What are the two types of ebola virus




















Facebook Twitter LinkedIn Syndicate. What is Ebola Virus Disease? Minus Related Pages. Ebola Virus Ecology and Transmission. Related Resources. Transmission Signs and Symptoms History of Ebola. Links with this icon indicate that you are leaving the CDC website. Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website.

This resulted in an outbreak that involved multiple regions in the three hardest hit countries. Additionally, it was the first time that Ebola was carried by air travel from one country to another. Further, the outbreak occurred in countries with weak healthcare infrastructure and a population that is distrustful of government and healthcare workers. Because it encompassed a much wider geographic area and denser population areas than previous outbreaks, containment was vastly more difficult and complex.

It was an immense challenge to control the outbreak in this impoverished part of the world, lacking many basic and essential medical supplies.

Workers faced the daunting task of identifying and quarantining large numbers of infected individuals and their contacts and providing medical care to patients - without sufficient numbers of health workers, personal protective equipment, adequate facilities, or sufficient numbers of hospital beds. Many infected individuals initially were turned away from health facilities and sent home, where they were more likely to infect others, due to lack of space in hospitals. Workers also needed to educate a fearful and mistrustful population about the dangers of Ebola and the proper procedures needed to minimize further infections, including safe burial procedures.

Health care workers themselves were at high risk of infection; more than became infected and at least died. Even outside of West Africa, there were several infections of health care workers - one in Spain and two in Dallas - within hospital settings in developed countries that employed rigorous infection control in workers wearing protective gear while treating Ebola infected patients.

The Ebola outbreak had a significant social and economic effect on the impacted regions in West Africa. Travel restrictions were put in place, schools were closed, and general panic and misinformation arose in some areas. Fear, and loss of health care workers and even attacks on these workers, led to the collapse of health care systems in some affected areas, which resulted in deaths due to other diseases that normally would be treatable.

The outbreak also created orphans, which were often unwanted by extended family members due to fear that the child could spread the disease. In the United States, the arrival of a person traveling from Liberia to Dallas and his subsequent diagnosis of Ebola infection, as well as the diagnosis of EVD in a doctor returning to New York after treating Ebola patients in West Africa also caused some panic in the United States.

This led to the institution of some mandatory quarantines and travel restrictions of persons returning from Ebola-affected areas. It also created a stigma associated with recovered patients or those who have treated Ebola patients.

Some of the policies were medically unnecessarily restrictive and may have discouraged volunteers from traveling to West Africa to treat patients at the source of the outbreak. The lack of approved drugs and vaccines highlights the general problem of inadequate funding for diseases that have previously occurred only in remote areas and afflicted small numbers of people.

A major problem during the height of the outbreak was that the experimental drugs and vaccines were available in extremely limited quantities and they had not undergone extensive prior testing in humans. Production was scaled up, but they were not widely available until late in the outbreak.

The availability of limited quantities of drugs and vaccines that have not been fully tested raises ethical concerns regarding the administration of unapproved drugs and determining which patients or workers should receive the drugs when there is a scarce supply.

A serious concern during any outbreak is the possibility that the virus could mutate to a form that is more virulent or contagious or becomes transmissible through the air where it could infect larger numbers of people. The reason for this concern is that when viruses pass through a large number of people, the number of mutations increases. Although some changes to the Ebola virus did occur, the strain that circulated during the Ebola outbreak is very similar to the strain initially discovered in , and the changes did not appear to affect the ability of the virus to cause disease.

In order to prevent another large Ebola virus outbreak, it is critical to maintain a high level of vigilance, so that any new cluster of infections can be swiftly identified and contained, as well as continuing the development and testing of vaccines and drugs that can be used in future outbreaks of the Ebola virus. One of the key steps in any virus infection occurs very early in an infection cycle. That is the step where a virus binds to and enters a cell in a susceptible host organism.

Because viruses are too small to reproduce on their own, they must invade a host cell in order to multiply and produce more copies of themselves that can then go on to infect other organisms and continue the infection cycle. Many viruses require a specific protein or other type of molecule on the surface of the host cell - called a receptor - which allows the virus to pass into a cell of a host organism.

If an organism or cell type does not possess this particular receptor, the virus is unable to infect that organism or cell type.

Knowing what this receptor is for any particular virus is a crucial piece of information for scientists, because it tells them which organisms or cell types are susceptible to infection by a certain virus. It is known that in humans, the Ebola virus appears to infect many different cell types. Ebola is also thought to have a broad host range, since it is capable of infecting diverse mammalian species, including primates, rodents, and bats. This knowledge can be used to design therapies that may be able to prevent a virus from entering into a cell and initiating an infection.

Based on evidence from other scientists that suggested that members of a group of proteins named the Tyro3 family might mediate entry of Ebola virus into cells, Dr.

They reasoned that if these proteins were necessary for entry into cells, reduction of their levels should diminish infection by Ebola. However, they observed little effect on Ebola virus infection when they reduced levels of expression of all three Tyro3 family genes.

They therefore concluded that it is unlikely that this family of proteins is the entry factor for Ebola virus. In addition, Dr. Peter Hotez , professor of Molecular Virology and Microbiology, and Pediatrics, and founding dean of the National School of Tropical Medicine at Baylor College of Medicine provided his expertise on the Ebola virus during the Ebola outbreak and gave interviews to numerous media outlets.

Department of Molecular Virology and Microbiology. Media Component. Ebola Virus Disease Ebola viruses cause a severe and often deadly illness known as Ebola virus disease EVD; previously referred to as Ebola hemorrhagic fever. Ebola Virus Classification Ebola viruses belong to a family of viruses termed Filoviridae.

Symptoms may appear anywhere from 2 to 21 days after contact with the virus, with an average of 8 to 10 days. Many common illnesses can have the same symptoms as EVD, including influenza flu , malaria, or typhoid fever. EVD is a rare but severe and often deadly disease. Studies show that survivors of Ebola virus infection have antibodies proteins made by the immune system that identify and neutralize invading viruses that can be detected in the blood up to 10 years after recovery.

Klenk, A. Garcia-Sastre, and P. USA 97 : Bowen, E. Lloyd, W. Harris, G. Platt, A. Baskerville, and E. Viral haemorrhagic fever in southern Sudan and northern Zaire. Preliminary studies on the aetiological agent. Lancet i : Bray, M. Davis, T. Geisbert, C. Schmaljohn, and J. A mouse model for evaluation of prophylaxis and therapy of Ebola hemorrhagic fever.

Chan, S. Empig, F. Welte, R. Speck, A. Schmaljohn, J. Kreisberg, and M. Cell : Colebunders, R. Ebola haemorrhagic fever—a review. Connolly, B. Steele, K. Geisbert, W. Kell, N. Jaax, and P. Pathogenesis of experimental Ebola virus infection in guinea pigs. Donnelly, J. Ulmer, J. Shiver, and M.

DNA vaccines. Feldmann, H. Bugany, F. Mahner, H. Klenk, D. Drenckhahn, and H. Nichol, H. Klenk, C. Peters, and A. Characterization of filoviruses based on differences in structure and antigenicity of the virion glycoprotein. Virology : Geisbert, T. Pushko, K. Anderson, J. Smith, K. Davis, and P. Evaluation in nonhuman primates of vaccines against Ebola virus. Gupta, M.

Mahanty, M. Bray, R. Ahmed, and P. Passive transfer of antibodies protects immunocompetent and immunodeficient mice against lethal Ebola virus infection without complete inhibition of viral replication.

Ito, H. Watanabe, A. Sanchez, M. Whitt, and Y. Mutational analysis of the putative fusion domain of Ebola virus glycoprotein. Takada, and Y. Ebola virus glycoprotein: proteolytic processing, acylation, cell tropism, and detection of neutralizing antibodies.

Jahrling, P. Geisbert, J. Swearengen, G. Jaax, T. Lewis, J. Huggins, J. Schmidt, J. LeDuc, and C. Passive immunization of Ebola virus-infected cynomolgus monkeys with immunoglobulin from hyperimmune horses. Geisbert, D. Dalgard, E. Johnson, T. Ksiazek, W. Hall, and C. Preliminary report: isolation of Ebola virus from monkeys imported to USA. Lancet : Johnson, K. Lange, P. Webb, and F.

Isolation and partial characterisation of a new virus causing acute haemorrhagic fever in Zaire. Kilby, J. Hopkins, T. Venetta, B. DiMassimo, G. Cloud, J. Lee, L. Alldredge, E. Hunter, D. Lambert, D.

Bolognesi, T. Matthews, M. Johnson, M. Nowak, G. Shaw, and M. Potent suppression of HIV-1 replication in humans by T, a peptide inhibitor of gpmediated virus entry. Kindzelskii, A. Yang, G.

Nabel, R. Todd III, and H. Malashkevich, V. Schneider, M. McNally, M. Milhollen, J.



0コメント

  • 1000 / 1000