After few weeks of waiting, i finally got my cd4 result it's 443, not bad, but the doctor said i have to start my treatment because of the new guidelines (if your cd4 goes down to 500 you may start medication right away). She said that it would lessen the risk of having OI (opportunistic infections). She gave me a week to think about it and also to have my x-ray again, because of my cough. Now I'm having fever again, hope its just because of the bad weather, not something serious.
I need to take care of myself more seriously.
Here are some info about CD4 and HIV:
T helper cells (also known as effector T cells or Th cells) are a sub-group of
lymphocytes (a type of
white blood cell or
leukocyte) that plays an important role in establishing and maximizing the capabilities of the
immune system. These cells are unusual in that they have no
cytotoxic or
phagocytic activity; they cannot kill infected
host (also known as
somatic) cells or
pathogens, and without other immune cells they would usually be considered useless against an infection. Th cells are involved in activating and directing other immune cells, and are particularly important in the
immune system. They are essential in determining
B cell antibody class switching, in the activation and growth of
cytotoxic T cells, and in maximizing
bactericidal activity of
phagocytes such as
macrophages. It is this diversity in function and their role in influencing other cells that gives T helper cells their name.
Mature Th cells are believed to always express the surface protein
CD4. T cells expressing CD4 are also known as CD4+ T cells. CD4+ T cells are generally treated as having a pre-defined role as helper T cells within the
immune system, although there are known rare exceptions. For example, there are sub-groups of
suppressor T cells,
natural killer T cells, and
cytotoxic T cells that are known to express CD4 (although cytotoxic examples have been observed in extremely low numbers in specific disease states, they are usually considered non-existent). All of the latter CD4+ T cell groups are not considered T helper cells, and are beyond the scope of this article.
The importance of helper T cells can be seen from
HIV, a virus that infects cells that are CD4+ (including helper T cells). Towards the end of an HIV infection the number of functional CD4+ T cells falls, which leads to the symptomatic stage of infection known as the acquired immune deficiency syndrome (
AIDS). There are also
some rare disorders that result in the absence or dysfunction of CD4+ T cells. These disorders produce similar symptoms, and many of these are fatal.
HIV infection
It has been proposed that during the non-symptomatic phase of HIV infection, the virus has a relatively low affinity towards T cells (and has a higher affinity for macrophages), resulting in a slow kill rate of CD4+ T cells by the immune system. This is initially compensated for via the production of new helper T cells from the
thymus (originally from the
bone marrow). Once the virus becomes
lymphotropic (or T-tropic) however, it begins to infect CD4+ T cells far more efficiently (likely due to a change in the
co-receptors it binds to during infection), and the immune system is overwhelmed.
At this point, functional CD4+ T cell levels begin to decrease, eventually to a point where the CD4+ T cell population is too small to recognize the full range of
antigens that could potentially be detected. The lack of full antigen cover results in the core symptoms of acquired immune deficiency syndrome (
AIDS). CD4 T cell depletion during AIDS allows various
pathogens to escape T cell recognition, thus allowing
opportunistic infections that would normally elicit a helper T cell response to bypass the immune system. While these complete bypass situations only occur when the helper T cell response is absolutely necessary for infection clearance, most infections increase in severity and/or duration because the immune system's helper T cells provide a weaker contribution to a less efficient immune response.
Two components of the immune system are particularly affected in AIDS, due to its CD4+ T cell dependency:
1.
CD8+ T cells are not stimulated as effectively during the AIDS period of HIV infection, making AIDS patients very susceptible to most viruses, including HIV itself. This decline in killing of
CD4+ T cells results in the virus being produced for a longer period (the infected CD4+ T cells are not killed as quickly), increasing the proliferation of the virus, and accelerating the development of the disease.
2.
Antibody class switching declines significantly once helper T cell function fails. The immune system loses its ability to improve the affinity of their antibodies, and are unable to generate B cells that can produce antibody groups such as
IgG and
IgA. These effects are primarily due to the loss of any helper T cell that can interact with the B lymphocyte correctly. Another symptom of AIDS is the reduction in antibody levels due to a decrease in Th2 cytokines (and less interactions by helper T cells). All of these complications result in an increased susceptibility to aggressive bacterial infections, especially in areas of the body not accessible by
IgM antibodies.
If the patient does not respond to (or does not receive)
HIV treatmentthey will succumb usually to either cancers or infections; the immune system finally reaches a point where it is no longer coordinated or stimulated enough to deal with the disease.
