How does the ebola virus attack and how do some people get away with it? Normally any virus would attack a cell with some kind of receptors and some kind of lock and key mechanism entering the cell and then multiplying.

What happens to the virus if a person manages to live through it, does the virus die and is thrown out or still remains inside the host?

I am not sure about a normal virus attack i tried to explain please correct on that also.


2 Answers 2


It is known that Ebola uses at least one cholesterol transporter called "Niemann-Pick C1" (NPC1) to enter its host cells. Cells with a mutated form of this transporter were not infected by the virus (this extends to other viruses from the Filovirus group as well), which seems like a proof that this can make people "immune" to the virus. However, these are only experiments in cell culture. Other experiments show that a small molecule inhibitor that mimics the transporter can inhibit Ebola from entering cells and infecting them.

There are two papers on this topic:

If a person manages to survive an Ebola infection the immune system fights the virus by making highly specific antibodies against it. These antibodies bind to the viruses and mark them for the immune system (mainly through mast cells) for take-up and degradation while inhibiting them from infecting other cells. Serum from Ebola survivors has been used as experimental treatment for infected people (here mainly the antibodies can be helpful). People who survive the infection are immune against another infection of the same virus strain.


Ebola enters the cells most probably using the NPC1 receptor, which is expressed by all cells. That receptor is important by other viruses as well e.g. by Marburg virus entry, HIV release, arenavirus entry, etc...

Coreceptors are not necessary required, but they can enhance ebola virus entry. Such coreceptors are:

  • TIM-1 (or HAVcr-1) - expressed mostly by epithelial cells,
  • C-type lectins,
  • β1 integrins,
  • Tyro3 (TAM) family tyrosine kinase receptors - expressed by lymphoid cells,
  • Rab7

It totally confuses the immune system with moves you can see only in Bruce Lee films e.g. by stimulate the expression of proinflammatory cytokines in the infected cells, so it can cause hemorrhagic fever.

By fighting the virus the adaptive immune system selects and proliferates the B- and T-cells which are specific to the virus and so B-cells can label the cell-free virus in the blood with antibodies for destruction, while T-cells can kill already infected cells. So if somebody manages to live through the symptoms her/his body will destroy the remaining virus after a few days maybe weeks.

The gene is part of a 3-member transmembrane receptor kinase receptor family with a processed pseudogene distal on chromosome 15. The encoded protein is activated by the products of the growth arrest-specific gene 6 and protein S genes and is involved in controlling cell survival and proliferation, spermatogenesis, immunoregulation and phagocytosis. The encoded protein has also been identified as a cell entry factor for Ebola and Marburg viruses. [provided by RefSeq, May 2010]

Recent studies have revealed that the TAM receptor protein tyrosine kinases — TYRO3, AXL and MER — have pivotal roles in innate immunity. They inhibit inflammation in dendritic cells and macrophages, promote the phagocytosis of apoptotic cells and membranous organelles, and stimulate the maturation of natural killer cells. Each of these phenomena may depend on a cooperative interaction between TAM receptor and cytokine receptor signalling systems. Although its importance was previously unrecognized, TAM signalling promises to have an increasingly prominent role in studies of innate immune regulation.

We showed previously that Niemann-Pick C1 (NPC1), a lysosomal cholesterol transporter, is required for filovirus entry. Here, we demonstrate that NPC1 is a critical filovirus receptor. Human NPC1 fulfills a cardinal property of viral receptors: it confers susceptibility to filovirus infection when expressed in non-permissive reptilian cells.

Ebolaviruses cause a severe hemorrhagic fever syndrome that is rapidly fatal to humans and nonhuman primates. Ebola protein interactions with host cellular proteins disrupt type I and type II interferon responses, RNAi antiviral responses, antigen presentation, T-cell-dependent B cell responses, humoral antibodies, and cell-mediated immunity. This multifaceted approach to evasion and suppression of innate and adaptive immune responses in their target hosts leads to the severe immune dysregulation and “cytokine storm” that is characteristic of fatal ebolavirus infection. Here, we highlight some of the processes by which Ebola interacts with its mammalian hosts to evade antiviral defenses.


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