Symptoms Of Hiv

The Science of HIV*
Written by Kimberly Dayton   
AIDS is not a single disease, but a syndrome -- a set of conditions that tend to occur together and include both the signs detected by a doctor, and the symptoms reported by a patient.  Scientists the world over have identified the Human Immunodeficiency Virus, or HIV, as the cause of AIDS.    

When HIV infects the human immune system, it attacks CD4 T helper lymphocytes -- the white blood cells that keep us healthy by digesting the dangerous bacteria and fungi it finds in our bodies.   CD4s travel everywhere the blood goes, catching and killing the germs that cause infections.   When the HIV enters the body, it latches onto the surfaces of CD4 cells and kills them, using their organic compounds to feed it and reproduce.   As HIV spreads, the CD4 count falls.  Surviving CD4 cells do continue to reproduce, but because HIV has invaded them, they also make more copies of the virus.  Thus, white blood cells infected by HIV effectively destroy themselves. 

As HIV spreads, the immune system weakens, and the body becomes much more susceptible to opportunistic infections.  These are diseases caused by all kinds of germs -- bacteria, viruses, funguses or protozoa- that a healthy immune system would usually kill off.    Since the HIV-infected body is short on CD4 lymphocytes, the germs and cancer cells that would ordinarily become a delicious dinner for a white blood cell can now survive and spread, going about their business of infecting their favorite parts of the human body.    

HIV infection has two phases  -- acute and chronic.   During the acute phase, in the first five weeks after the virus first infects the immune system, it commits mass murder of the CD4 lymphocytes in the lining of the intestine.   Intestinal white blood cells are the most vulnerable to HIV because their surfaces have CCR5 receptors; in simple terms, this means that their shape is a good fit with the shape of HIV cells.   The virus kills some CD4s; while other CD4s may actually kill themselves off in a process called apoptosis, or programmed cell death, triggered by HIV.  After the first few weeks of HIV infection, the immune system reasserts itself and dramatically slows the spread of the virus to other parts of the body.  However, the worst damage has already been done.   HIV has invaded and conquered the intestine, and the weakened immune system cannot regain the lost territory.  Like troops defending a city under siege, immune cells settle into a holding pattern.  They are able to prevent the worst; most life threatening infections while the body is still strong overall.  However, HIV stays in the body indefinitely, waging low-grade guerrilla war against the immune cells.  It still seeks out CD4 cells to attack, and the immune system remains on active alert trying to hold HIV at bay. 

One of the consequences of the constant "amber alert" in the immune system in response to the presence of HIV is the constant release of cytokines, messenger molecules that help cells communicate with one another.  The message delivered by cytokines is basically "Strangers nearby, stand guard!"   Some cytokines trigger an immune response.  White blood cells migrate to the danger zone, where they encircle, attack and eat the foreign organisms.  We experience this normal, non-specific immune response as inflammation.  The zone of the body under surveillance by immune cells becomes red, warm, swollen, and usually painful.    Because of this, HIV-positive people are highly susceptible to inflammations, particularly of the intestinal area where the dearth of CD4 cells creates more opportunities for "opportunistic infection" by the many microorganisms that live there.  To an HIV positive person, frequent inflammation shows up as diarrhea, stomach pains, and other gastrointestinal difficulties. 

Although an HIV-infected person may not experience severe symptoms for many years after the initial infection, the number of CD4 T-cells gradually declines.  There are two main reasons for this. 

First of all, every time one of the remaining stocks of CD4 lymphocytes reproduces, it creates a copy of HIV as well.  The HIV in turn keeps the immune system active, and leads to more white blood cell reproduction, which leads to more HIV.  As HIV spreads, it continues to attack CD4 T cells.  This isn't the only factor in CD4 decline, however, because only a small number of CD4 T cells -- anywhere from 1 in 1000 to 1 in 10,000 -- is infected in HIV-positive people who have progressed to the chronic phase of infection. 

A second reason for the gradual decline of CD4s is the activated immune system itself.   In HIV patients, CD4s kill themselves in large numbers through apoptosis.  The most recent HIV research suggests that apoptosis is a normal response in an activated immune system; old CD4s appear to commit suicide so they can clear the way for fresh cells that fight off infections more easily.    The problem for patients with HIV infection, however, is that the body has lost much of its capacity to create new CD4 cells.   Among the small number of CD4s infected by HIV, a large proportion are thymocytes, the specialized white blood cells that make up organ called the thymus, whose only job is to produce T-lymphocytes. 

Imagine the immune system as an army of cells that works together to repel foreign invaders.  CD4s are the actual killer cells, which do the front-line work of attacking and killing the bacteria, fungi, viruses and other creatures that are invading the body.  The killer cells are effective, but not invincible.  Eventually, they wear themselves out; they cannot absorb any more foreign substances, so they commit suicide.  The body then must produce more killer cells to continue the work of repelling invaders.   The reason HIV is so dangerous is that it doesn't just kill the killer cells -- it also kills the mother cells that give birth to the killers.    Over time, as the mother cells die off, the body loses its ability to produce more killer cells, and as a result, more and more invaders fight off the immune system and invade the body. 

In people who never take medicines to fight off HIV, the virus eventually kills most of the body's CD4+ T cells.   Once their concentration in the blood falls below 200 per microliter (1 millionth of a liter) of blood, most of the body's cells have lost their immunity, and can no longer fight off most infections.   This marks the onset of the syndrome known as AIDS, in which infection after infection weakens the body so much that the patient dies.   Hence, the actual killer is not AIDS itself, but the opportunistic infections that result from the disappearance of the body's CD4 T-cells.   The time between initial HIV infection and AIDS-related death takes ten years on average, although actual death rates vary between two weeks and twenty years depending on the overall health of the HIV infected person. 

Anti-retroviral drugs, which slow the reproduction of the HIV virus, are the only known treatment that can slow the onset of AIDS.  They can lengthen the time between the onset of infection and the critical point when CD4 T-cell count falls below 200 per microliter.   As yet, no one has been able to develop a vaccine against HIV.  

*This article is based on the information at http://www.cdc.gov/hiv/resources/factsheets/, http://www.hivla.org/factsheets/index.html, http://www.webmd.com/hiv-aids/default.htm, http://aidsinfo.nih.gov/, http://en.wikipedia.org/wiki/HIV/AIDS/, http://www.avert.org/aids.htm, http://www.mayoclinic.com/health/hiv-aids/ds00005
 
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