Mode of transmission of Ebola virus infection: Transmission of Ebola virus occurs when man consumes the flesh of fruit bats, flesh of animals fed on infected fruit bats, or through contacting or touching any contaminated matter with the virus  

Mode of transmission of Ebola virus infection: Transmission of Ebola virus occurs when man consumes the flesh of fruit bats, flesh of animals fed on infected fruit bats, or through contacting or touching any contaminated matter with the virus  

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Ebola hemorrhagic fever is a lethal viral disease transmitted by contact with infected people and animals. Ebola infection represents a worldwide health threat causing enormous mortality rates and fatal epidemics. Major concern is pilgrimage seasons with possible transmission to Middle East populations. In this review, we aim to shed light on Ebola...

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... Cytokines including TNFα, IFNγ, IL-1β, IL-2, IL-6 and IL-10 have been linked to the pathogenesis of other viral hemorrhagic diseases, such as dengue [73][74][75][76][77], and Ebola [78,79]. However, data have so far been lacking as to whether cytokines facilitate the immune response in fighting infection, suppression of the immune response is part of EEHV pathogenesis, or whether over activation contributes to disease progression through a 'cytokine storm' that often occurs in the terminal stages of Ebola and other viral diseases [80]. ...
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Hemorrhagic disease (HD) caused by a group of elephant endotheliotropic herpesviruses (EEHV) is one of the leading causes of death for young elephants in human care. These viruses are widespread and typically persist latently in adult elephants with no negative effects; however, in juvenile Asian and more recently young African elephants, the onset of disease can be rapid and the mortality rate high. Measuring biomarkers associated with the immune response could be beneficial to understanding underlying disease processes, as well as the management of infection and HD. The goal of this study was to measure acute phase proteins and cytokines in serum collected from elephants infected with EEHV (13 Asian and 1 African) and compare concentrations according to presence, severity and outcome of disease. Serum amyloid A (SAA) and haptoglobin (HP) were higher in elephants with EEHV viremia than those without; concentrations increased with increasing viral load, and were higher in fatal cases compared to those that survived. In Asian elephants, SAA was also higher during EEHV1 viremia compared to EEHV5. Cytokine concentrations were typically low, and no statistical differences existed between groups. However, in individuals with detectable levels, longitudinal profiles indicated changes in tumor necrosis factor alpha (TNF-α) and interleukin-2 (IL-2) that may reflect an immune response to EEHV infection. However, the overall low concentrations detected using previously validated assays do not support the presence of a ‘cytokine storm’ and suggest more work is needed to understand if sub-optimal immune responses could be involved in disease progression. These results highlight the potential benefit of measuring circulating biomarker concentrations, such as APPs and cytokines, to improve our understanding of EEHV viremia and HD, assist with monitoring the progression of disease and determining the impact of interventions.
... It has severely affected the areas of central Africa and sub-Saharan Africa, principally Gabon, Congo, Uganda, and Sudan. In 2014, approximately 11,325 people have passed away due to EVD (66). For this reason, WHO stated this outbreak as a public health emergency of global alarm (67). ...
... Evaluation of natural products (including TQ) for the treatment of EVD may be recognized as a progressed drug, as TQ could be a medicinal nutrition or nutritional supplement for treating EVD (67,68). TQ has been reported to inhibit the lipopolysaccharide-induced inflammatory processes by suppressing the activities of potent inflammatory mediators along with reducing the concentration of NO that plays a major role in the pathogenesis of EVD (66). However, more experiments are needed to use TQ against EVD clinically. ...
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... Some patients have been observed to experience pulmonary edema, vascular leakage, tachypnea, dyspnea, hypoxemia, and pneumonia, which may cause acute respiratory failure and even acute lung injury in later stages of EVD. 15,19 ...
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... Acute "DIC" is due to DIT-associated hepatic coagulopathy One remaining, very pertinent question is: "what is the correct diagnosis for acute/decompensated/overt "DIC" that is associated with abnormal coagulation profile?" The answer is clear since "DIC" is often associated with hepatic diseases [1,15,[116][117][118][119][120]. In endotheliopathy-associated DIT, hepatic coagulopathy could occur as a phenotype of acute fulminant hepatic failure or acute hepatic necrosis as seen in critical illnesses [15,90,[116][117][118][119][120]. ...
... The answer is clear since "DIC" is often associated with hepatic diseases [1,15,[116][117][118][119][120]. In endotheliopathy-associated DIT, hepatic coagulopathy could occur as a phenotype of acute fulminant hepatic failure or acute hepatic necrosis as seen in critical illnesses [15,90,[116][117][118][119][120]. The pathogenesis unknown hepato-renal syndrome [121][122][123] and hepatic encephalopathy [15,121] are very much consistent with endotheliopathy-associated DIT similar to "DIC" syndrome. ...
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TTP is characterized by microangiopathic hemolytic anemia and thrombocytopenia associated with brain and kidney dysfunction. It occurs due to ADAMTS13 deficiency. TTP-like syndrome occurs in critically ill patients with the similar hematologic changes and additional organ dysfunction syndromes. Vascular microthrombotic disease (VMTD) includes both TTP and TTP-like syndrome because their underlying pathology is the same disseminated intravascular microthrombosis (DIT). Microthrombi are composed of platelet-unusually large von Willebrand factor multimers (ULVWF) complexes. TTP occurs as a result of accumulation of circulating ULVWF secondary to ADAMTS13 deficiency. This protease deficiency triggers microthrombogenesis, leading to “microthrombi” formation in microcirculation. Unlike TTP, TTP-like syndrome occurs in critical illnesses due to complement activation. Terminal C5b-9 complex causes channel formation to endothelial membrane, leading to endotheliopathy, which activates two different molecular pathways (i.e., inflammatory and microthrombotic). Activation of inflammatory pathway triggers inflammation. Activation of microthrombotic pathway promotes platelet activation and excessive endothelial exocytosis of ULVWF from endothelial cells (ECs). Overexpressed and uncleaved ULVWF become anchored to ECs as long elongated strings to recruit activated platelets, and assemble “microthrombi”. In TTP, circulating microthrombi typically be lodged in microvasculature of the brain and kidney, but in TTP-like syndrome, microthrombi anchored to ECs of organs such as the lungs and liver as well as the brain and kidneys, leading to multiorgan dysfunction syndrome. TTP occurs as hereditary or autoimmune disease and is the phenotype of ADAMTS13 deficiency-associated VMTD. But TTP-like syndrome is hemostatic disorder occurring in critical illnesses and is the phenotype of endotheliopathy-associated VMTD. Thus, this author’s contention is TTP and TTP-like syndrome are two distinctly different disorders with dissimilar underlying pathology and pathogenesis.
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... Currently there is a predominant call for increasing and fast-tracking research on diagnostic, preventive and curative interventions. 24 It is obvious that a rapid test, cure or vaccine would be true game changers, but as always the delivery of such new interventions will require complementary innovative programmatic approaches. ...
... The virus enters through mucosal surfaces, cut or lesions of the skin, or direct transfer. Cells like monocytes, macrophages, dendritic cells, hepatocytes, and endothelial cells are the targets of EBOV (Feldmann et al. 1996;El Sayed et al. 2016). Epithelial, endothelial fibroblasts, hepatocytes, and adrenal gland cells are also infected (Olejnik et al. 2011). ...
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Ebola virus (EBOV) is an extremely contagious pathogen and causes lethal hemorrhagic fever disease in man and animals with high fatality rates. The recently occurred Ebola virus disease (EVD) outbreaks in the West African countries have categorized it as an international health concern. For the virus maintenance and transmission, the non-human primates and reservoir hosts like fruit bats have played a vital role. Furthermore, the virus may also get transferred through contaminated biological fluids like breast milk, tears, urine, semen, blood, etc. For curbing the disease timely, we need effective therapeutics/prophylactics, however, in the absence of any approved vaccine, timely diagnosis and monitoring of EBOV remains of utmost importance for restraining the EVD incidences. The technologically advanced vaccines like a viral-vectored vaccine, DNA vaccine and Virus-like particles (VLPs) are underway for testing against EBOV. In the absence of any effective control measure, the adaptation of high standards of biosecurity measures, strict sanitary and hygienic practices, strengthening of surveillance and monitoring systems, imposing appropriate quarantine checks and vigilance on trade, transport, and movement of visitors from EVD endemic countries remains the answer of choice for tackling the EBOV spread. Herein, we converse with the current scenario of EBOV giving due emphasis on animal and veterinary perspectives along with advances in diagnosis and control strategies to be adopted, lessons learned from the recent outbreaks and the global preparedness plans. To retrieve the evolutionary information, we have analyzed a total of 56 genome sequences of various EBOV species submitted between 1976 and 2016 in public databases.
... Another word, "What is the correct diagnosis for "DIC" that is associated with abnormal coagulation profile?" In Ebola, acute fulminating hepatitis/acute hepatic necrosis, especially multifocal necrosis type, occurs without a good explanation [5,[36][37][38][39][40]. With "two-activation theory" this can be easily explained by endotheliopathyassociated DIT/VMTD causing hepatic microthrombosis and acute hepatic necrosis syndrome, leading to hepatic coagulopathy [5]. ...
... Another word, What is the correct diagnosis for "DIC" that is associated with abnormal coagulation profile?" In viral hemorrhagic fevers, acute fulminating hepatitis/acute hepatic necrosis, especially multifocal necrosis type, occurs regularly without a good explanation [42][43][44][45][46]. Acute fulminant hepatitis and hepatic necrosis are not due to viral hepatitis, but are due to DIT. ...
Chapter
Male infertility is a condition where the males either become sterile or critically infertile. The World Health Organisation assessed that approximately 9% of the couple have fertility issues where the contribution of the male partner was estimated to be 50%. There are several factors that can amalgamate to give rise to male infertility. Among them are lifestyle factors, genetic factors and as well as several environmental factors. The causes of male infertility may be acquired, congenital or sometimes idiopathic. All these factors adversely affect the spermatogenesis process as well as they impart serious threats to male genital organs thus resulting in infertility. Viruses are submicroscopic pathogenic agents that rely on host for their replication and survival. They enter the host cell, hijack the host cell machinery to aid their own replication and exit the cell for a new round of infection. With the growing abundance of different types of viruses and the havoc they have stirred in the form of pandemics, it is very essential to decipher their route of entry inside the human body and understand their diverse functional roles in order to combat them. In this chapter, we will review how viruses invade the male genital system thus in turn leading to detrimental consequence on male fertility. We will discuss the tropism of various viruses in the male genital organs and explore their sexual transmissibility. This chapter will summarise the functional and mechanistic approaches employed by the viruses in inducing oxidative stress inside spermatozoa thus leading to male infertility. Moreover, we will also highlight the various antiviral therapies that have been studied so far in order to ameliorate viral infection in order to combat the harmful consequences leading to male infertility.