The Human Immunodeficiency Virus (HIV) likes to replicate (live) in the group of white blood cells called lymphocytes, or "T-Cells" for short. (There are five major groups of white blood cells.) Among the T-cells, HIV's favorite is the T4-cell. Figure 2 illustrates the life cycle of HIV in the T4-cell.
The T4-cell, also called the "helper/inducer" T-cell, performs a vital job in the immune system. The T4-cell finds germ invaders by circulating through the bloodstream and bumping into them. After recognizing the invading germ, the T4-cell releases a chemical alarm that triggers other parts of the immune system into action.
The T-4 cell recognizes only viral, fungal (fungus) and parasitic invaders, and triggers only those portions of the immune system that act against these invaders.
Once the T4-cell triggers the alarm, other parts of the immune system come into play. Other T-cells, called "effector/killer" cells, release chemicals to kill the invader. Sometimes they succeed. The T4-cell's alarm also tells the B-cells, another kind of lymphocyte, to change their structure and to begin manufacturing antibodies. A third type of lymphocyte migrates towards the T4-cell's alarm and engulfs and digests germ invaders. These large, roving lymphocytes are called macrophages.
Antibodies are proteins which neutralize (stop) invaders. Antibodies prevent viruses from latching onto host cells. A virus and its antibody fit together like a lock and key. B-cells, another type of lymphocyte, make antibodies. New antibodies must be tailored for each new viral invader. Figure 2 shows how antibodies work.
Any substance or object that triggers the creation of antibodies is called an antigen. The protein coats of viruses are antigenic.
After the antibody and virus join together, they are eaten by macrophages. Macrophages are large white blood cells that engulf and digest germs. The T4-cell's alarm also increases macrophage production.
Certain B-cells, called memory cells, remember the shape of the antibodies they have created. If, after being defeated, the same virus gets into the bloodstream again, these cells rapidly begin antibody production. Hopefully, these antibodies stop the invader before it gets a foothold. However, if the virus has changed (mutated), as the flu does in its yearly journey around the world, the old antibodies cannot stop it. New antibodies must be manufactured to neutralize the mutated virus. While this antibody production is taking place, the viral invader has time to multiply, and the infected person suffers the symptoms.
HIV's infection of the T4-cell seems to create a defect in the body's immune system which eventually causes AIDS.
Once HIV hijacks a T4-cell, the lymphocyte stops functioning normally, although this change is not immediately apparent. Evidently, very little or no viral replication takes place for an indefinite amount of time. HIV's takeover is a quiet event.
[Figure 2]
Figure 2: HIV latches onto host cell, injects its RNA inside. The viral RNA creates viral DNA, which hijacks the host cell, turning the host cell into a virus-making factory. The host cell's DNA is represented by solid black
When the T4-cell does become active, rather than functioning normally, the T-cell manufactures viral RNA strands. An infected T4-cell no longer detects invaders and triggers alarms. Eventually, the infected T4-cells begin to die, gradually decreasing the T4-cell alarm network and allowing opportunistic disease to enter and grow within the body. (Other unknown co-factors may contribute to T4-cell failure and death.)
T4-cells trigger immune system alarms when they encounter fungi, viruses, and parasites. The opportunistic diseases associated with HIV infection are caused by fungi, viruses and parasites, many of which we encounter daily. Some of these organisms live permanently in our bodies, although they are usually held in check by the immune system.
HIV does not attack the anti-viral system on purpose. Viruses have no brains; they can't make decisions. The virus inhabits any host cell that it can successfully infect and replicates within any suitable host organism it encounters.
B-cells make antibodies in response to the T4-cell's alarm, but slowly. The viral infection often runs ahead of the immune system's response for awhile, then the immune system gradually catches up.
This situation is exampled by influenza (the flu). A person becomes infected and develops flu symptoms before the body can make antibodies to kill the virus. With the flu, however, the body usually is able to destroy the virus within matter of days.
The situation is different with HIV infection. First, anti-HIV antibodies may not develop for weeks or months after the initial infection. HIV's initial infection may be so slow, or so "quiet" that the body doesn't notice anything wrong for a while.
Also, when the body does notice the infection and produces antibodies against HIV, the antibodies don't seem to work; infected people, rather than getting better, usually continue to sicken.
In several experiments where HIV has been isolated from blood, large numbers of anti-HIV antibodies were also present in the blood. This situation indicates that, even though the anti-HIV antibody is present, it has difficulty latching onto the virus and, therefore, provides little protection inside the human body.
Antibodies cannot enter blood cells. An antibody can only attack viruses in the plasma. Plasma is the fluid part of the blood (blood is composed of fluid, red and white blood cells, antibodies, etc.) Once inside a host cell, HIV has nothing to fear from antibodies. Cells can generate anti-viral chemicals within themselves, but these chemicals too seem ineffective against HIV.
Once a virus gets a foothold within a host cell, it is likely to remain there for the rest of the host's life, unless some other anti-viral mechanism within the body, or some artificial chemical is able to destroy the virus or the infected cell. HIV-infected cells seem to slip by a number of other immune system safeguards, such as the "natural killer" cells which normally destroy cells infected by viruses.
The Human Immunodeficiency Virus (HIV) successfully infects and replicates in a number of cells in the human body besides the T4-cell.
Other lymphocytes, such as the T8-cell, are vulnerable to infection. T8-cells help the immune system recognize (and not attack) cells of its own body. Some T8-cells die during HIV infection, and as a result, some AIDS patients have an auto-immune response, meaning that parts of the immune system attack their own body.
HIV also infects macrophages, but it does not kill them. Consequently, the macrophage is like a "Trojan horse" which hides the invader and carries it to protected places, namely the brain-where HIV-infected macrophages presumably disrupt the function of brain cells-and the bone marrow, the site of T-cell and B-cell generation.
HIV may also infect the cells of the retina, a part of the eye. HIV also seems to infect (at least in the laboratory) cells of the rectum and colon. The colon is basically the large intestine, and the rectum is the lowest part of the large intestine, directly inside the anus. The ability of HIV to infect these cells means HIV may be transmitted via anal intercourse more easily than previously suspected.
HIV also seems to infect lung tissue, but only in children. In adults, HIV seems able to marginally infect the interstitial cells of the lungs, that is, the connective tissue that connects the lungs to the surrounding tissues. Interstitial tissue is not part of the air passageways -- HIV remains sealed in the body. Thus, little or no HIV is present in sputum, and little or no HIV is expelled by coughing.