Let's first look at hepatitis A, which is an acute disorder in which the immune response usually manages to prevent a long term problem. Much of what follows is going to sound much like our initial discussion of influenza A.
First, there are the innate processes that can happen immediately.
After one to two weeks, the adaptive, specific immune mechanisms begin and include both B cells and T cells.
The immune responses for hepatitis A, in general, are going to work, which is why the disorder is acute. But with hepatitis B and C these immune responses may well not be enough, and thus the infection becomes chronic with long-term repercussions.
It's interesting to note that the treatment of chronic hepatitis can include IFN-alpha. An important action of this cytokine is to increase the placement of MHC I molecules on the surface of cells. This makes it much easier for cytotoxic T cells to attack the cells in which the virus is so effectively hiding. As the liver cells are attacked, the patient at first becomes ill, a necessary effect if the infected cells are to be removed. Antiviral drugs are also given at the same time.
As you know, tuberculosis bacteria, after they have been phagocytized, have a mechanism which can prevent lysosomes from fusing with the phagosomes. Thus, they can remain alive in the phagosome. But at the same time, a dendritic cell phagocytizes some of the bacteria and carries them to a lymph node where this leads to the creation of a clone of TH1 helper T cells.
Can you characterize the situation the dendritic cell "sees" that cause it to release cytokines that cause the helper T cells to become TH1 helper T cells (rather than TH2 helper T cells)?
Now some of the TH1 helper T cells travel out to the location of the macrophages and bind to them.
How does a helper T cell know which macrophage to bind to with its T cell receptor?
Once bound to the macrophages, the helper T cells release of IFN-gamma, which "activates" the macrophages.
Can you list some things that happen in the macrophage with this activation?
But if the activation of the macrophages does not wind up killing the bacteria, what tends to happen?
But if the bacteria are now walled off, why is the tissue damaged? Why might the patient, for example, be coughing up blood?
But if the formation of the granuloma is successful, with time the bacteria may remain contained, the stimulation by the helper T cells may decrease and the symptoms of tuberculosis disappear. However, later, if the immune system becomes comprised by old age or a disorder with immunodeficiency, the quiescent bacteria can emerge and cause secondary tuberculosis.
There is limited, good information available because of the difficulty of performing studies under outbreak conditions. Most comes from laboratory experiments with animals. The following information is largely taken from uptodate.com.
In animal experiments, it has proved possible for Ebola to be transmitted through the air, but there is no evidence that this happens in humans. The virus ends up in most of the body fluids and first enters the next human through a mucous membrane or breaks in the skin. The first cells infected are macrophages and dendritic cells, which, as we have discussed, are normally found throughout the tissues acting as sentinels. The virus then replicates unusually rapidly, especially because the virus suppresses the interferon alpha and interferon beta response in the cells. This leads to necrosis and the release of large number of viral particles, which can then infect many other types of cells.
Eventually, a systemic inflammatory response develops due to the release of cytokines, chemokines and various other inflammatory paracrines from macrophages and other cells. It is the release of these that leads to the fever, malaise, vasodilation, increased endothelial permeability.
The vasodilation of blood vessels and the loss of fluid from the blood due to the increased endothelial permeability leads to hypotension and eventually shock.
Also, infected macrophages synthesize tissue factor and this begins to trigger the blood coagulation system throughout the body. This consumes the blood coagulation proteins. In monkeys, additional D-dimer is present in the blood within 24 hours of infection. After 3 or 4 days, platelets become activated as they stick to endothelial cells. Again, this consumes the platelets in the blood. The lack of blood coagulation factors and platelets results in poor blood clotting. This is is why Ebola is classified as one of the "hemorrhagic fevers".
Specific immunity is affected because dendritic cells are a major site of viral infection. Lymphocytes are not infected, but many undergo apoptosis as "bystanders" during the inflammation and impairment of the dendritic cells. The resulting weak specific immunity causes great difficulty in containing the rapidly replicating virus.