One Health
Rebecca A. Krimins in Learning from Disease in Pets, 2020
Ebola virus disease (EVD) was first recognized in 1976 in two separate outbreaks that occurred in the Democratic Republic of Congo (DRC) and what is now known as South Sudan.47 There is some evidence that implicates fruit bats of the Pteropodidae family as the reservoir host of this virus, and initial infection in humans is through close contact with bats or other infected animals, such as chimpanzees, gorillas, monkeys, forest antelope, and porcupines.48 Once infection in a person takes hold, person-to-person transmission is easily accomplished through close contact with blood, vomitus, sweat, urine, and other secretions and body fluids.49 The first case in the massive 2014–2016 outbreak that resulted in over 28,000 cases and 11,000 deaths is thought to have been an 18-month-old boy from a remote village in Guinea, who is speculated to have had contact with a bat.50,51 Further evidence of the role of bats in Ebola virus comes from the outbreak in the DRC in 2007, which was linked to people buying fresh-killed fruit bats to eat, bats that had migrated in large numbers and settled in fruit trees and palm trees of an abandoned plantation.52 Ebola virus was discovered in a bat in Liberia in 2018,53 and a new strain of Ebola (Bombali virus) was discovered in a bat in Sierra Leone in 2018,54 as well as in bats in Kenya and Guinea in 2019.55,56
Out of Nowhere
Rae-Ellen W. Kavey, Allison B. Kavey in Viral Pandemics, 2020
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.
African Cities and Ebola
Igor Vojnovic, Amber L. Pearson, Gershim Asiki, Geoffrey DeVerteuil, Adriana Allen in Handbook of Global Urban Health, 2019
Ebola virus disease (EVD), formerly known as Ebola hemorrhagic fever (EHF), is a severe viral illness caused by infection with one of the five known Ebola virus species (Zheng et al. 2015). The first cases of EVD occurred in 1976 in two simultaneous outbreaks, one in Nzara, Sudan (currently South Sudan) and the other in Yambuku, Zaire (currently the Democratic Republic of Congo (DRC)). The Zaire cases were mainly from Yambuku, a small village near the Ebola River, from which the disease takes its name. Similarly, the virus species have taken the names of places where subsequent outbreaks have happened, and these are: Zaire ebolavirus (ZEBOV), Sudan ebolavirus (SEBOV), Tai Forest ebolavirus (TAFV) (formerly known as Côte d’Ivoire ebolavirus), Bundibugyo ebolavirus (BEBOV) and Reston ebolavirus (REBOV). Of the five species, ZEBOV is the most pathogenic in humans, followed by SEBOV, BEBOV and lastly TAFV. REBOV is known only to be pathogenic to non-human primates (Feldmann and Geisbert 2011).
Ocular Toxoplasmosis Associated Dark Without Pressure
Published in Ocular Immunology and Inflammation, 2023
Paul J. Steptoe, Catherine M. Guly, Andrew D. Dick
The majority of DWP areas published to date have been observed in isolation (and therefore of unknown aetiology), commonly in the mid-peripheral fundus5–7,14 and regarded as benign entities.15 However, cases of perilesional DWP enable an insight into their underlying aetiology, where the cause is known. While perilesional areas of DWP have been reported adjacent to non-infectious lesions such as congenital hypertrophy of the retinal pigment epithelium,16 and choroidal osteomas,17 they have also been associated with infectious aetiologies such as Ebola retinal lesions.8 Over a 12-month observational period, 1 year following Ebola virus disease (EVD) infection, areas of DWP were observed to retract back towards EVD lesions in some cases, while in other examples were observed to both simultaneously expand and contract at opposing DWP margins suggesting the presence of an unknown prolonged intraretinal stimulus post-infection.8
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.
Related Knowledge Centers
- Body Fluid
- Ebolavirus
- Filoviridae
- Marburg Virus
- Mononegavirales
- Nucleotide
- Viral Hemorrhagic Fever
- Ebola
- Western African Ebola Virus Epidemic
- Species