AIDS Has Changed

Excerpt from The Real AIDS Epidemic

The following is an excerpt from the foreword to The Real AIDS Epidemic. You can purchase the whole book here on Kindle and in hardcover.

AIDS Has Changed

If you treat only healthy people you can claim great therapeutic success.

—Claus Kohnlein, 2005

This topic is covered extensively in chapter four of the original text, so I will discuss it only briefly here. It is my contention that AIDS in the early 1980s is not the same disease or even the same syndrome as it is now, or even as it was by the early 1990s. In the early 1980s, the latency period between infection and full-blown AIDS was estimated to be between one and three years, and the diseases that proved fatal were pneumocystis pneumonia, candidiasis, and Kaposi’s sarcoma, the latter of which is rarely seen anymore and is not even attributed to HIV any longer. Globally, the most common AIDS-defining disease is now tuberculosis, which is by no means exclusive to HIV-positive individuals.

Another AIDS-defining condition is nothing more than a laboratory result. A one-time CD4+ T cell count of less than 200 per milliliter is sufficient for a diagnosis of AIDS in the US. Interestingly, from the beginning researchers were looking for an infectious agent that was tropic for CD4+ T cells, and “HIV disease” was considered for years to be defined by the loss of such cells via direct or indirect HIV-mediated destruction. Forty years into the epidemic, there is still no agreed-upon mechanism of said depletion, and the presence of so few infected T cells rendered this assumption suspicious. Modes of destruction involving healthy T cells somehow being primed for destruction have been proposed, but never witnessed.

Furthermore, there are other laboratory anomalies often to be found in AIDS patients and HIV-positive individuals, including elevated levels of circulating antibodies of many kinds, and deficiencies in the levels of natural killer cells. Chronic inflammation is often seen as well. Interestingly, elevated levels of many types of antibodies are a known cause of so-called false positive HIV tests, which might lead the reader to wonder if the entire construction might be circular in its logic.

The question has to be asked: What would have happened if, from the early days of AIDS, we had been looking for an agent capable of causing depletion in natural killer cells and other abnormalities now known to be associated with AIDS? If we hadn’t been so laser focused on CD4+ T cells, would we have found something different?

The changing face of AIDS, as well as the prevalence of certain immunological disorders and dysregulation in populations outside the risk groups, strongly suggest that we have lost our way—or that something is being concealed from the public through fraud, incompetence, or plain old self-deception. Given that the AIDS of the 1980s had changed significantly in its severity by the early 1990s (AIDS deaths began to drop between 1993-95, before the advent of highly active antiretroviral therapy), it would not be unreasonable to say that the “HIV disease” of the 1990s and beyond is more akin to “long haul AIDS,” of necessarily decreased severity than proto-AIDS of the early days.

Given that HIV-positivity is nowhere near zero, in any population, including groups such as repeat blood donors who are at no known risk of AIDS, it seems entirely reasonable to assume that HIV positivity is either incidental to, or is the direct result of disease/dysfunction rather than its cause.

Consider also the prevalence of immune disorders and autoimmune illnesses that bear more than a passing resemblance to AIDS. AIDS-defining illnesses often prove to be more like autoimmunity or a very specific decline in cell-mediated immunity, rather than being similar to classical immune deficiencies from cancer chemotherapy, for example. Chronic inflammation, for example, is known to be common in AIDS patients, but inflammation is not an immune deficiency but rather closer to an immune over-reaction.

There are also diseases and syndromes seen outside the classical risk groups that bear more than a passing similarity to AIDS; so much so that the category of “HIV-negative AIDS” was introduced in 1993. One such striking example is myalgic encephalomyelitis, more commonly known as chronic fatigue syndrome. Another name for this disorder is “chronic fatigue immune dysfunction,” and it is characterized by debilitating fatigue, susceptibility to infection, and cognitive disturbances. Additionally, it is common for ME/CFS patients to experience lymphadenopathy, night sweats, and bowel disturbances. All of these symptoms are common to AIDS as well, making ME/CFS look awfully like “non risk group, HIV-negative long haul AIDS.” Inflammation and depletion of natural killer cells are commonly observed in ME/CFS as well as AIDS, but the difference is almost entirely in who gets which disease. ME/CFS appears almost as a mirror image of AIDS, being more common in women than men, and almost never to be seen in AIDS risk groups.

Other immune disturbances that are clinically similar to AIDS include lupus and Lyme disease.

The question I will pose to close this section is the following: Does the HIV/AIDS designation exist solely to ghettoize the risk groups, so that they can be “retained in care” to take drugs that either are (in the case of TDF) or should be the subject of class action lawsuits?