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Out of Nowhere
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
Over the past 30 years, three basic methods for detecting infection and/or disease with Ebola virus have been developed for use in clinical laboratory settings: serologic tests that detect host antibodies generated against the virus; antigen tests that detect viral proteins; and molecular tests that detect viral RNA sequences. In the early years, serologic tests were used to confirm the cause of disease outbreaks because antiviral antibodies persist for years following infection. However, the variable onset of antibody responses during acute illness makes serology much less useful in the acute setting. Antigen detection and molecular tests are very effective for acute diagnosis as virus levels in the blood typically rise to high levels as soon as symptoms begin. No tests reliably detect Ebola virus prior to the onset of symptoms.
Diagnostic Approach to Fulminant Hepatitis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Ebola, also called Ebola hemorrhagic fever, is a viral hemorrhagic fever of humans caused by the Ebola virus, a member of the Filoviridae family. It is spread by direct contact with body fluids, such as blood, stool, and vomitus of an infected human. Ebola is characterized by fever, fatigue, vomiting, diarrhea, rash, kidney, liver failure, and occasionally bleeding. It is associated with a high case fatality rate of 54.7%, with fatality rates reported to increase with age and high viral load [28]. Patients with Ebola virus disease were found to have AST/ALT levels of more than five times the upper limit of normal and, in severe cases, levels of more than 15 times the upper limit of normal [29]. Diagnosis of Ebola can be made by serum PCR on blood drawn within 3 days of the onset of symptoms. A rapid chromatographic immunoassay (ReEBOV) that detects Ebola virus antigen can provide results within 15 minutes; however, this has been associated with false-positive results in 10% of patients who tested negative by PCR [30]. On postmortem liver biopsy, hepatocellular necrosis with minimal inflammation is the primary histological finding. There is no specific therapy for Ebola, and treatment includes fluids and supportive care.
Marburg and Ebola Virus Infections
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
The index case in Zaire may have been a man who had been admitted to Yambuku hospital with suspected malaria about 2 months after EHF was first recognized in Sudan. He was treated with parenteral chloroquine, recovered rapidly and went home. About 5 days later his fever recurred, and he was readmitted to the hospital with gastrointestinal bleeding. He died a week after onset of the second illness. At the time of his admission, one of two autoclaves in the hospital broke down. Consequently, the autoclaving program for most of the hospital was temporarily suspended. This included the routine autoclaving of syringes and needles. Instead, clean syringes were issued daily with instructions that these were to be rinsed in alcohol followed by sterile saline each time they were used. This was not done, but sometimes the syringes were boiled at the end of the day. Investigations revealed that Ebola virus was transmitted by injection to many patients.10 These included 82 pregnant women who attended the antenatal clinic, as well as hospital staff who received typhoid vaccine in an attempt to control what investigators believed might be a typhoid epidemic. Up to 25% of the pregnant women aborted before they died. Injection was believed to be the prime mechanism by which a massive secondary infective pool was generated from a common source; from this pool further spread occurred, mainly by direct contact, and up to five generations of virus transmission were recorded.
The roles of epidermal growth factor receptor in viral infections
Published in Growth Factors, 2022
So far, there is no specific drug to treat DENV infection. Bekerman et al. (2017) have revealed the antiviral activity of combined treatment of erlotinib and sunitinib in two DENV-infected IFN-α/β and IFN-γ receptor-deficient murine models, AG129 and AG-B6. Erlotinib is a reversible EGFR inhibitor approved for the treatment of metastatic NSCLC and pancreatic cancer, whereas sunitinib is an ATP-competitive multitargeted tyrosine kinase inhibitor approved for the treatment of renal cell carcinoma, gastrointestinal stromal tumour, and pancreatic neuroendocrine tumour (Shukla et al. 2009; Blumenthal et al. 2012). Prophylactic and daily combined treatment of erlotinib and sunitinib at 30 mg/kg respectively resulted in 11-fold reduction in DENV viremia in infected AG-B mice. This combined treatment also reduced morbidity and mortality in AG-129 and AG-B6 mice infected with lethal DENV inoculum. In addition to DENV, Bekerman et al. also demonstrated that the combined treatment inhibited Ebola virus (EBOV) infection in vivo. EBOV is one of the members of family Filoviridae that causes haemorrhagic fever associated with 50–90% human mortality. It is an enveloped virus that consists of non-segmented, single stranded and negative-sense RNA genome (Lee et al. 2008). Prophylactic and daily treatment of erlotinib and sunitinib at 45 and 5 mg/kg respectively reduced morbidity and mortality in EBOV-infected mice, as evidenced by greater weight gain and 50% survival (Bekerman et al. 2017). However, little is known on the role of EGFR in EBOV infection.
Characteristics of patients with ST-segment elevated myocardial infarction (STEMI) at the initial stage of the COVID-19 pandemic: a systematic review and meta-analysis
Published in Infectious Diseases, 2021
Yuhang Zhu, Wanying Xing, Hui Wang, Jun Song, Zhixia Sun, Xingzhao Li
An increased time from symptom onset to FMC was also observed, which could be caused by the following reasons [1]: At the initial stage of the COVID-19 pandemic, STEMI patients were likely to be worried that they would come into contact with patients infected with SARS-CoV-2 in the hospitals so that they would also become infected. When they had only mild symptoms, some STEMI patients were likely to not call for emergency treatment and went to medical institutions on their own. Only when the symptoms became serious, a medical contact became necessary, resulting in a longer time from symptom onset to FMC [31]. In the Ebola epidemic in West Africa in 2013, a similar situation occurred due to the fear of being infected by Ebola virus in the hospital, which was proven by an investigation after the outbreak [50]. Citizens of various countries have taken different self-isolation measures [2]. Some people voluntarily isolate themselves due to fear of being infected by SARS-CoV-2, while others only self-isolate under the pressure of the government or dissuasion by their relatives [51]. When typical symptoms of STEMI such as chest pain occurred in patients who lived alone, it may have been difficult for them to seek medical treatment by their own efforts.
Defibrotide: potential for treating endothelial dysfunction related to viral and post-infectious syndromes
Published in Expert Opinion on Therapeutic Targets, 2021
Edward Richardson, David García-Bernal, Eleonora Calabretta, Rubén Jara, Marta Palomo, Rebecca M. Baron, Gregory Yanik, Jawed Fareed, Israel Vlodavsky, Massimo Iacobelli, Maribel Díaz-Ricart, Paul G. Richardson, Carmelo Carlo-Stella, Jose M. Moraleda
Severe manifestations of the Ebola virus including overt hemorrhage, shock, lymphopenia, and thrombocytopenia. Excessive proinflammatory cytokine production and absence of immune responses are recognized as major factors in the development of these phenomena [69]. As the Ebola virus infects monocytes, macrophages, dendritic cells, and ECs, direct infection may also contribute to disruption of endothelial homeostasis [70]. Widespread endothelial activation and dysfunction are an integral component of pathogenesis, leading to loss of vascular integrity, increased vascular permeability, and activation-dysregulation of the coagulation pathway [66]. This presents the endothelium as an attractive target in therapeutic approaches for Ebola virus infection, a disease with few established therapeutic strategies. Indeed, statins and ARBs have been utilized for their endothelial protective effects in the treatment of Ebola virus infection, with reported improvements in patient mortality [71]. As DF also protects endothelium and may similarly downregulate the Ang-II signaling axis, DF may also achieve therapeutic effects in patients with Ebola virus infection. As cytokine storm is recognized as a critical factor in Ebola virus disease; moreover, DF may stand to modulate the impact of excessive cytokine production on the endothelium. To our knowledge, DF has not been utilized in the treatment of these infections.