Search

Introduction: Reactivation of cytomegalovirus can complicate the evolution of patients with gastritis induced by immune checkpoint inhibitors., Methods: The experience in our center is described and a review of the literature is performed., Results: A case of severe gastritis induced by treatment with a programmed cell death receptor-1 (anti-PD1) inhibitor, associated with reactivation of cytomegalovirus (CMV) is described. In the systematic review, we identified 5 cases of immune-related gastritis associated with CMV reactivation. Ganciclovir treatment contributed to clinical improvement in most patients., Conclusion: The early identification of a CMV infection in patients with severe or refractory immune-related gastritis will allow the initiation of targeted treatment, and may avoid increasing immunosuppressive therapy., (Copyright © 2022 Sociedad Española de Enfermedades Infecciosas y Microbiología Clínica. Published by Elsevier España, S.L.U. All rights reserved.)

Apoptosis is one of the most effective mechanisms against the spread of pathogens such as viruses. However, viruses have developed measures to counter the protective role of apoptosis in infected cells. Cytomegalovirus (CMV) represents the major cause of congenital infection worldwide triggering important damage in the developing central nervous system (CNS). Several mechanisms of apoptosis prevention during CMV infection have been described, among them, viral proteins and RNAs are capable of prevent apoptosis by the intrinsic and extrinsic pathways as well as the one mediated by stress in the endoplasmic reticulum. Nevertheless, the CMV pro-apoptotic effect remains enigmatic and it has been suggested as a bystander effect in non-infected cells. This review summarizes the mechanisms by which CMV modulates the signaling pathways involved in apoptosis. It also includes a brief description of the permissiveness of the CNS to CMV infection and the generated cell death after infection, which may relate to the observed damage during a congenital infection.

Although advances have been made in the prevention, diagnosis and treatment of cytomegalovirus (CMV), this infection continues to be a major complication in transplant recipients, causing considerable morbidity and occasionally mortality. There is wide variability in definitions of CMV infection, which can lead to conceptual errors. The present article attempts to standardize the definitions used, which have recently been revised and recommended by the American Society of Transplantation for the purpose of developing consistent reporting of CMV in clinical trials. The concepts of infection and viral replication, persistence and recurrence of infection, viremia and disease are discussed, together with the diagnostic criteria for febrile syndrome and visceral involvement. Methods for preventing CMV infection, universal prophylaxis and preemptive therapy are also mentioned., (Copyright © 2011 Elsevier España S.L. All rights reserved.)

Cytomegalovirus (CMV) is a β herpesvirus and a significant human pathogen. After primary infection establishes life long latency. In immunocompetent individuals cell-mediated host immune responses prevent the development of overt CMV disease. It has increasingly come to be recognized that critically ill patients are at risk for CMV reactivation from the latency. The risk factors associated to CMV reactivation in the critically ill are infection, sepsis, trauma, transfusions, major surgery, prolonged mechanical ventilation, steroids and vasopressors. In the pathogenesis are involved immunodysfunction and imbalance in immunomodulatory mediators principally tumor necrosis factor (TNF) and nuclear factor κB (NF-κB). Several studies have shown an association between CMV reactivation in immunocompetent critically ill patients and poor clinical outcomes. Further studies are warranted to identify subsets of patients who are at risk of developing CMV reactivation and to determine the role of antiviral agents on clinically outcomes in critically ill patients.

Introduction: The possible "infection"/interaction processes between sperm and different microorganisms are being under discussion nowadays. This process might include some viruses and even recent investigations are aiming to elucidate the mechanisms and the receptors that may be involved in this interaction. Furthermore, it has been reported the presence of some viral genomes within the sperm DNA, raising the possibility of transmitting the infection to the partner and offspring., Objective: The aim of this review is to describe the mechanisms by how viruses could possibly infect some seminal fractions. This is pursued by performing a literature review for answering the question: how the sexually transmitted virus could be infecting sperm?, Materials and Methods: We carried out a bibliographic review about sperm and virus interaction., Results: Some viruses interact with sperm cells; and sperm cells could transfer the viruses to offspring, however, in most cases, the receptors that allow this interaction are not clearly described., Conclusions: Based on the current information, new in vitro studies are needed to determine the role of sperm in spreading viruses of sexually transmitted infections.

Objective: To study the impact of initial cytomegalovirus (CMV) viral load on virological response to ganciclovir preemptive therapy in allogeneic stem cell transplant (SCT) recipients after 4 weeks of treatment., Methods: Eighty-one consecutive allogeneic SCT recipients were included. Preemptive therapy was initiated when CMV load was positive for 2 consecutive weeks or when a viral load >5000copies/mL was detected in 1 sample. If viral load was >400copies/mL after 2 weeks of treatment, maintenance treatment with ganciclovir was continued for 2 additional weeks. Virological failure was defined as a CMV load >400copies/mL after 4 weeks of treatment., Results: Ganciclovir preemptive therapy was initiated in 32 patients (39.5%) who had 39 episodes of CMV replication. Virological failure occurred in 16 patients (50%) after 18 episodes of replication (46%). Clinical failure additionally occurred in 2 episodes (5%). The only risk factor for virological failure was a peak viral load >20,000copies/mL at the beginning of treatment (OR 5.88; 95% CI: 1.49-25, P=.03). The main risk factor for CMV replication >20,000copies/mL at the start of treatment was the presence of grade II-IV acute graft-versus-host-disease (OR 16; 95% CI: 8.5-45)., Conclusion: CMV viral load >20,000copies/mL is the main risk factor for virological failure after 4 weeks of ganciclovir preemptive therapy following SCT., (Copyright 2008 Elsevier España, S.L. All rights reserved.)

Ganciclovir is the drug of choice for the treatment of acute cytomegalovirus infections. This antiviral agent is a nucleoside analog of guanine whose activity is dependent upon its intracellular phosphorylation to the triphosphate derivative. Foscarnet is used to treat immunosuppressed patients such as organ transplant recipients and AIDS patients with cytomegalovirus who do not tolerate or develop resistance to ganciclovir. Foscarnet is a pyrophosphate analog that directly inhibits viral DNA polymerase. Resistant isolates have been recovered from immunocompromised patients treated with both anticytomegalovirus compounds. The aims of this study were to prepare a plaque reduction assay to study the in vitro susceptibility of cytomegalovirus to ganciclovir and foscarnet, and to apply it to the knowledge of in vitro susceptibility values of cytomegalovirus isolated from clinical samples. Eighty isolates from patients who had never been treated with ganciclovir or foscarnet were tested for antiviral susceptibility. The plaque reduction assay took 6-8 weeks. The results are expressed as ID(50) (inhibitory dose 50), and the ID(50) values of ganciclovir were between 2.14 and 13.49 microM. The ID(50) for ganciclovir was higher that 12 microM in only two cases (2%). The molecular study of the DNA of these did not show any mutation in the UL97 gene. The ID(50) values of foscarnet were between 46.65 and 460.22 microM. In 78 cases (98%) foscarnet ID(50) was lower than 400 microM. These results were comparable with those obtained by other authors. To summarize, the frequency of cytomegalovirus strains resistant in vitro to ganciclovir and foscarnet in previously untreated patients was low and when it was present it did not involve therapeutic failure since the patients progressed favorably.

We performed an evaluation of early cytomegalovirus antigen detection (Shell-vial method) for rapid diagnosis of cytomegalovirus infection in patients at risk. A comparative, parallel, prospective study against conventional cell culture in 913 clinical specimens was carried out. Shell-vial technique detected an early cytomegalovirus antigen in culture using an indirect immunofluorescent method with monoclonal antibodies. Cytomegalovirus was detected in 210 specimens (23.0%). In 24 instances (11.4%), cytomegalovirus was only detected by culture, in contrast with 54 specimens (25.7%) that were only positive in Shell-vial (p less than 0.001; McNemar test). Mean detection time for cell culture was 9.2 days, and 16-24 h for the Shell-vial technique. This is a rapid, sensitive, specific and simple to perform method for diagnosis of cytomegalovirus infection. Nevertheless, the predictivity of cytomegalovirus disease was not improved by this technique.