E' pericolosa? Come si cura? Seguici su. Ultima modifica Classificazione dei virus Vaccini antivirali. Pap test e prevenzione Vedi altri articoli tag Pap test - Screening. Moltiplicazione dei virus Vedi altri articoli tag Virus. Virus I virus, termine che in latino significa "veleno", sono microrganismi acellulari parassiti obbligati. Malattie causate da virus e farmaci antivirali Quando il virus infetta l'organismo si parla di patogenesi virale; essa consta di fasi distinte: 1a tappa: ingresso del virus nell'ospite tratto respiratorio e digerente, per via sessuale, attraverso punture di antropodi, ferite ecc.
HCV antibodies were detected in 4. Moreover, globally it is estimated that more than 70 million people have been infected with HCV, which is increasingly being associated with CV disease 28 and is considered a major cause of viral myocarditis in Japan Yet still, our epidemiological data is likely vastly under-representative of the true prevalence and contribution of viruses in heart failure, given that the majority of viral infections are asymptomatic or subclinical and are frequently not suspected or recognized as contributing to or exacerbating disease in the context of heart failure.
Confounding these issues, due to our inability to suspect viral involvement from the onset our ability to screen for viruses and diagnose these conditions is severely limited 8 , 9 , Treatment options thus remain mostly supportive, often consisting of mechanical circulatory support and heart transplantation as a means of ensuring patient survival 59 , Previous studies have implicated the detection of cardiotropic viral genomes, including adenoviruses, B19V, EBV, CMV, enteroviruses and herpes simplex viruses, with adverse outcomes and premature cardiac transplant rejection 61 , One study demonstrated that the patients in which viral genomes were detected were 6.
Moreover, adenovirus detection was associated with the highest mortality rate among heart transplant recipients who were virus postive CMV seropositivity was also identified as a risk factor for poor outcomes in the context of transplant rejection The prevalence and types of viruses identified in the context of transplant rejection has also shifted over time, with enteroviruses giving way to adenoviruses in the s, followed by an increase of B19V in the s In our cohort, we report the detection of cardiotropic viruses in In both patients, EBV was detected.
Our results merely indicate that the prevalence of viruses in transplant patients is higher than perhaps previously anticipated. However, given the findings in previous studies that viral genome presence results in poor outcomes of graft rejection, the case can be made that standard of care for individual cardiac transplant recipients could include the screening for cardiotropic viruses as a part of their routine endomyocardial biopsy process if causation is further established with future research.
Moreover, further consideration and research may be devoted to the treatment of such conditions. However, a delicate balance must be found with patients receiving immunosuppressive therapies. Among the key findings in the present study is the detection of replicating viruses within a lesion of cardiac sarcoidosis Fig. To our knowledge, this is the first report of actively replicating virus within a granulomatous lesion consistent with sarcoidosis.
Such findings could implicate viruses as antigenic triggers for the underlying granulomatous inflammatory response, the hallmark of sarcoidosis. Currently, immunosuppressive therapy is standard of care treatment for sarcoidosis, despite inconclusive evidence of its benefit 64 , Thus, as with many modalities of heart failure, therapy is largely supportive, involving standard of care heart failure medications, mechanical assist devices and cardiac transplantation 66 , Our findings speak to the need for further investigation in order to rule out viral etiology as a pathogenic trigger responsible for causing genetically susceptible individuals to develop cardiac and systemic sarcoidosis.
In the current study, B19V was detected in 3. Our study revealed the presence of actively replicating B19V among The prevalence of B19V among patients with DCM or myocarditis in our cohort is considerably lower than the prevalence quoted in previous reports 18 , A recent meta-analysis demonstrated that the prevalence of B19V in endomyocardial biopsies of patients with myocarditis or DCM It is noteworthy that of all three patients in our cohort positive for B19V 2 DCM and 1 eosinophilic myocarditis , at least one additional actively replicating virus was detected within the same tissue.
Our study thus supports that B19V acts as a bystander virus, or at least that actively replicating B19V is at a much lower prevalence than has been reported in previous studies, which were reliant upon PCR for detection and did not provide spatial or morphological context of actively replicating viruses within the heart.
The contribution of cardiotropic viruses in initiation and exacerbation of heart failure is often not suspected or confirmed clinically and therefore is likely significantly underreported.
Moreover, when virus-associated heart failure is suspected clinically most commonly in myocarditis , current diagnostic techniques such as PCR are insufficient to detect viral RNA in the heart in a manner that would affirm causation.
As such, PCR does not provide the spatial context 36 , 69 i. In addition, PCR has considerable potential for false positivity 46 , 70 , as viral presence in the blood is indistinguishable from viral presence in tissue 71 , making it exceedingly difficult to implicate viruses as potential pathogenetic agents.
For example, EBV is among the most prevalent, ubiquitous infections worldwide Thus, it is difficult to determine whether EBV infection is causative under certain conditions of heart failure or whether the virus is merely a bystander. Although in rare cases EBV has been implicated in acute myocarditis 49 , exacerbation of coronary events 50 and heart failure 51 , definitive evidence of causation remains elusive.
Further, these studies were reliant upon detection of neutralizing antibodies for EBV in patient blood. The method of in situ hybridization demonstrated here corrects for and addresses these challenges by providing morphological context as to whether virus is present in the tissue and in which cell types, while simultaneously distinguishing between replicating and template strands of viral RNA and detecting low copy RNA.
Our method thus applies a highly sensitive technique of in situ hybridization capable of detecting single copies of RNA with high specificity and reduced background. While our study has found that viral prevalence in patients with end-stage heart failure is much more common than currently reported, causation cannot be attributed.
Accordingly, our research may serve to inspire future research in order to determine the causative relationship between viruses and various heart failure conditions. In the present study, we designed and developed advanced methodology for the detection of cardiotropic viruses in a heart failure cohort to examine the prevalence and phenotype of cardiotropic viruses associated with a spectrum of conditions.
Specifically, we designed and developed a custom tissue microarray from explanted and autopsy hearts with a variety of clinically diagnosed, pathologist-confirmed, acute inflammatory viral myocarditis, lymphocytic myocarditis, eosinophilic myocarditis, transplant rejection, sarcoidosis, GCM , chronic chronic active myocarditis in the context of DCM, non-inflammatory DCM and CAD and genetic HCM, ARVC conditions from selected regions of pathological significance.
Subsequently, we employed a newly emerging in situ hybridization technology uniquely capable of detecting a single RNA molecule with high specificity to identify a panel of common cardiotropic viruses. This method further provides spatial context within our cohort of heart failure patients, creating a snapshot of viral prevalence among various heart conditions.
Overall, AAV2 was the most prevalent virus in our cohort, detected in AAV2 was associated with concurrent infection in AAV2 and CMV were both detected in one patient described above, which likely contributed to the exacerbation of orthotropic rejection. The finding of AAV2 in the context of transplant rejection is consistent with previous literature 52 , 61 , We additionally report several novel findings, including the first account of the detection of HCV and EBV within a lesion of cardiac sarcoidosis, and the presence of CVB3 in GCM and the overall presence of viruses across a spectrum of heart failure manifestations, all of which warrant further investigation.
Considering the high rate of virus detection in our cohort Thus, the combination of a TMA and a highly specific and sensitive in situ hybridization method yields a powerful, high-throughput diagnostic tool which may be implemented in clinical settings to identify pathogenetic viral agents in the context of heart failure.
In turn, implementing such as standard of care in the settings of patients for whom reoccurring endomyocardial biopsy is performed may provide avenues for personalized treatment i. Our cohort of heart failure patients is diverse, which is representative the variability of diagnosis among patients at our research center and in the general population. Patient selection also resulted from the availability of samples in our biobank. As a result of the limited sample size and high heterogenity among patient clinical presentation, even among those with the same diagnoses, some of our research results have only been observed in a small cohort of patients.
For example, our novel finding of viral involvement in cardiac sarcoidosis was only reported in one patient due to these limitations. As such, our research is a starting point for further investigation of the role of cardiotropic viruses in heart failure, for which it is recommended that larger sample sizes of more homogenous patient tissues are utilized for pathological review.
Another limitation of the current study was not including an exhaustive panel of all known cardiotropic viruses, including human herpesvirus 6 HHV6 , another virus responsible for causing cardiomyopathy. However, our rather extensive panel of cardiotropic viruses includes those that have historically and regionally been shown to play a role as initial triggers and in the exacerbation of heart failure.
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Coronavirus Actualidad Enfermedades Virus Medicina. Foto: Cordon Press. Virus de la rabia El virus de la rabia Familia Rhabdoviridaees , es un virus monocatenario. Norovirus Estos virus de la familia Caliciviridae son los responsables de fuertes gastroenteritis.
Virus de la viruela bovina El virus de las viruela bovina, Cowpox virus , pertenece a la familia Poxviridae,.
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