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Resting Cells
I am slightly puzzled. I have been researching the way hiv replicates and am a little confued by one aspect. The virus targets t cells primarily. T cells can be in two different states, either active or resting. My research has led me to discover that hiv can only actively reproduce inside activated t cells and not resting. Inside resting cells it can lay dormant until that cell becomes active, thereby facilitating it's reproduction.
The confusing part is, 95% of our t cells are in a restng state. If someone is newly infected and the virus enters their blood stream, if the few viruses that enter only infects resting cells then how can it replicate immediately? In other words, how can it not lay dormant until these cells are triggered by another pathogen? e.g. longer window period.
The confusing part is, 95% of our t cells are in a restng state. If someone is newly infected and the virus enters their blood stream, if the few viruses that enter only infects resting cells then how can it replicate immediately? In other words, how can it not lay dormant until these cells are triggered by another pathogen? e.g. longer window period.
MEDICAL PROFESSIONAL
Sorry if my assumption about motivation was unwarranted. But there are plenty of better resources than this forum for this sort of question. My reply should be viewed only as a starting point for understanding of the questions you ask, not definitive by any means.
Good luck in your studies.
Good luck in your studies.
Thank you Dr
Incidentally, the question is not related to any of the questions last year. I've been studying various sections of microbiology at uni and this was my motive for coming back to this.
I understand this is not your area of expertise but thank you for your indepth response, very helpful.
Kind Regards
AD
Incidentally, the question is not related to any of the questions last year. I've been studying various sections of microbiology at uni and this was my motive for coming back to this.
I understand this is not your area of expertise but thank you for your indepth response, very helpful.
Kind Regards
AD
MEDICAL PROFESSIONAL
Welcome back to the HIV forum. Of course this forum emphasizes HIV prevention, not the biological aspects of HIV infection, except to the extent biological factors might influence the answers to specific questions. I'm not a virologist, but I'll do my best.
First, there are plenty of cell types other than T lymphocytes that are susceptible to HIV because their surface membranes have the CD4 protein, to which HIV attaches as the first step in entering a cell. These include macrophages, Langerhans cells embedded in the skin (especially common in the foreskin of uncircumcised men, partly explaining the association of being uncircumcised with HIV risk), and others.
Second, I'll assume your statement is accurate about 95% of T lymphocytes being in a resting state at any one time. That sounds about right, but I cannot vouch for it. But even if it were 99%, the remaining 1% seems like plenty to allow infection to take hold. Further, I imagine that as soon as some cells are invaded by HIV, it and other T cells "turn on" in response to the infection, accelerating it and providing more susceptible cells. Much of this process takes place in a matter of hours. And our T cells are turning on all the time, as we are exposed to continuing immunological insults. A skinned knee, a pimple, swallowing various chemicals in foods and the environment, and innumerable other things are going on all the time. In each, some T cells probably activate. Finally, I'm not so sure that resting T cells cannot be infected at all. Resting cells have a certain amount of metabolic activity and I believe they still have CD4 on their surfaces. The difference in susceptibility between resting and active cells probably is one of degree, not absolute susceptibility.
All of this is entirely unrelated to the seroconversion window. The time to develop measurable antibodies to HIV does not depend on a resting period for the virus or infected cells. The window is pretty much the same in every newly infected person.
Your two previous threads a year ago, one each on this and the STD forum, suggest you are pretty anxious about HIV despite low risk for it. If that is your motivation for this question, I would suggest it probably is not in your interest to try to understand the biology of HIV infection. The epidemiologic facts -- i.e. the statistics about transmission risk, window period, etc -- are all that is needed. Scientifically untrained persons can draw all sorts of unwarranted conclusions from the biology of the virus that just don't matter. In addition to seroconversion window, the time that HIV can survive outside the body is another example.
Because the forum emphasizes practical issues in prevention, and because I'm really not an expert in the virology of HIV, I'm not going to permit an ongoing dialog on this topic. Best wishes-- HHH, MD
First, there are plenty of cell types other than T lymphocytes that are susceptible to HIV because their surface membranes have the CD4 protein, to which HIV attaches as the first step in entering a cell. These include macrophages, Langerhans cells embedded in the skin (especially common in the foreskin of uncircumcised men, partly explaining the association of being uncircumcised with HIV risk), and others.
Second, I'll assume your statement is accurate about 95% of T lymphocytes being in a resting state at any one time. That sounds about right, but I cannot vouch for it. But even if it were 99%, the remaining 1% seems like plenty to allow infection to take hold. Further, I imagine that as soon as some cells are invaded by HIV, it and other T cells "turn on" in response to the infection, accelerating it and providing more susceptible cells. Much of this process takes place in a matter of hours. And our T cells are turning on all the time, as we are exposed to continuing immunological insults. A skinned knee, a pimple, swallowing various chemicals in foods and the environment, and innumerable other things are going on all the time. In each, some T cells probably activate. Finally, I'm not so sure that resting T cells cannot be infected at all. Resting cells have a certain amount of metabolic activity and I believe they still have CD4 on their surfaces. The difference in susceptibility between resting and active cells probably is one of degree, not absolute susceptibility.
All of this is entirely unrelated to the seroconversion window. The time to develop measurable antibodies to HIV does not depend on a resting period for the virus or infected cells. The window is pretty much the same in every newly infected person.
Your two previous threads a year ago, one each on this and the STD forum, suggest you are pretty anxious about HIV despite low risk for it. If that is your motivation for this question, I would suggest it probably is not in your interest to try to understand the biology of HIV infection. The epidemiologic facts -- i.e. the statistics about transmission risk, window period, etc -- are all that is needed. Scientifically untrained persons can draw all sorts of unwarranted conclusions from the biology of the virus that just don't matter. In addition to seroconversion window, the time that HIV can survive outside the body is another example.
Because the forum emphasizes practical issues in prevention, and because I'm really not an expert in the virology of HIV, I'm not going to permit an ongoing dialog on this topic. Best wishes-- HHH, MD
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