The complicated and delicate process that HIV "uses" to put us ill?
Almost thirty years after the first cases of AIDS, we still do not know exactly how 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. The research is reviewing the way the virus is understood - and how it can be tackled more 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 remain healthy, with better white blood cell counts with the CD4 Receptor, in those who are medicated and have at least 90 five percent (in fact, my membership is one hundred percent, but can still have an overwhelming life annihilated, people's lives are at risk of contracting or developing opportunistic infections such as cytomegalovirus (CMV) retinitis) , which can cause the person to lose sight and their ability to see becomes inferior in quality and acuity, which can leave him completely blind in an irretrievable way and there is, for example, Pneumocystis pneumonia ( PCP), problems such as cardiovascular diseases (I, Cláudio Souza, suffered two pulmonary embolisms, one of which was mass, as well as generalized kidney diseases. anti-retroviral therapy - such as increased cholesterol - do not fully explain such complications: HIV infection itself is now understood to significantly increase metabolic risks.
Several emerging concepts can shed some light on these issues. Inflammation - the prolonged state of immune activation resulting from the ongoing immune system of battle with the virus - appears to be a key factor of metabolic disorders and cardiovascular diseases (my pulmonary embolism has been triggered by these triggers). The research also revealed that the digestive tract may play a much larger role in the progression of HIV disease than previously done and in fact may be one of the strongest sources of immune activation.
early infection and intestines
The course of HIV infection largely follows 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 becomes markedly droplets. Tests now suggest that by looking only at CD4 cells in the blood, which may have underestimated the overall measure of this early decline. Only a small fraction (2%) of the body CD4 cells are effectively found in circulating blood. Most live on 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:
"Once we thought that CD4 cells were lost slowly but surely during the course of the disease. But we note that most outer memory T cells - which are the majority of CD4 cells in an adult - are lost extremely quickly. " About 60% of memory cells can become infected and, in most people, may 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 cellular interactions, limiting the ability of the immune system to fully regenerate lost CD4 cells in early infection. Intestines and tissue damage may also contribute to inflammation that helps lead to later stages of HIV disease - a point we will 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. (this is all that can be said about "chronic disease" - AIDS is a syndrome that has little or nothing to do with chronic disease ... AIDS has, yes, everything to do with Acquired Immune Deficiency - AIDS in if it 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.
It is the virus directly who kills CD4 cells? It is easy to assume that should be the main reason for the eventual fall of CD4 counts. But the truth is more complex. Considerably less than 1% CD4 circulating cells are actually infected with HIV during chronic infection - too few to explain the overall loss - and millions of new CD4 cells are created every day. In recent years, researchers have discovered other possible means by which HIV leads to loss of CD4 cells. These include toxic viral proteins, flashes infected cells, which can kill uninfected cells in the so-called "bystander effect". HIV can also trigger the cells to '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 the activation of immune cells is an essential part of immune function. However, there is increasing evidence that prolonged and excessive immune activation - inflammation - underlies much of the ongoing damage of HIV disease.5
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