Ebola Infection via Endocytosis

Ebola Infection via Endocytosis

Michael Mauvais
3/26/2015
4891193

Ebola Infection via Endocytosis

Ebola takes advantage of a cells endocytic pathway because the membrane receptors that bind to viral glycoproteins are non-specific, resulting in numerous carbohydrate proteins. As a result the cell engulfs the Ebola virus via micropinocytosis, Once Ebola is enveloped into endosome, viral glycoprotein is cleaved and bind to NPC1 before fusion into endosome membrane. TPC2 calcium channel is then activated to release viral genome into the cell where it will be replicated.
Ebola virus disease (EVD; also Ebola hemorrhagic fever, or EHF), or simply Ebola, is a disease of humans and other primates caused by ebolaviruses. Signs and symptoms typically start between two days and three weeks after contracting the virus with a fever, sore throat, muscular pain, and headaches. Then, vomiting, diarrhea and rash usually follow, along with decreased function of the liver and kidneys. At this time some people begin to bleed both internally and externally.[1] The disease has a high risk of death, killing between 25 and 90 percent of those infected, with an average of about 50 percent.[1] This is often due to low blood pressure from fluid loss, and typically follows six to sixteen days after symptoms appear.[2]

The virus spreads by direct contact with body fluids, such as blood, of an infected human or other animals.[1] This may also occur through contact with an item recently contaminated with bodily fluids.[1] Spread of the disease through the air between primates, including humans, has not been documented in either laboratory or natural conditions.[3] Semen or breast milk of a person after recovery from EVD may still carry the virus for several weeks to months.[1][4] Fruit bats are believed to be the normal carrier in nature, able to spread the virus without being affected by it. Other diseases such as malaria, cholera, typhoid fever, meningitis and other viral hemorrhagic fevers may resemble EVD....

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