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,
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
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.