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Natural Immunity and HIV

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7 Comments

Benjamin

Hello Dr.Joe, It's is clear that you article is entirely based on an assumption and there is no practical eveidence corroborating your theory. This is similar to your claim while denying the fact 'HIV caused AIDS', later very comfortably you have changed your stance on that. I respect your contributions especially in promoting the safe sex, at the same time the mere purpose of this article based on your wild imagination and some flawed research by Dr. Imagawa some 20 years back is to create controversy. Have you ever thought about implications of this article on some anxious person not trusting their conclusive results. It adds fuel to their anxiety and they may never get out of it. I suggest you to focus on promoting useful things leveraging on your credibility rather than creating controversies. History will never forgive you then..

September 22, 2014

My name

I have really wondered about the claims that some people have completely asymptomatic infection. I've seen some surveys suggestion that symptoms occur in 90% and other surveys suggesting 50%. Intuitively, it is hard to understand how an infection with HIV could occur without any symptoms at all, especially given the very severe symptoms some people get! As Joseph points out, many factors could affect the initial phases of infection. One explanation could be people who have very slow initial replication of virus (due to either viral or host factors) meaning that the acute phase takes place more slowly and is thus "diluted by time" leading to fewer symptoms. It would enable the body to get the virus under the control with antibodies (and CD8+ cells) when the replication was at a lower level than if the initial replication had been fast. Before HAART some studies suggested disease progression was faster for people with severe ARS symptoms. This again goes back to Joseph's original complaint about how people view HIV infection as having just "one couse" instead of being open to different courses even if they may be rarer than the standard course. For other viruses, asymptomatic infection and silent carriers are not uncommon. You can get infected by hepatitis and not get any symptoms at all for instance, whereas other people might get severe jaundice. There are clearly host factors at play - some people tend to get relatively high fevers even from mild infections like the common cold, whereas others only run fevers with more serious infections like the flu. Some get sick (with fevers etc.) from a vaccine whereas others don't (in that case the agent is the same, so this difference must definitely be caused by host factors). Then there's also the subjective component. One person's "I feel sick" maybe another persons "I'm not feeling totally on top, I will just take a nap at lunch". Some symptoms may be subtle and not noticeable in the lighter courses - a swollen lymph node could easily be overlooked. Then there's the problem Joseph points out about recall. Some people are not even sure when they were infected so that may cause confusion in recalling ARS (for instance if they were infected way longer back and by a different encounter than they think). Other people may have plainly forgotten they were sick or may not even have thought they had symptoms (i.e. relating to the subjective component). So all in all there are biological reasons why people's acute courses may vary (and at least theoretically not cause any symptoms at all), and there are practical reasons why symptoms might be forgotten even when they occur. How much of each explanation contributes to the "asymptomatic" cases are not known. To someone who is sexually active, getting symptoms that resemble ARS might be a good reason for getting an HIV test taken (at the appropriate time) and taking care not to infect other people (after all, if you have symptoms, you could have another disease that you could also infect with!) However, it wouldn't be wise, for many reasons, to conclude you are definitely HIV negative, just because you didn't have symptoms of ARS.

November 14, 2010

Joseph Sonnabend

James, thanks for your comment. Why do only some people experience an illness of varying severity when they seroconvert? As you suggest one reason may be that, as with many pathogenic microorganisms, there are HIV strains with greater or lesser virulence or replicative competence. But this would only be one factor which determines if a primary illness occurs at all and if it does how severe it will be. The size of the infecting dose of virus and how it’s introduced into the body will have an influence. Host factors will also play a role; these may be genetic and immunologic, conferring relative degrees of resistance. Concomitant infections may also have an effect on the initial response to infection. The primary illness is associated with the appearance of HIV in the blood stream, which in turn is a reflection of the extent of HIV replication. So the primary illness will be affected by all those factors, both related to HIV and the host that can influence HIV replication. The proportion of infected people who experience an illness at seroconversion can only be estimated very roughly. The illness can be mild and forgotten; it can also resemble other mononucleosis like viral illnesses. It’s even possible that occasionally the illness was indeed mononucleosis like illness caused by another virus which then activated HIV that had been present as proviral HIV DNA in the host genome.

November 2, 2010

Joseph Sonnabend

Thank you for your comment. Perhaps one reason why there seem to be loose threads in HIV research is that we were presented with a description of HIV disease at the end of the 1980s, only 5 years after HIV was discovered. This description, illustrated in the very familiar graphic I reproduced could not have been based on extensive observations, yet it was eagerly accepted seemingly without question. When observations were made that were inconsistent with the model they often were either ignored or as in the case of David Imagawa, aggressively rejected. This preference for theoretical constructs rather than empirical evidence is quite odd in a society where scientists pride themselves in their respect for evidence. Maybe not, as noted by Oliver Wendell Holmes in 1860: "The truth is that medicine, professedly founded on observation, is as sensitive to outside influences, political, religious, philosophical, imaginative, as is the barometer to the changes of atmospheric density” Your theory that some of the symptoms of the seroconversion illness result from activation of other infections seems perfectly reasonable, and if these add substantially to immune activation at that time, might determine a more rapid progression of HIV disease. There is a reciprocal relationship between HIV and herpes viruses, particularly CMV and EBV, which can mutually enhance each other in a positive feedback interaction. So both your idea and what I proposed could exist. There could be some seroconversions that are triggered by another infection and I’m reminded of very early evidence of EBV reactivation preceding HIV seroconversion. Here is another example of an observation that did not fit with the model and was simply ignored. I hope your wise words to the worried well will be heeded. Certainty is an unrealistic expectation but we can recognize relative risk, and in this regard a negative test is a great reassurance.

November 2, 2010

James

Interesting and promising! I'm not a scientist and I've only begin educating myself on this disease a couple weeks ago. The more I read, the more questions I have .. I'm sure all of us experience this. They are still calling this a "new" disease? True, it's not as old as measles and the common cold, but 28 years? I so wish this theory would have been focused on and studied more. We very well might have found our vaccine or cure by now. Oh well, I give credit to the pioneers of this theory and applaud all the hard-working scientist' today who are doing their best help understand and to help defeat this virus once and for all. Okay ... now a question I have that I can't seem to find an answer to or anything remotely close to an answer. Strains of the virus. Not really HIV-1 and HIV-2 in that sense but more like how after an infection the patient will take a test to see what kind of antivrals will fail or work based on the virus type in their body. They say 1 in 3 people do not know they are infected because they have no symptoms while 2 of 3 experience mild / moderate symptoms and lastly, most of those infected say they get the worst flu of their life. Most of the people I've heard talk about their acute infection and seroconversion have stated they experienced the worst illness ever. Here is my question: Can it be possible that symptoms of an acute infection can be based off a certain type of strain their infected parnter pass on to them? Example: Poz partner contracted the vius and became VERY ill during seroconversion 6 weeks after infection, thus, he passes the virus onto his un-infected and again, 6 weeks after exposure the newly infected becomes gravely ill. While someone with a different strain experienced no symptoms and any person me infects may not experience symptoms. Thus, the 1:3 ratio. It might explain certain dates of serconversion as well as symptom severity. My hypothesis is very basic and not too scientific and I apologize, I'm not a scientist. Rather, someone who is tired of seeing people suffer over something so natural. It's even extended into the innocent children. It breaks my heart.

November 2, 2010

My name

Hi thank you very much for this article. I too have wondered about the seemingly loose threads in HIV research. There are several reports of unusual HIV infections and observations regarding testing, but none of these reports seem to be followed up by new research, but are not rebutted either, so it's hard to know what to think of it. Another example of this is the studies showing delayed seroconversion after needle-stick injuries in health care workers. This setting has the benefit that one knows exactly the day of exposure and the affected individuals were intensively tested often over long periods. At least one report found that in some cases, it took more than a year after exposure for seroconversion to happen. I've heard someone trying to explain this by the insensitive HIV antibody tests in use at the time. However, this argument doesn't stand up to scrutiny, because these workers were not only screened for HIV antibodies but also for p24 antigen and HIV RNA, for which they were negative too. The samples were even sent to the CDC for additional analysis. What seemed to happen in these cases was that after a long period of absolutely no detectable sign of HIV infection, suddenly there was a burst in viremia, often accompanied by symptoms associated with primary HIV infection. This was followed by HIV seroconversion shortly after. In other words, it was not the production of the antibodies that was the delayed - it was the onset of viremia! I believe this might be a case of the patient havingly only one or a few latently infected T-cells (or even another type of cell). These cells have have the HIV virus in their genome but for some reason, perhaps because the particular T-cells are not activated, there's no production of virus proteins and thus no viremia or antibodies. At some point something happens that activate these cells, thereby kicking off the production of virions. From this point on the infection follows the classical course that would usually have happened a few weeks after the exposure. Finally, I find your idea of a secondary disease triggering primary HIV very interesting. I agree that it could explain the symptoms associated with primary HIV. I have often wondered why there's such a high degree of variability in the reported symptoms. It seems almost any symptom can occur. My own theory has been that at least some of the symptoms are not a result of HIV itself but rather (re)activation of other latent infections as a result of the dramatic weakening of the immune system seen during primary HIV infection, where many patients seem to reach AIDS-like CD4 counts temporarily. This could at least explain the variability in symptoms and can also explain why not everyone gets symptoms. I suspect some of the symptoms, like fever, swollen nodes and perhaps sore throat, might be "core HIV" symptoms brought on by HIV itself, whereas many of the others (rash, mouth sores, genital ulcers etc.) might be due to activations. Finally: to all the worried well out there, don't be afraid that you can't trust you HIV negativ tests. In all likelihood your negative test represent that you don't have HIV. If you are still worried, focus that worry on the other (probably much bigger) risks in your live. You can always get tested again if you experience symptoms or feel sick, but don't freak out. Regarding the health care worker study, keep in mind one can never be absolutely sure that the workers involved didn't get infected by some later, after their needle-stick injury. However, in at least one case a phylogenetic analysis indicated that the person did get infected from the needlestick.

October 30, 2010

Wayne (poz)

This is encouraging. I find there is little to no support for those who are in Poz/Neg relationships as to help support the emotional factors involved with the threat of cross-infection. Thank you for posting this article. It is a step in the right direction of FULLY understanding all the aspects of this epidemic. As stated in the end of the blog, it is to bad this was not a leading thought process in the beginning of this epidemic. It might have lead to better understanding the mechanics of the virus and host interaction and possibly lead to a cure/vaccine sooner. Wayne

October 24, 2010

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