The human immunodeficiency virus (HIV) is the etiologic agent that causes acquired immunodeficiency syndrome (AIDS). AIDS is the last stage of HIV infection.
HIV infects and eventually destroys cells of the immune system so that the body is susceptible and/or unable to fight against other viruses, bacteria, parasites, fungi and diseases. AIDS is the resulting syndrome where the body is depleted of its ability to defend against these secondary or “opportunistic” infections. If left untreated, these secondary illnesses are usually the cause of death for people living with HIV/AIDS.
How the virus attacks the body
HIV is a retrovirus that attacks the cells of the immune system. HIV first attacks macrophage cells, the large cells that destroy foreign organisms and establish a “memory” to fight off future attacks from the same organism. HIV then moves on and kills T-lymphocyte CD4+ or helper cells, the white blood cells that organise the immune system’s response against infection. When these cells can no longer perform their function or are depleted, the immune system cannot defend itself from other infections and diseases.
|
|
INFECTION OF HOST CELL
HIV binds to the receptor on the surface of the host cell. Following the fusion of the viral and cell membranes, HIV’s genetic core and enzymes are injected into the host cell. |
|
INTEGRATION INTO HOST CELL
HIV’s DNA is inserted into the host cell’s nucleus - the site of it’s DNA. | |
The viral attack begins when HIV enters the body and recognises the cell-surface of a macrophage cell. A protein made by the HIV virus (gp120) connects with a protein (CD4 receptor) found on the surface of the macrophage cell. When the two proteins come into contact, the shape of the HIV protein changes to a shape that fits with another protein (CCR5 receptor) also found on the macrophage cell. Contact with this second protein starts a process that results in HIV being "swallowed into" the macrophage cell. Once inside the macrophage, the HIV genome (RNA) integrates into the cell’s genome (DNA). HIV then duplicates and multiplies within the cell. When it is finished replicating, HIV leaves the macrophage cell to perform the same procedure in other macrophage cells. The original macrophage cell does not die but becomes a permanent “reservoir” of HIV in the body. The HIV attack against macrophage cells continues for years without any visible external symptoms.
|
|
ACTIVATION OF THE VIRUS
The host cell is now latently infected. When activated, the viral genes integrated in the cell’s DNA are expressed resulting in the formation of new HIV virions |
|
BUDDING AND FURTHER INFECTION
The newly-formed HIV then “buds” out and is released from the infected host cell to repeat the same process of infection in other cells. | |
Eventually, and without notice, HIV changes its structure so that it now attaches to the protein (CXCR4 receptor) found on the exterior of T-lymphocyte CD4+ cell rather than the CCR5 receptor. HIV enters this cell and performs a similar replication process as described above. However, unlike its departure from macrophage cells, HIV ruptures out of the T-lymphocyte cell destroying it on its journey to find and infect more T-lymphocyte cells. HIV’s destruction of T-lymphocyte cells continue until the body deteriorates to a level of such severe immune deficiency (AIDS) that it is defenceless against attack from secondary infections and disease. Patients ultimately succumb to one or more of these illnesses.
|
