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Anonymous
Unregistered

How common is it?
      #198583 - 07/02/06 12:44 PM

How common is it to be infected with HIV and test negative 6 months or more after being infected. Could different strains of the virus cause it not to be picked up? Also, I have only tested for HIV-1, is it necessary to test for HIV-2 ?

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Anonymous
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Re: How common is it? new
      #198600 - 07/02/06 04:31 PM

people who have symptpms take longer to seroconvert. what was your exposure ? did you have flu like symptoms 2-4 weeks after the exposure to HIV or you just think you were exposed ?

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Anonymous
Unregistered

Re: How common is it? new
      #198602 - 07/02/06 06:30 PM

I'm a gay male, the incident was receptive anal intercourse without protection. Happened only once. I've had burning sensations in my legs and feet on and off since about four weeks after the incident. Tested at 13 weeks and 19 weeks by Elisa blood test. Both tests were negative. I'll test again at 26 weeks.

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Anonymous
Unregistered

Re: How common is it? new
      #198607 - 07/02/06 07:12 PM

You do not need to test again. You already have not 1, but 2, conclusive negatives.

OH and people with symptoms do not take longer to sero-convert. Acute Retroviral Syndrome is the name for those symptoms. It's when the body is seroconverting. Not everyone has symptoms, but everyone will have a conclusive test at 3 months.

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MiamiLat
Guardian

Reged: 12/30/05
Posts: 396
Loc: Miami, FL
Re: How common is it? new
      #198613 - 07/02/06 07:42 PM

"Anon", that is incorrect information. People who have symptoms DO NOT take longer to seroconvert. ARS is when the body is actually seroconverting. Most experience it, but some do not. Yet, 12 or 13 weeks (3 mos) is considered conclusive for all.
To the original "Anon" poster, to answer your question, it is extremely unlikely for you to be pos and test neg at 6 mos. You have tested conclusively NEG up till now. Since you're exposure was high risk, a test at 6 mos wouldn't be a bad idea for your own peace of mind and to confirm your NEG status.
As for your question about HIV-2, some ELISAs screen for both HIV-1 and HIV-2 as well as the OraQuick Rapid Advance. Find out which test was actually performed...

--------------------
"Education, prevention, awareness, research, and support"

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Anonymous
Unregistered

Re: How common is it? new
      #198618 - 07/02/06 08:39 PM

no it is true people who have severe ARS take longer for the body to produce antibodies. people who do not have ARS have stronger immune systems and produce antibodies to fight the infection and they show up quicker on the elisa test. i have studied HIV for almost 15 years and read this in one of the medical journals. also with the testes used in 2006 6 weeks is sufficient for a accurate status in the old days late 80s and 90s the window was 6-12 weeks. there have only been a few documented cases where it took longer.

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Anonymous
Unregistered

Re: How common is it? new
      #198622 - 07/02/06 09:13 PM

You've studied this for 15 years...and read this in a medical journal? What year, which one. Was the study long term? How many people were studied? Is this true with all disease or just HIV? What were the parameters? Are you working in the field or have an overwhelming curosity about everything HIV? Or just an overwhelming curosity about ARS and testing, to hell with the actual disease and it's long term effects eh?

Odd with all that research you don't understand basic body function. When people get sick, that is the body fighting off the infection. That's is what causes the 'symptoms' The harder the body fights off an infection (more severe symtoms) the stronger the immune function, the quicker antibodies are developed for whatever disease the body has encountered. A lesser or no reaction does not mean a better immune function. It actually means a poor immune response.

You need to look no further than people in late stage disease to see that a poorly working immune system will not recognize a threat and will not react with illness (symptoms). People in late stage will develop illness that have the ability to take hold because of the very fact the person has no severe reaction to the disease. Study up on reconsistion syndrome. It showed up when anti-retrovirals got better and people started to be able to recover immune function. Funny thing. Once they did, they got sick with all sorts of things. Why, because the immune function started to once again recognize invading disease.

You need to study a bit more.



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Anonymous
Unregistered

Re: How common is it? new
      #198625 - 07/02/06 09:32 PM

it's pretty well known that people who have severe ARS symptoms take longer to show positive on a Elisa Test. I agree with the other guy.

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Anonymous
Unregistered

Re: How common is it? new
      #198627 - 07/02/06 09:53 PM

Since it 's pretty well known, I'm sure you won't have a problem providing links to medical studies citing this will you?

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Anonymous
Unregistered

Re: How common is it? new
      #198630 - 07/02/06 10:16 PM

What do you mean with "it take longer"??? How long? 3 months??? 6 months a year, it would ne nice to know?

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Anonymous
Unregistered

Re: How common is it? new
      #198634 - 07/02/06 10:56 PM

yes i have studied HIV for 15 years and you can find the links yourself. i do not have access to the old medical journals anymore so you will have to find it yourself. i studied everything from the library at stanford university in palo alto california from 1990 when people i went to school with were dying of AIDS.




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Virgo
Grand Master

Reged: 06/01/06
Posts: 171
Loc: Massachusetts
Re: How common is it? new
      #198648 - 07/03/06 08:20 AM

Please do not listen to ANYONE other than the experts!! A 3 MONTH test is conclusive!! Doesnt matter how bad your "ARS" symptoms were, if ya had a cold, or any other illness.

The ONLY people who MIGHT take a little longer are those with SEVERLY COMPROSMISED immune systems. And IF you had a SEVERLY COMPROISED IMMUNE problem YOU WILL KNOW!!

A test at 6 weeks is probably around 98-99% accurate. So a test at 13 weeks is like 99.9999%. NOTHING in this world is ever 100% accurate.

If you tested 3 months past your possible exposure, then you need to put this behind you. Experts would not be recommending a 3 month test as being conclusive if they did not truely trust it!!

Congrats on your negative result, and remember is YOUR job to protect your status!!

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SteveR
Legend

Reged: 07/19/05
Posts: 576
Re: How common is it? new
      #198691 - 07/03/06 03:07 PM

It's virtually unheard of (as in, only a few cases ever) to test negative at 6 months and actually be positive.

You do not need to test for HIV-2 specifically unless you've been in West Africa or been exposed via someone from West Africa. HIV-2 is very rare outside of that part of the world. Besides, most HIV tests will pick up HIV-2 anyway.

Re. the other posters and the discussion of severity of acute illness vs. appearance of antibodies, I don't believe a link between the two has ever been proven. In other words, some very sick people make antibodies right away and some take longer; some people who have little or no ARS illness have antbodies quickly and some don't.

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Anonymous
Unregistered

Re: How common is it? new
      #198702 - 07/03/06 05:05 PM

[quote]yes i have studied HIV for 15 years and you can find the links yourself. i do not have access to the old medical journals anymore so you will have to find it yourself. i studied everything from the library at stanford university in palo alto california from 1990 when people i went to school with were dying of AIDS. [/quote]

I see, so your saying your 'latest' information is from 1990? Since you say you only have links to OLD medical journals, that blows your 15 years of study. That's 16 years ago. I wouldn't bother to try and find those links. Times change. I don't know about in 1990, but now you should be able to supply links if you really want anyone to take you seriously.

I'll start:

Here are links to the studies that were done that showed that once an immune function started working again, people had symtoms of OI's. Hence, the better the immune function, the more symptoms, the quicker reaction to infection.

8th Conference on Retroviruses and Opportunistic Infections


Chicago, IL - February 4 - 8, 2001




Relative significance of different pathways of immune reconstitution in HIV-1 infection as estimated by mathematical modeling.
Conf Retroviruses Opportunistic Infect 2001 Feb 4-8; 8:157 (abstract no. 382)
Kaufmann G, Zaunders J, Murray J, Kelleher AD, Lewin SR, Solomon A, Smith D, Cooper DA; NCHECR, Sydney, Australia.



--------------------------------------------------------------------------------

Background: A major goal of antiretroviral HIV-1 therapy is the reversal of HIV-1-associated immunological dysfunction. However, the pathogenetic mechanisms involved and their significance are largely unknown.

Methods: Based on the life cycle of na´ve, activated and memory CD4+ T cell subsets, a mathematical model of immune reconstitution was developed and applied to data for T cell subsets in individuals with acute (n = 28) or chronic (n = 30) HIV-1 infection receiving potent antiretroviral therapy. The final model considered three pathways of immune reconstitution for na´ve cells, including thymic production, peripheral expansion and re-distribution of na´ve cells from lymphoid tissue. The reconstitution of the memory compartment was fitted through antigen- dependent activation, differentiation and expansion of na´ve cells and peripheral expansion of memory cells as well as re-distribution of memory cells, trapped in the lymphoid tissue.

Results: Estimated median half-lives for na´ve and memory CD4+ T cells were 114 and 21 days, while total production rates were 9.1 x 10(7) and 2.4 x 10(9) cells/day, respectively. Peripheral expansion and thymic production contributed equally to the regeneration of na´ve cells, but peripheral expansion of memory cells was larger than production of these cells by differentiation of na´ve cells. A comparison of subjects with acute and chronic HIV-1 infection revealed that the main difference was the more rapid release of a larger number of na´ve cells in treated acute HIV-1 infection. Thymic function and peripheral expansion rates of na´ve cells as well as the parameters for memory cells, however, were similar in both cohorts.

Conclusions: In conclusion, a model of immune reconstitution was developed that fitted well the time course of CD4+ T cell subsets and provided realistic estimates for the turnover of these cells. The model appears to be a useful tool to compare immune reconstitution in different cohorts of HIV-1-infected individuals.


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Keywords: AEGIS, HIV Infections, HIV-1, Antiretroviral Therapy, Highly Active, T-Lymphocyte Subsets, Acquired Immunodeficiency Syndrome, Models, Theoretical, Models, Immunological, T-Lymphocytes, Thymus Gland, AIDS
010204
382


************************************************************************

14th International AIDS Conference


Barcelona, Spain - July 7-12, 2002




HAART allow the reconstitution of cytomegalovirus (CMV)-specific cell-mediated immunity in HIV-infected patients.
Int Conf AIDS 2002 Jul 7-12; 14:(abstract no. ThPeA7140)

Diaz MA, Blanc D, Troadec C, Eliaszewicz M, Gonzalez G, Algara DS
Institut Pasteur, Paris, France


--------------------------------------------------------------------------------

BACKGROUND: Because CMV retinitis could be observed after initiation HAART, we aimed better understand how HAART reconstitute the CMV-specific immunity. We prospectively studied patients receiving HAART whose CMV retinitis was quiescent in order to establish the degree of T lymphocyte reconstitution obtained during one year of therapy.

METHODS: We measured the number of circulating T-cells and their subsets, the plasmatic HIV-RNA concentration, the specific proliferation cellular (LPR), the specific secretion of cytokines (IL-2, IL-4, IL-5, IL-10, IFN-γ and TNF-α), and the cytolytic activity of CD8+ T cells against autologous fibroblasts infected with CMV. All tests were done prospectively at five time points during follow-up: baseline, 3 months, 6 months, 9 months and 12 months.

RESULTS: In untreated patients, we found a CMV-specific CTL activity despite the absence of CMV-specific LPR, secretion of IFN-γ, TNF-α and IL-2. However, the reconstitution of these CMV- specific responses was observed (LPR and cytokines secretion) after 6 months of HAART simultaneously with a significant increase of CMV-specific CTL activity and a suppression of HIV load. Moreover, the reconstitution of CD4+ T cells during HAART, showed a characteristic delay of increase in na´ve CD4+ T cells compared to the memory CD4+ T cells.

CONCLUSIONS: Our findings suggests that one year of HAART, allowed the recovery of various CMV-specific responses, probably by a redistribution of memory CD4+ T cells in our cohort of patients. Measurements of CMV-specific responses during the reconstitution by HAART are needed to reduce the risk of CMV disease when the anti-CMV therapy could be discontinued in HIV-infected patients.


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Keywords: AEGIS, Antiretroviral Therapy, Highly Active, HIV, Cytomegalovirus, Cytomegalovirus Retinitis, HIV Infections, Immunity, Cellular, CD4-Positive T-Lymphocytes, Cytomegalovirus Infections, HIV Seropositivity, Anti-HIV Agents, Cytokines, Human, immunology
020707
ThPeA7140

***************************************************************

Evaluation of immune reconstitution during HAART.
Int Conf AIDS 2004 Jul 11-16; 15:(abstract no. MoPeA3062)

Gomez FA, Romero SP, Bernal JA, Ruiz P, Rosety M, Garcia-Gil D, Rivera C
Hospital Universitario Puerto Real, Department of Medicine, University of Cadiz, Cadiz, Spain


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BACKGROUND: Immune reconstitution is one of the goals of HIV treatment. IL-7 is critical for thymopoiesis and for the regulation of T cells in the periphery. An inverse correlation has been reported between plasma IL-7 and CD4 count, suggesting that IL-7 may be a part of the compensatory mechanisms of CD4 depletion. Objectives: We have performed a prospective study to assess whether, high levels of IL-7 prior to HAART may contribute to immune reconstitution and to the increased CD4 count associated with this treatment in a cohort of 48 na´ve patients before HAART (M0), then at 6 (M6), 12 (M12) and 24 (M24) months while on HAART.

METHODS: Naive CD4 cells were identified by double expression of CD45RA/CD621, and functionality by CD28. Activation markers of CD8 cells were HLADR and CD38.

RESULTS: Viral load (pVL SD) at M0 (236,124 2,189 copies/mL) became undetectable (<50 copies/mL) at M6, M12 and M24. Increases of CD4 cells were very heterogeneous (from 112 to 865 cells/mL). CD4 counts (SD) increased from 178 69 at M0 to 239 98 at M6, 354 130 at M12 and 489 227 at M24. Levels of IL-7 were elevated at M0 (11.5 12.8 pg/mL) in comparison to a witness group of non-HIV infected patients (1.7 1.1 pg/mL; p<0.001), and progressively decreased during HAART to 3.9 5.2 pg/mL at M24 (p<0.0001). An inverse significant correlation was observed between plasma IL-7 and CD4 count during HAART (r = -0.879; p<0.001). Patients presented a persistent hyperactivity of CD8CD38 cells, more na´ve CD4 cells and, a decreased functionality of CD4 cells (p<0.003), that became non significant at M24.

CONCLUSIONS: Immune reconstitution is feasible in patients with sustained plasma RNA undetectability. IL-7 levels may predict CD4 recovery during HAART.


--------------------------------------------------------------------------------
Keywords: AEGIS, Antiretroviral Therapy, Highly Active, CD4 Lymphocyte Count, Viral Load, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Antigens, CD45, Acquired Immunodeficiency Syndrome, Antigens, CD4, ADP-ribosyl Cyclase, Antigens, CD28, Interleukin-7, T-Lymphocytes, Antigens, CD, Prospective Studies, CD38 antigen, Humans, immunology, methods

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This should keep you busy for a while

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Anonymous
Unregistered

Re: How common is it? new
      #198703 - 07/03/06 05:06 PM

[quote]Please do not listen to ANYONE other than the experts!! [/quote]

I hope you aren't including yourself in that category.

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