My CD4 among other things!

It’s official I am transferring to RITM. After a couple of cancelled appointments I went to RITM last Tuesday (September 2, 2008) to undergo my 3rd CD4 test since I was diagnosed positive of HIV, my 1st viral load, Urinalysis, CBC and PPD. When I arrive there I saw Ate Ana and she gave me the requests for all the test that the hospital need to make. After that I went to the lab so that they can extract blood from me I was kinda afraid of needles and there was a time when the medtech is having a hard time extracting blood from me. The med tech said to me to relax so I closed my eyes and think of a HAPPY PLACE (I’m still trying to overcome that fear) after it was finished I went back to Ate Ana and she guided me to another nurse for the PPD test. Meaning another injection for me. PPD test is to determine if you have been expose to a TB environment (I hope there’s cable or satellite included) luckily the result turned negative. After that Ate Ana instructed me to go to the X-ray room. When I was there the attendant an old lady told me to comeback around 10:30 AM because they are still fixing the X-ray machine. When I looked at my watch its around 9:30 AM I still have 1 hour to wait. I went to Ate Ana’s office and waited there until around 10:45 AM the attendant called and told Ate Ana that the X-ray machine is already fixed. So I went to the X-ray room again followed the instructions of the old lady to put my chin on top of the plate and breathe deeply. After that, the old lady told me to stay outside and wait for the result. After around 5 minutes the old lady told me that I need to repeat my X-ray. I said to myself Why? Am not a lab rat! The old lady said that there a certain portion that the X-ray machine didn’t get. Now I am imagining a scene from a movie wherein the guy was left on the X-ray room and was over exposed from the radiation of the X-ray machine and he was starting to decay. I don’t want to die like that. I still followed the old lady and told me to put my chin on top of the plate and inhale, hold your breathe and we’re done. She told me to wait again outside so that she can be sure that the X-ray is ok. After 5 minutes she said the X-ray is clear she will just give the result to Ate Ana. So I went back there and told Ate Ana that I will just comeback next Thursday for the results of the exams.

The next day I was excited to know the results of my CD4 test and to check if my ARV is working I texted Ate Ana. “Ate Ana ask ko lng po kung nandyan nap o yung result ng CD4 test ko.” Then Ate Ana replied “ Oo, very good your CD4 is 574. Keep up your healthy lifestyle.” Wow I was so happy when I received that message imagine from 504 that was the first result of my CD4 then after 9 months I got my 2nd test and it turned out that my CD4 went down to 360. So my doctor advised me to undergo ARV meds. As a good patient I followed my doctor and drink my ARV meds for almost 9 months now. Now here’s the result my 3rd CD4 test an all time high of 574. I hope that I can maintain this level.
Tuloy ang ligaya, but of course be RESPONSIBLE!

By the way I’ve been sexless for 2 weeks now I don’t know why? Actually I think this is the longest time. May be that’s why I got sick because of the mounting pressure inside of me, don’t you think? Kidding!!!

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

Perhaps the best example of the importance of CD4+ T cells is demonstrated with human immunodeficiency virus (HIV) infection. HIV targets cells that express CD4, and can infect macrophages, dendritic cells (both groups express CD4 at low levels) and CD4+ T cells.
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 treatment they 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.