75 (2) ◽  
pp. 280-283
Author(s):  
ELIZABETH H. DANISH ◽  
BEVERLY B. DAHMS ◽  
MARY L. KUMAR

Virus-associated hemophagocytic syndrome, first described by Risdall and co-workers in 1979,1 is a rare histiocytic proliferative syndrome characterzed by fever, hepatosplenomegaly, pancytopenia, and erythrophagocytosis by histiocytes that appear benign by histologic criteria. The clinical course and pathologic findings may be identical with another histiocytic disorder, familial erythrophagocytic lymphohistiocytosis, which occurs predominantly in infants. Diagnosis of virus-associated hemophagocytic syndrome depends entirely on evidence of concurrent viral infection, usually of the herpes group. Epstein-Barr virus has been associated with this syndrome in the few cases reported in children without underlying disease, whereas cytomegalovirus (CMV) has been implicated in immunosuppressed patients. We report a case of fatal CMV-associated hemophagocytic syndrome which occurred in a previously healthy infant.


2019 ◽  
Vol 16 (1S) ◽  
pp. 40-44
Author(s):  
V. V. Neroev ◽  
L. A. Katargina ◽  
L. A. Kovaleva ◽  
G. I. Krichevskaya ◽  
N. V. Balatskaya

Purpose: to study the role of human herpesviruses (HHV) in the pathogenesis of prolonged bacterial corneal ulcers. Patients and methods. 117 patients with bacterial corneal ulcer were examined. Two groups were identified: a favorable course-with duration of bacterial corneal ulcer epithelialization for 17 days (62 people) and a prolonged course with a persistent ulcer more than 17 days (55 people). Blood samples (n = 117) and scrapes from corneal ulcer (n = 117) were investigated in polymerase chain reaction (PCR) for the presence of deoxyribonucleic acid (DNA) of Herpes simplex virus (HSV1, 2), Epstein-Barr virus (EBV), Human herpesvirus type 6, 7 (HHV-6, HSV-7). Results. The HSV1, 2 and EBV genomes were detected in the cornea significantly more often in BCU of prolonged course compared with a favorable course (HSV1, 2 p = 0.012; EBV p = 0.012), and HHV-6 was detected not only in the cornea (p = 0.000), but also and in blood (p = 0.007). In patients with HHV DNA in corneal scarps and/or blood, after resorption of purulent infiltrate, corneal epithelialization was absent, and the use of antiherpetic drugs allowed to reduce the completion time of BCU epithelialization. Conclusion. The role of HHV-6, EBV, HSV 1, 2 in the pathogenesis of bacterial corneal ulcer of protracted course was revealed. The expediency of examination of patients with bacterial corneal ulcer on HHV is shown, a method of treatment is proposed, including antiherpetic therapy, which makes it possible to prevent the development of a protracted course.


Author(s):  
Randall C. Walker

The following types of viral infections are discussed in this chapter: viral infections that have the capacity for multiorgan or systemic disease; infections that affect adults who may be otherwise healthy or at least not in special populations such as herpes simplex virus (HSV) type 1, varicella-zoster virus (VZV), Epstein-Barr virus, adenovirus, mumps virus, human parvovirus B19, and coxsackievirus. Reviews of these viruses focus on differentiating clinical features, diagnostic tools and treatment, and salient microbiologic and epidemiologic factors.


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