HIV and Immune system

Creator: Dr. Reeja Tharu
Keywords: HIV and Immune system, T-cells, HIV infection, B-Cell function, Monocytes and HIV

Medically Reviewed by The Medindia Medical Review Team on Nov 12, 2014

HIV eventually destroys many of the white blood cells, which protect us against disease.
HIV infection leaves people helpless against many other serious infections and cancers.

Different viruses invade different kinds of cells. HIV invades and destroys helper T cells, the very cells that direct the body's defenses. By destroying helper T cells, HIV disables the entire immune system that protects us against disease.
Lymphoid organs play a central role in HIV infection.
Know Our Body's Defense System: The immune system is made up of many different kinds of white blood cells. White blood cells work together to protect us against disease-causing germs. White blood cells defend against germs.
The RBC carries heme and iron that help in carrying oxygen around the body. The WBC fights against infection and there are many sub-types of WBC.
Macrophages identify germs - When a germ invades our bodies, macrophages gobble up the germ and display its surface shape, or antigen, for other immune cells to see.
Helper T cells direct the defense - Helper T cells spot the foreign antigen on the macrophage and begin to multiply. They alert other white blood cells and direct the body's defense.
Killer T cells destroy germs Alerted by helper T cells; killer T cells multiply and destroy the invading germs.
B cells make antibodies - B cells start to make chemicals called antibodies. Antibodies lock onto foreign antigens making it easier for other immune cells to destroy them.
Working together, our white blood cells can usually destroy invading germs.

T-cells and HIV infection

There is a significant drop in number of circulating CD4 T cells at this early stage.
An immune response to HIV occurs 1 week to 3 months after infection, when the levels of CD4 cell increases. But the immune response is unable to clear the infection completely, and HIV-infected cells persist in the lymph nodes.
This period of clinical latency may last for as long as 10 years. Although very few infected cells are in the blood.
HIV found in patients with late-stage disease is usually much more virulent and harmful than the strains of virus found early in infection.
Decrease of CD4 T-lymphocytes causes a decrease in Immune response and affects the lymphoid and non-lymphoid cell functions.

Further Reading:

HIV and B-Cell function:

AIDS infected persons show an abnormal B cell function.
It produces an inability to mount an adequate immunoglobulin M (IgM) response against the HIV.

Monocytes and HIV:

Monocytes and macrophages play a major role in the spread and pathogenesis of HIV infection.
These phagocytic cells can engulf the virus.
Monocytes express the CD4 surface antigen and therefore bind to the envelope of HIV.
The infectivity of monocytes with HIV suggests that the monocyte serves as a major reservoir for HIV in the body.
Neurologic abnormalities are common in AIDS
HIV encephalopathy, myelopathy, peripheral neuropathies, and most serious, AIDS dementia complex.
gp120, may be involved in tissue damage without actual infection of all cells.
It is speculated that gp120 may activate macrophages, microgilia, and astrocytes and cause the release of cytokines and neurotoxins that injure neighboring neuronal cells.
In HIV infected individual, a wide range of invivo antigenic stimuli seems to serve as cellular activators.
Other concomitant viral infections - EB virus, Cytomegalo virus, Herpes simplex virus, or hepatitis B virus can act as cofactors for AIDS.

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