The complicated and delicate process that HIV “uses” to make us sick?
Almost thirty years after the first cases of AIDS, we still don't know exactly how the HIV destroys the immune system (!!!). But inflammation - sustained immune activation - is now seen as a key factor in the process in which they do their damage, much like fire under the tundra. Research is reviewing how the virus is understood - and how it can be combated most effectively and forcefully.
Untreated HIV infection is evidently from the onset of the epidemic haphazard demonstrated that, sooner or later, HIV easily causes a massive loss of CD4 cells and the immune defenses of the human body. If CD4 cell count drops to sufficiently low levels and HIV unfortunately does so easily, the body becomes easy prey for opportunistic infections and cancers that the previously healthy immune system can efficiently and quietly defeat in the highest part of the time.
Perhaps, surprisingly, and yet not fully understood, the process as HIV depletes CD4 cells. In addition, while antiretroviral treatment has enabled people living with HIV to be able to stay healthy, with better white blood cell counts with the CD4 receptor, in all those who are medicated and have at least ninety-two adherence. five percent (in fact my membership is one hundred percent but it can still have its life overwhelmingly annihilated, people's lives are at risk of contracting or developing opportunistic infections, such as cytomegalovirus (CMV) retinitis, which can cause a person to lose vision and their ability to see becomes inferior in quality and acuity , and that can leave you completely blind, irremissibly and there is still, for example, Pneumocystis pneumonia (PCP), problems such as cardiovascular diseases (I, Cláudio Souza, suffered two pulmonary embolisms, one of which it was massive, as well as widespread kidney diseases.The toxicities of antiretroviral treatment - such as the increase in cholesterol - do not fully explain such complications: HIV infection itself is now understood to significantly increase metabolic risks.
Several emerging concepts may shed some light on these issues. The inflammation - the prolonged state of immune activation resulting from the ongoing immune system of battle with the virus - Seems to be a key factor in metabolic disorders and cardiovascular disease (my pulmonary embolism was triggered by these triggers). Research has also revealed that the digestive tract may play a much larger role in the progression of HIV disease than previously performed and, in fact, may be one of the strongest sources of immune activation.
early infection and intestines
The course of HIV infection follows largely as a characteristic pattern for most people. During the first few weeks - acute infection - the immune system has not yet learned to respond to the new intruder. HIV levels are elevated throughout the body and the number of CD4 cells in the blood plasma drops dramatically. Tests now suggest that looking at only CD4 cells in the blood, which may have underestimated the overall measure of this early fall. Only a small fraction (2%) of the body's CD4 cells are actually found in circulating blood. Most live in lymph nodes (these include the 'glands' you can sometimes feel in the neck and inguinal region when you have an infection), in the intestines associated with lymphoid tissue (GALT Note to Translator, GALT is an acronym in English for the text marked in red above, which in English is defined as: Gut-associated lymphoid tissue ) where they are present as clumps of immune cell lining throughout the intestines in mucous membranes of other organs exposed to foreign substances such as lungs and genitalia. The researchers observed a massive loss of CD4 memory cells in this bowel tissue rapidly after infection. (Note: If I left here only the text with memory cells this would not be understood in its dramatic importance and the severe loss that this represents for us people living with HIV or AIDS. I searched the net and found on Wikipedia the following definition:
memory T cells are derived from other T lymphocytes that have learned to respond to a specific invader, for example a kind of bacterium, or a type of fungus or even a allergen and were successful in eliminating them. They go live for many years, and can be re-activated for a faster response to an attacker similar to the one they fought in the past. For example, a lymphocyte that has been activated to combat measles (by direct contact or by vacina) Can follow combating new invasions by the measles virus ensuring lifelong immunity to that individual. At the end of this text you will find a link that leads directly to the entire Wikipedia page
Danny Douek, researcher at US National Institute of Allergy and Infectious Diseases (NIAID), studied the process closely:
“Since we thought CD4 cells were lost slowly but surely during the course of the disease. But we note that most of the outer memory T cells - which is most CD4 cells in an adult - are lost extremely quickly. ” About 60% of memory cells can become infected, and in most people it can disappear within the first two weeks of infection (…).
Ideally, the treatment of HIV might need protection against both pacing and immunodeficiencies. It is likely that this is a complex goal, and the consensus is that considerable research is still needed.
In Stripping (removal of internal layers of less virus) with tissue CD4 many cells, HIV also causes structural damage to the intestinal tissue, and immune to the lymph nodes where many immune cells normally reside. Recent studies have found that these tissues have become marked with collagen during infection aguda.2
Researchers speculate that this damage interferes with normal cell growth and cell interactions, limiting the ability of the immune system to fully regenerate CD4 cells lost in early infection. Intestines and tissue damage can also contribute to inflammation that helps lead to later stages of HIV disease - one point we'll return to.3
Chronic infection: Why CD4 cells die?
After the intense activity of a few weeks of acute infection, the body begins to produce antibodies and immune cells that specifically target HIV. During this period (known as seroconversion), viral load levels drop and the CD4 cell count returns to near normal levels. At this point, the disease enters a prolonged phase known as Chronic infection. (That's all you can say about “chronic disease” - AIDS is a syndrome that has little or nothing to do with chronic disease… AIDS does have everything to do with Acquired Immune Deficiency - AIDS in itself is not a chronic disease)
In the early years of the epidemic, the virus was even thought to sleeping during the long period of chronic infection. This proved to be completely wrong: the advent of viral load testing in the mid-proved that the virus continues to infect actively CD4 cells and other from the time of infection on, producing millions of new copies of every day.
Is it the virus that directly kills CD4 cells? It is easy to assume that this should be the main reason for the eventual drop in CD4 counts. But the truth is more complex. Considerably less than 1% circulating CD4 cells are actually infected with HIV during chronic infection - too few to explain the overall loss - and millions of new CD4 cells are created each day. In recent years, researchers have discovered possible other ways in which HIV leads to CD4 cell loss. These include toxic viral proteins, flashes from infected cells, which can kill uninfected cells in the so-called bypass effect. HIV can also trigger cells in "suicide" in a process called apoptosis., or programmed cell death.
Other mechanisms are likely to be at work well, including - ironically - the immune system's own response to HIV. The virus can infect only activated CD4 cells - those that have been “linked” to fight the infection. In other words, by the very act of taking action against the virus, CD4 cells themselves become targets for infection. This paradox is inevitable to some degree, since immune cell activation is an essential part of immune function. However, there is growing evidence that prolongation and excessive immune activation - inflammation - underlie much of the continuing damage from HIV disease.5
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