What is the most powerful virus on Earth?

The "Ebola" virus has the highest mortality rate ever discovered by mankind, ranging from 50% to 90%. This virus was first discovered in 1967 in Marburg, Germany, but at that time did not attract people's attention. 1976 in southern Sudan and Zaire that is now the Democratic Republic of the Congo (DRC) in the Ebola River region again found its existence, only to attract the medical profession's widespread concern and attention, "Ebola" thus named. "Ebola" virus is shaped like the ancient Chinese "Ruyi", extremely active, the virus is mainly transmitted through body fluids, such as sweat, saliva or blood, the incubation period of about 2 weeks. The incubation period is about 2 weeks. Infected people suddenly develop high fever, headache, sore throat, weakness and muscle pain. This is followed by vomiting, abdominal pain, and diarrhea. Within two weeks after the onset of the disease, the virus spills over, leading to internal and external bleeding, blood coagulation, necrosis of the blood quickly spread to various organs throughout the body, the patient eventually develops symptoms such as bleeding from the mouth, nose and anus, and the patient can die within 24 hours. Its mortality rate is as high as 50% or even 90%. According to the World Health Organization, so far, the virus has infected about 1,500 people, of which about 1,000 died. In addition to the transmission of the "Ebola" virus through blood and human secretions, contact with medical equipment contaminated by the patient's blood may also be infected. The disease spreads so quickly that all patients must be quarantined as soon as they are detected, and those who have been in contact with the patient must undergo regular checkups. At present, the global medical community has not yet found a vaccine to prevent this disease or a drug that can cure it. However, with timely control measures and strict isolation of the affected area, the spread of the virus can be quickly contained. Chronicle: Tracking Ebola and the Marburg Virus Marburg, Germany - This quiet town north of Frankfurt, with its beautiful scenery and many famous historical monuments, doesn't look like it has ever been ravaged by the deadly virus that gave it its name. in August 1967, when a lab worker had a sudden attack of high blood pressure, he was in the middle of an attack on a laboratory. The town's tranquility was shattered when a lab worker suddenly developed high fever, diarrhea, vomiting, hemorrhaging, shock and circulatory failure. Local virologists quickly investigated the cause - such symptoms were also seen in Frankfurt and Belgrade (the capital of Yugoslavia) - all three laboratories had used monkeys from Uganda for research such as the polio vaccine. In one case, 37 people, including lab workers, medical staff, and their relatives, were infected with the inexplicable disease, and a quarter of them died. 3 months later, German experts found the culprit: a dangerous new virus, in the shape of a serpentine rod, that had been transmitted from monkeys to humans. The Marburg virus disappeared as mysteriously as it came, with only one case reported in South Africa as late as 1975. But by 1976, a close relative of the virus, Ebola, struck another wave of terror in the Democratic Republic of the Congo*** and country (DRC, formerly Zaire), killing 280 people. Since then, Ebola, Marburg and other deadly "hemorrhagic fever viruses" have become almost mythical. Last month, in the run-up to the Ebola outbreak in Uganda and in the middle of the Marburg rampage at the DRC, about 100 experts on Ebola and Marburg met in Marburg to discuss recent findings. This is despite the fact that there are many unanswered questions, such as where do the viruses lurk when they are not prevalent and how do they cause these devastating symptoms? The truth is that there have been new breakthroughs in research for new treatments and vaccines. Research includes the creation of genetically engineered Ebola viruses, a powerful molecular tool for analyzing their pathogenic mechanisms, in addition to studies using Ebola vaccines in monkeys. Mysterious host While the Ebola outbreak in Uganda has dominated newspaper headlines, the DRC is suffering from an invasion of the Marburg virus. According to Jean Muyembe-Tamfum of the National Institute of Biomedical Research (NIBR) in Kinshasa (Zaire's capital) and Stuart Nichol of the Centers for Disease Control (CDC) in Atlanta, GA, the epidemic began in November 1998 north of the town of Durba, and gold miners outside Durba were among the first to die. But the remoteness of the area and the government's war at the time meant that CDC and WHO experts did not learn of it until the following May. the epidemic reached its peak in mid-1999, and new cases were not known until September 2000, by which time 99 people had been infected, with a death rate of more than 80 percent. More than half of the deaths were among gold miners, which provides insight into the origin of the virus. Nichol and colleagues at the National Institute of Virus Research in Johannesburg, South Africa, along with virologist Robert Swanepoel, sequenced some of the genes of the Marburg virus. Strikingly, the virus is extremely genetically variable, coming from the same ancestor, with a full 16 percent of the nucleotide sequences differing. In contrast, the strain of the virus that caused the 1995 Ebola pandemic in Kuwait, DRC, which infected 315 people, had no genetic variation at all. From Durba, it is known that Marburg virus infected the population at least seven separate times. These findings suggest that this rare microbe is creating new transmissions in populations. In search of an animal host for the virus, the team captured at least 500 bats in the gold mine. Many scientists believe that the natural hosts of Marburg and Ebola are animals, such as rodents or monkeys, because people are in constant contact with them (Science, 22 October 1999, p. 654.) Swanepoel had experimentally caused bats to become infected with Ebola in the early days, so bats could have been the earliest source of infection. But today Nichol announced that this speculation is probably wrong, as most of the bats tested up to this meeting showed no signs of Marburg virus infection. But there is a glimmer of hope: some bats may carry the virus, and other hosts-including arthropods, insects, spiders, etc.-should be considered. Broken capillaries? The mechanism of the devastating symptoms (shock and hemorrhage) caused by Marburg and Ebola are equally complex. Earlier studies have shown that the virus attacks a wide range of cells, particularly the giant eosinophils of the immune system and hepatocytes. Whether vascular endothelial cells are directly attacked by Ebola and Marburg is unclear. Some researchers (not all) believe that damage to these cells causes blood in the capillaries to flow backwards into peripheral organs, resulting in a collapse of the circulatory system and rapid death. The critical role of endothelial cell damage has been affirmed by CDC pathologist Sherif Zaki, who found severe damage to the capillary endothelium through autopsies of Ebola victims in Kuwait, and by virologist Gary Nabel, director of the NIH Vaccine Research Center. To find the cause of the damage, Nabel's team, along with CDC and NIH, genetically engineered human endothelial cells to express the Ebola protein GP (GP protein is the viral capsid protein), and the results were published in the August issue of Nature Medicine. The results of the experiment were astonishing; within 24 hours, the cells stopped adhering to each other, and within a few days, the cells died. If the gene encoding GP is expressed directly on blood vessels from humans or pigs, the vessels lose most of their endothelial cells within 48 hours, become more permeable, and turn into flowing fluid. In Ebola and Marburg virus damage, "increased endothelial permeability and damage to capillaries appear to be key to the pathologic damage," says CDC virologist Brian Mahy. However, other researchers disagree, with Susan Fisher-Hoch, a virologist at Jean Mérieux Laboratories in Lyon, arguing that victims of Ebola and Marburg viruses do not have symptoms of capillary leakage, such as pulmonary edema and head and neck swelling, and that it is only survivors recovering from severe shock-like symptoms who have severe endothelial cell damage. This is supported by preliminary findings of Ebola virus infection in experimental monkeys reported by Thomas Geisbert of the Institute for Research on Infectious Diseases at the U.S. Army Hospital in Maryland (USAMRIID). Their results of looking at different stages of infection at the time of symptom severity showed that, knowing the end of the disease course, there was only a small amount of damage to the endothelium. This issue requires continued deliberation. Designing Ebola A study by Viktor Volchkov, a molecular virologist at the Claude Bernard University of Lyon, has made it potentially easier to study the mechanism of infection: genetically engineering the Ebola virus, which has made it possible to study the function of key lethal genes and proteins by mutation. "That's the most exciting thing about this meeting," Fisher-Hoch said. Last year, Volchkov, along with colleagues at the Marburg Institute for Virus Research, clarified the genetic sequence of Ebola: 18,959 bases of single-stranded RNA.The researchers are now employing the complementary strands of the Ebola genome to construct a DNA molecule.Introducing this DNA into a cell line with expression of the four key proteins of Ebola, including the structural protein GP, the cell line can then produce a new RNA Ebola virus. The result is that the lab has created a virus that can be transfected to other cell lines and is fully infectious. "We can now answer all the questions about Ebola virulence and pathogenesis," says Bray. By altering the sequence of complementary DNA, Volchkov's group has developed an Ebola mutant that accounts for the virus' lethal effects. mutations in the genes encoding the GP proteins (the most virulent proteins) allow the virus to replicate more proteins. volchkov has determined that the virus has a GP-producing "self-control" mechanism that prevents the virus from developing a "self-control" mechanism. Volchkov determined that the virus had a GP-generating "self-control" mechanism that prevented those infected cells from being killed before the virus could spread to other, non-infected cells, and Feldmann saw in this a strategy that could lead to the creation of a genetically engineered vaccine. For several years, vaccine researchers have been working to make vaccines against Marburg and Ebola, and experiments in Guinea pigs and monkeys have been successful. At the conference, Nabel reported on his new advances in DNA vaccines. Using a so-called "prime-boost" vaccine technique, Nabel and colleagues-including Nancy Sullivan, a postdoctoral fellow at NIH, and Anthony Sanchez of the CDC-injected four monkeys with DNA vaccines containing "naked DNA. Nabel and colleagues - including Nancy Sullivan, a postdoctoral fellow at NIH, and Anthony Sanchez at CDC - injected the four monkeys with a vaccine containing "naked DNA" that was complementary to the gene for Ebola's GP protein, and then injected the gene with an adenoviral vector. The immunized monkeys were spared death by the Ebola vaccine, while the unimmunized controls died quickly. Although the conference gave the impression that there has been quite a bit of progress in virus research, the rampage of Ebola and Marburg viruses in Africa will continue, and until we actually work out an effective vaccine, we will not be able to defeat them. Mechanisms of Ebola Virus Attacks in the Human Body After decades of research, human understanding of the Ebola virus remains limited. It is generally believed that the virus destroys the body's resistance by invading and killing white blood cells that fight infection. The virus hides from the immune system by hiding in macrophages, the "patrolling guards" of the immune system. Macrophages can clear bacterial infections, but can be attacked by the virus. Macrophages don't die instantly; they sound a red alert and frantically release cytokines as they move through the bloodstream. Under normal circumstances, the release of cytokines would alert the rest of the immune system to join forces to fight the virus. But, when attacked by Ebola, the program is disrupted. The surge of cellular hormones will break through the walls of the blood vessels and the blood seeps into the surrounding tissues. This cycle would repeat itself until the infected person bled out. No one knows why this happens. The only thing that is known is this: once the process has begun, it is almost impossible to stop the massive bleeding. Simply put, it's progressively spreading organ damage. It's a bit like dying by a thousand cuts. Your entire body would be covered in countless tiny wounds.

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