Are You Positive?

by Stephen Davis

  Chapter Ten

  Sarah had decided to try Walter’s Country Kitchen at The Big Chill for lunch. It was within walking distance of the courthouse, and they advertised “meat and three,” meaning that you had your choice of a meat dish and three side dishes for one price. She thought she should try southern cooking at some point; and besides, it was a non-smoking restaurant, still unusual in South Carolina, she was told.

  She passed on the meat, vegetarian that she was, and actually enjoyed the side dishes quite a bit, especially the mashed potatoes – real mashed potatoes. Maybe southern cooking isn’t that bad after all, as long as you remember to ask for “unsweet” tea.

  On the walk back to the courthouse, she noticed that the temperature had dropped significantly, maybe even ten or fifteen degrees. At least, it felt like it. Must be a big cold front coming in.

  Inside, the courthouse was nice and warm, and the judge wasn’t late returning this time. Court resumed promptly at two p.m. and Dr. Fowler is back on the witness stand.

  “Dr. Fowler, I want to concentrate for a few minutes on these antibodies that our immune system creates.”

  “Okay. What would you like to know that I haven’t already told you?”

  “For example, does the average human being produce a lot of these antibodies?”

  “That depends entirely on what kind of life they lead, what kind of life their parents led, and whether they had the good fortune of being breast-fed.”

  “Will you please explain that?”

  “As I said this morning, we can get antibodies at least two different ways. One is to create them when we are invaded by a previously unknown organism; the other is to inherit antibody memory chips from our parents. But our parents also created antibodies only when their bodies felt threatened as well. So, basically, the number of different antibodies anyone has will be mainly dependent on how many dangerous things they and their parents had been exposed to that their immune systems decided needed to be guarded against.”

  “Are you saying that the more diseases we get, the more antibodies we will create to protect us in the future?”

  “Yes, basically. And that makes good common sense, doesn’t it? If we get sick, our immune system goes to work to fight the invasive organism; and when it’s successful, it creates antibodies to protect us from getting that same illness again. The more often we encounter a new or different disease, the more antibodies we will create. But remember, we don’t actually have to get sick to make antibodies.”

  “Tell us again, please.”

  “Like with vaccinations, whenever we are exposed to a sufficient amount of a foreign substance – even if it’s not enough to create obvious symptoms of disease – our immune system goes through the same process of creating antibodies so we won’t get sick in the future.”

  “You’re saying that those who have more illnesses than others, and those exposed to more illnesses even though they don’t actually get sick, will have more antibodies.”

  “As a general rule, yes.”

  “So someone who has led a normal life, has been careful about their health and their bodies and what they get exposed to, might have a lot fewer antibodies than someone, say, who lives on the street, or lives a dangerous lifestyle, and develops a lot of health problems.”

  “Absolutely.”

  “Dr. Fowler, how does this translate when we talk about the HIV tests?”

  “I can say it very simply, and then I’ll explain it. The more antibodies someone has – to anything – the more likely they are to test Positive on an HIV Antibody test.”

  “Why?”

  “First and foremost, because there are more antibodies in their blood to react with the test kit proteins.”

  “And why would that make a difference?”

  “Because antibodies are not monogamous.”

  There’s a buzz in the courtroom, and even a couple jurors turn to each other and ask, “What did he just say?” loud enough for Dr. Fowler to hear.

  “I said, antibodies are not monogamous, and I meant that exactly as it sounds. I could have also said it the other way around and maybe that would make more sense: Antibodies are very promiscuous, in that they will try to mate with lots of different invaders.”

  The judge gavels the courtroom whispers into silence. “Continue, Dr. Fowler.”

  “Look, I have said a number of times that the human body is extremely efficient and very lazy. When a foreign substance enters the body, the first thing the immune system wants to do is find out if it already has an antibody to counteract the attacker. It will send out its entire collection of antibodies, if necessary, to see if there is already one with the right key to fit into the lock, if you remember the video presentation. In other words, antibodies that were created to handle one virus, for example, will try to fit into the lock of a different virus when it appears, thinking that there may be enough of a match to unlock it. Hence, antibodies will try to mate with almost anything when there’s a chance to save the body some work and not make it develop new antibodies from scratch.”

  This is such an important point for later testimony that Campbell wants to see how many times he can get Fowler to explain it. “I’m beginning to get the picture, Dr. Fowler. Someone with more antibodies, inherited from their parents or created as a result of exposure to a lot of different illnesses, will stand a better chance of having one of their existing antibodies be enough of a match to deal with a new foreign substance.”

  “Right – as long as their immune system is working properly. An antibody created against one kind of flu, for instance, might easily work against another kind of flu; or even against a completely new virus causing a brand new disease we’ve never heard of. So when a foreign invader comes along, these antibodies run around as fast as they can trying to mate with anything they can get their hands on. Therefore, as I said, they are not monogamous. So when you asked about how this translates if we talk about an HIV antibody test, if someone has a lot of antibodies already coursing through their blood, there’s a greater chance that one of those antibodies will find a lock that it fits on one of the test kit proteins – even if it’s not a perfect match – and cause a positive reaction on the test.”

  Campbell doesn’t want to get too deep into the question of false positive test results yet, but he can’t let this opportunity go. “I assume, Dr. Fowler, you’re suggesting that those with more antibodies could get more false positive results on an HIV test.”

  “More false positives, yes, but also more true positives, if there actually is such a thing.”

  “Well, I want to talk to another witness about false positives, but what do you mean when you say ‘more true positives’ as well?”

  “I mean that the more antibodies someone has, the more positive results we’re going to get on an HIV test, regardless of whether the test proteins come from the actual Human Immunodeficiency Virus or not, because that person will have more antibodies that could match up with the test proteins and produce a reaction.”

  Campbell is not sure he totally understood that. “What exactly did you just say?”

  Fowler realizes he wasn’t that clear. “Let me put it this way… if the test kit proteins are not specific or unique to HIV, then these same proteins will be found in other viruses or bacteria as well. The more antibodies someone has, the better the chance that they will test Positive on an HIV test when, in fact, their antibodies were designed for one of these other diseases.”

  “Is this just a theory, or is there evidence to support what you’re saying?”

  “There’s evidence – no doubt about that. For example, the CDC says that the majority of those testing HIV-Positive in the U.S. today are African-American – at a rate of about 2 to 1 over White Americans. But scientific studies have also found that African-Americans naturally have about twice as many antibodies than White Americans. And, of course, we hear so much about how many Africans are testing HIV-Positive. Well, other studies show that Africans have t
wice as many antibodies as African-Americans, and four times as many as White Americans.”

  Campbell figures that the best he can do at the moment. “Can what you just said explain why those who were drug addicts and high-risk gay men were mostly the ones testing HIV-Positive on the ELISA when it first came out?”

  “Very much so. And hemophiliacs as well. Hemophiliacs, for example, had to take injections of other people’s blood about twice a week. That means they were receiving foreign proteins from literally hundreds of other people. The problem with this is that their own bodies would then have to create a whole host of new antibodies in attempt to get rid of these foreign proteins. This would have given them an enormous number of diverse antibodies that could react on an HIV ELISA test.”

  “And the drug addicts and high-risk gay men?”

  “They both have a lifestyle of contracting quite a lot of diseases, from sexually transmitted diseases to hepatitis to herpes, you name it. Yes, both those groups will have a disproportionately higher number of antibodies, and a wider range of antibodies, than the rest of us.”

  “So it didn’t surprise you in the mid-1980’s when these three groups – drug users, high-risk gay men, and hemophiliacs – were the ones who were predominantly testing HIV-Positive?”

  “Not in the least. It’s what you would expect from this kind of antibody test.”

  “But were they testing positive for HIV?”

  “There’s absolutely no way to tell that. I heard your previous witness, Dr. Richardson, explain to you that the test kit itself has never been proven to accurately identify HIV antibodies. Maybe it does; but probably it doesn’t – at least according to the scientific studies I’ve read. The only thing I can add from my perspective is that a virus like HIV is not, by definition, capable of choosing its victims by gender. The fact that drug addicts, who are mostly men; hemophiliacs, who are all men; and sexually-overactive gay men, made up 99-plus percent of those testing HIV-Positive was evidence, at least to me, that one of two things had to be true: first, the HIV ELISA test itself was so overly sensitive that it was reacting with a lot of different antibodies these particular people carried around more than others; or two, the test proteins themselves were not specific or unique to HIV and therefore allowed antibodies created against other diseases to react with the test kit too often. And frankly, I’ve decided that it was probably both.”

  Campbell has to remind himself to save the question of false positives for later. “Again, I want to get into this concept of false positives – of antibodies to other things causing a positive reaction on an HIV test – with another witness. But I want to ask you more about the sensitivity of the test to a wide range of antibodies.”

  “Well, this is the problem with any antibody test, not just with the HIV test. Whenever you design an antibody test, you have to go through a procedure to try to make the test not react with antibodies other than the ones you want it to.”

  “And how is this accomplished?”

  Fowler seems pleased that he has the opportunity to repeat what he thought was the most important point in this trial. “First, by ensuring that the proteins used in the test are as specific and unique as they can be to the agent you want to test for. You’ve already heard that this was apparently not done for the HIV test. But you can never be 100% successful with that. So the second way is to dilute the blood sample from the patient you’re testing to limit the number of antibodies that will react with the test kit.”

  “Dilute the blood?”

  “Yes. Sorry, not clear? Okay, let’s use an example. Let’s say you want to design an antibody test to see whether someone has Antibody A in their blood. First, you do the best you can to make sure the test kit proteins are as specific and unique as possible to Antibody A. Then you run your test, and it comes out positive. But when you do a validation study on it, you find out that the person really didn’t have Antibody A in their blood after all; they had Antibodies B, C, and D instead, which apparently reacted with the test kit protein. So you want to try to get rid of B, C, and D so they don’t cause a positive reaction, because you’re looking for Antibody A. You can often accomplish that by diluting the blood and limiting the number of antibodies that interact with the test kit.”

  “Are all antibody tests done on diluted blood?”

  “Many of them, yes; otherwise there are too many antibodies available to cause false positive reactions.”

  “What kind of dilution are we talking about?”

  “Usually 5 to 1, 10 to 1, maybe even 20 to 1. You keep experimenting until you find the best balance between too much sensitivity and too much specificity.”

  “And what does the HIV ELISA test call for in terms of diluting the patient’s blood?”

  “That’s the amazing thing: It calls for 400 to 1 – many times more than any other antibody test I’m aware of.”

  “And why do you think it’s necessary to dilute the blood 400 times for an HIV test?”

  “I don’t know the exact answer to that question. I assume that there were too many other antibodies reacting to the test kit at lesser dilutions, creating too many false positives. We also have to remember that the so-called AIDS experts started with the idea that AIDS was caused by HIV, and therefore only people who were getting AIDS should have positive HIV-antibody tests. So they had to keep diluting the blood until at least most of the HIV-Positive test results occurred in the high-risk groups for the disease. And we’ve already discussed the fact that these same high-risk groups were those who would have more antibodies in general, from their exposure to other diseases; so apparently they had to use an astronomical dilution for the test to appear accurate.”

  “But you don’t know that for a fact, Dr. Fowler?”

  “No, but it makes sense, doesn’t it? What I do know is that an experiment was done by a doctor in New York where he ran HIV ELISA tests on completely undiluted blood from HIV-Negative people, and all of them came out Positive!”

  “Everyone was HIV-Positive?”

  “That’s correct. If we ran an HIV ELISA test on everyone in this room – including the judge and the jury – without diluting their blood 400 times, we would all test HIV-Positive.”

  There’s an audible gasp that makes its way around the room.

  “What does that say to you about the HIV ELISA test?”

  “It says that the test kit proteins themselves are so generic – so non-specific and non-unique – that a large number of antibodies created to fight things other than HIV will react with them and cause a positive test result.”

  Campbell can’t think of a better lead in to his next witness. But is he finished with Fowler? He checks his notes and is still not sure. “Dr. Fowler, before I go on, is there anything else we need to know about the antibodies our immune system creates as they relate to the HIV antibody tests?”

  “Actually, yes, there is. I’ve talked about people with higher levels of antibodies in their blood being more likely to test Positive on an HIV ELISA. What I haven’t said, because we don’t know for certain, is that at some point, high levels of antibodies may indicate a broken immune system rather than a healthy one – a bad sign instead of a good one. In other words, it’s possible that if the immune system should start to break down for some reason, it could stop functioning normally – like sending out existing antibodies to fight an unknown invader to see if it already has one that works. Instead it might start producing more and more antibodies from scratch until the system gets overloaded. Frankly, we just don’t know enough yet about how this whole thing works.”

  “But that would explain why people whose immune systems are in trouble might also be reacting positively on an HIV test, wouldn’t it – simply from having too many antibodies?”

  “That’s a possibility, yes.”

  “Well, that brings us to the next topic I want to discuss, and that is the Helper T-cells of the immune system that you described in the video. They have another name, don’t they?”

&n
bsp; “Yes, they’re also called CD4 cells.”

  “We sometimes count these CD4 cells, don’t we?”

  “Yes, sometimes.”

  “Why would we count the number of CD4 cells someone has?”

  “That’s really a good question. It used to be because we thought that the number of CD4 cells was a direct indication of the health of the immune system.”

  “But that’s not true any more?”

  “Well, there is a lot of contradictory evidence that suggests maybe there’s not such a direct correlation after all.”

  “Such as…”

  Fowler pauses to decide where to begin his answer. He looks at the jury to try to see how well they have been following him so far. Since no one’s eyes appear to be completely glazed over, he assumes they can handle a little more technical information.

  “As you know, HIV is supposed to be the cause of the demise of the immune system, which then leads to the body being unable to fight off opportunistic diseases; the person gets AIDS and dies. Part and parcel of that definition of AIDS is a broken immune system. So for years – and still today, as a matter of fact – an HIV-Positive’s CD4 cell count was thought to be an indication of progression to AIDS. But a major study in 1991 – I think the researcher’s name was Hill – found that CD4 counts were not really a reliable marker to predict progression to AIDS in HIV-Positive subjects. What Dr. Hill said exactly was that ‘variance in CD4 from… non-HIV related longitudinal fluctuations needs to be accounted for in analysis of the prognostic power of CD4 in HIV infection.’ Since then other studies have found HIV-Negative people to have low CD4 cell counts as well.”

  “When you say ‘a low CD4 count,’ what constitutes a normal CD4 cell count?”

  “The normal range is usually considered to be between 500 and 1500.”

  “500 and 1500 what?”

  “Sorry. 500 to 1500 CD4 cells in a cubic millimeter of blood.”

  “That’s a fairly wide range, isn’t it?”

  “Yes, and a person’s CD4 cell count can vary widely within that range, depending on a lot of factors, even in the course of 24 hours. Just go out and lie on a beach for a while and your CD4 cell count will go down. Any time we don’t need our immune system to be actively fighting some perceived threat, it will rest – take a nap, if you will, and fade into the background.”

  It was a really good example that Campbell had never thought about. He’s glad Fowler had.

  “What other factors will impact a CD4 cell count, Dr. Fowler?”

  “Well, it’s now been well documented that malnutrition is one of the biggest things that can lower a CD4 cell count. Malnutrition, chronic stress and fatigue. On the other hand, infections, and even vaccinations, will make the CD4 count go up as the immune system responds to a foreign invader and builds up its armies. Generally speaking, if you have high CD4 cell counts, your immune system is considered to be doing pretty well; and if you have very low CD4 cell counts, you're considered to be in trouble.”

  “But you said that healthy people who were HIV-Negative could also have low CD4 cell counts.”

  “Yes, they can. Another recent study in Africa found HIV-Negative people with lower than normal CD4 cell counts – around 350. That’s why there is so much controversy about using CD4 cell counts to diagnose AIDS or to begin HIV drug therapy.”

  “But isn’t that exactly what the CDC has been doing ever since 1993? Doesn’t the CDC define some AIDS cases based solely on the fact that someone is HIV-Positive and has a CD4 cell count of 200 or less?”

  “Yes; and frankly, it’s totally ridiculous. There are a lot of very healthy people running around out there with low CD4 counts. But I understand that since the mid-1990’s, more than half of the AIDS diagnoses are based on this CD4 cell count definition. So even though many of these people have no symptoms whatsoever – they’re not sick by any stretch of the imagination – they are being told they have AIDS. And to make matters worse, you only need to have one CD4 count of 200 or less to be diagnosed as an AIDS case. One low count, one time, and you are forever branded. But I would suggest to you that we all probably have a CD4 cell count of 200 or less at some time in our lives, based on the amount of stress we are under, or how much sleep we’ve gotten, or a poor diet, or any number of other factors. Remember that the CD4 count normally goes up if we are under attack by a foreign invader, and goes down when there’s no need for the immune system to be so active. So if we are not sick, or there’s no threat, but we simply haven’t gotten enough sleep or food due to a prolonged stressful situation, it’s quite possible for our CD4 cell count to drop to 200 temporarily. And if we should happen to take a CD4 count at that moment, we’re liable to be told we have AIDS and are likely to die soon – if we have tested HIV-Positive.”

  Campbell looks up suddenly, as if he just had a major revelation. “Dr Fowler, what would happen to a person’s CD4 cell count when they are told they are HIV-Positive, especially if they have no symptoms of any disease?”

  Fowler thinks for a moment and then has the same look of surprise. “Well, now that you mention it, I can’t think of any more stressful situation than being told you are HIV-Positive! After all, it’s the equivalent of a death sentence – intense emotional and psychological stress, not to mention the family and social stress. It’s easy to imagine someone losing a lot of sleep and not eating well in the coming days and weeks after such a diagnosis, and it wouldn’t surprise me at all if their CD4 cell count plummeted because of it. If they were to take a CD4 count at that time – which most do shortly after a Positive diagnosis – it’s very probable that it would be quite low. Therefore, rather than a low CD4 cell count being the cause of AIDS, it is entirely possible that exactly the opposite is true: an HIV-Positive diagnosis could be the cause of a low CD4 cell count. In fact, as I said before, if HIV were actively attacking the immune system as the so-called AIDS experts want us to believe, you would expect the CD4 cell count to go up, not down.”

  Campbell looks back at his notes, wanting to pick up where he left off before that short but very important detour. “Dr. Fowler, in the last few minutes you’ve used words like ‘very probable’ and ‘entirely possible.’ Don’t we know any of these things for sure?”

  “Unfortunately, we don’t. One of the reasons is the lack of enough statistical data to make a definitive statement on this topic. For example, we don’t normally run CD4 cell counts on healthy people, unless, of course, they are HIV-Positive. Bottom line is that we simply do not know enough, and there are too many conflicting studies and theories to be able to say with any certainty that a low CD4 cell count has anything to do with HIV or AIDS.”

  “You mean, there’s a reasonable doubt?”

  “More than a reasonable doubt, Mr. Campbell – a very big doubt.”

  “Is that why Canada, for example, doesn’t recognize the CDC’s definition of AIDS based on a low CD4 cell count?”

  “I assume so, Mr. Campbell, and it just points out one more absurdity in this whole HIV=AIDS mess. Can you name me one other disease that no longer exists if you drive one hour north from Buffalo, New York? It’s ludicrous!”

  Campbell, of course, doesn’t answer Fowler’s rhetorical question. He goes for the key question instead. “Dr. Fowler, the defendant in this case supposedly tested Antibody-Positive on an HIV ELISA test. In your mind, what does that mean?”

  “Assuming he really is HIV-Antibody-Positive, which I understand is highly doubtful based on the results of an HIV ELISA test, he should actually be pleased that his immune system was working well enough to defeat the Human Immunodeficiency Virus, if in fact that virus exists and is a dangerous pathogen.”

  “And in your expert opinion, does his HIV-Antibody-Positive status pose a threat to anyone – himself, or anyone else?”

  “Not according to antibody theory, as we understand it today. No.”

  “Thank you, Dr. Fowler. Your witness, Mr. Armand.”

  Sarah again notices that Armand does no
t seem perplexed or upset by Fowler’s testimony. She wonders why, and what he knows that she doesn’t – or what he might have planned to counteract all this damning evidence about the HIV tests. Maybe the other shoe is about to drop on his cross-examination.

  “Dr. Fowler, you said in the beginning that… let me quote you,” as Armand consults his legal pad, “‘in the vast majority of cases, the presence of HIV antibodies would indicate a past infection rather than a present one.’ You were testifying that having the antibodies to a foreign invader, as you put it, meant that there was no current infection. Is that correct?”

  “I said that having antibodies to a foreign invader would mean that the immune system was working well and that the T-cells had to be doing their job of killing off the pathogen or the antibody would not have been created in the first place.”

  “But you do acknowledge that having the antibodies to a disease could also mean having that disease in the present time….”

  “No one knows enough about the human immune system to say anything with absolute certainty, Mr. Armand. I, for one, never want to say something is an indisputable fact without the scientific studies to back me up, unlike some other people I know.”

  Armand ignores Fowler’s dig at the AIDS experts. “So is it your testimony, Dr. Fowler, that it is possible that someone could have the antibodies to HIV and also have HIV disease at the same time.”

  “Possible? Yes, anything’s possible – but highly unlikely; and if it’s true, Mr. Armand, we in the field of immunology must reexamine our theories from the ground up, because, as I said, it would violate the entire premise of vaccinations, for one thing.”

  “But you admitted that there are other diseases we know about where we have the antibodies to the disease and yet have an active case of the disease at the same time.”

  “There are a couple diseases where we believe we have an accurate positive antibody test result, and there is evidence of concurrent disease symptoms, yes. Not many – I can count them on one hand, Mr. Armand. Plus, most of those antibody tests in question have appeared in the last twenty years or so, after medical science threw out all the usual protocols to establish the accuracy of antibody tests – such as validation studies – in order to vindicate the HIV tests.”

  Armand looks directly at Fowler with a piercing stare, as if challenging him to a ‘no blink’ contest. “But you do admit that these diseases do exist, such as Hepatitis C, where we have a positive antibody test and yet an active case of Hepatitis going on?”

  “As far as I know, the Hepatitis C antibody test has never been validated either, using the generally accepted rules of establishing a gold standard.”

  Armand blinks first. He knows he isn’t going to get anywhere going down that path, so he changes course. “Dr. Fowler, you also stated that CD4 cell counts can vary a lot from individual to individual, did you not?”

  “Yes, I did, Mr. Armand, and within a particular individual during any particular day.”

  “But would you agree that virtually all of those diagnosed with AIDS have low CD4 cell counts?”

  “From what I have read, I would have to agree, yes. But so do other people who do not have AIDS – or HIV.”

  Armand sees no point in continuing. “No further questions of this witness, Your Honor.”

  The judge looks at Campbell. “Re-direct?”

  “Just a couple questions, Your Honor. Dr. Fowler, you just agreed that virtually all diagnosed AIDS patients have a low CD4 cell count.”

  “Yes, I did.”

  “Would you also agree that all diagnosed AIDS patients are HIV-Antibody-Positive?”

  “Yes, by definition.”

  “What do you mean by that?”

  “I mean that since 1991, the CDC has defined AIDS one of two ways: being HIV-Positive and having one of about thirty different diseases, or being HIV-Positive and having a CD4 cell count under 200.”

  “And I believe you said that more than half of those diagnosed with AIDS are people who are not sick, but are HIV-Positive and have a CD4 cell count below 200.”

  “Yes, that’s true.”

  “So isn’t the fact that the majority of AIDS patients have a CD4 cell count of less than 200 the result of the definition of AIDS rather than a medical finding, just like you have to be HIV-Positive in order to have AIDS?”

  Fowler looks confused, as if he didn’t understand the question. Campbell is quick to clarify.

  “I mean, if a person is HIV-Positive and has a T-cell count of 400, they won’t be diagnosed with AIDS as long as they have no symptoms of disease. But if they have a T-cell count of 150, they’ll have AIDS, according to the CDC. So the fact that virtually all AIDS patients, as Mr. Wilson just said, have low CD4 cell counts is meaningless and depends entirely on the definition rather than on cause-and-effect.”

  “I suppose that’s right, Mr. Campbell. What you’re saying is that a low CD4 cell count doesn’t mean you have AIDS; having AIDS means you have a low CD4 cell count. I hadn’t thought about it that way; but yes, that would be true. It’s also typical of the way the CDC manipulates the statistics.”

  Campbell’s not sure what Fowler means, but he’s curious. “In what way?”

  “Well, the CDC keeps saying that 40,000 people get ‘newly infected’ with HIV each year in the United States. First of all, that’s an estimate and an extrapolation and has no basis in statistical fact. But there’s a bigger problem with their statement, and it’s a mistake that everybody seems to make, for some reason.”

  “Which is?”

  “They don’t have prior HIV-Negative tests on these people to prove that their positive HIV test results mean they have been, quote: ‘newly infected.’ The assumption is always that no one is HIV-Positive unless they get infected by somebody else. But that’s not true, and the CDC’s own statistics prove that. So at least some of these people – and unfortunately, we don’t know how many – may have been HIV-Positive all their lives; and when they finally take their first HIV test, they show up as Positive. But they were not, quote: ‘newly infected.’ They’ve been Positive the whole time and simply not known it.”

  “So when the CDC says these people are newly infected…”

  “…they have no proof of that, and frankly, no scientific basis to say it.”

  “Why do you think they make that claim, then?”

  “I can only guess…”

  “Objection. This witness is not qualified to talk about the motivations of the CDC, much less ‘guess’ about them.”

  Armand was right, of course, but Campbell wanted to try to get Fowler’s answer on the record anyway. “Your Honor, I’m simply asking Dr. Fowler for his personal opinion – not as an expert on the CDC, but, as he said, his guess.”

  “I’ll allow it. You may finish your answer, Dr. Fowler.”

  Campbell’s beginning to think that the judge has a lot of sympathy for the defense in this case. He didn’t have to make that ruling, and so far he’s been quite lenient when questions have come up. It doesn’t hurt to have the judge on your side, especially in a murder trial. Campbell makes a mental note not to do anything to jeopardize the relationship.

  Fowler is also pleased he can finish his answer. “I can only guess that it helps create the appearance that HIV is contagious – which it isn’t – and is still infecting large numbers of people – which they can’t prove without prior HIV-negative test results.”

  “But you said…”

  The judge interrupts. “That’s enough of that line of questioning, Mr. Campbell. I gave you the chance, now move on to something else.”

  Maybe not quite as sympathetic as Campbell thought! “I have no further questions of this witness, Your Honor.”

  Picking up his gavel, the judge says, “Then the witness may step down; and in light of the time, this court will stand in recess until ten a.m. tomorrow morning.”