], we would like to point out that, although we agree with his overall contention regarding the beneficial effects of transfer factor even on advanced-stage AIDS patients, our polymerase chain reaction (PCR) data, albeit limited, do not confirm his equally limited observations, suggesting a dramatic drop in the PCR counts. In our experience, only one out of three patients showed an important decrease in PCR counts following transfer factor administration.
Nevertheless and notwithstanding the aforementioned results, most patients who received HIV-specific transfer factor over long periods have shown arrest of disease progression with clinical and/or laboratory improvement.
Furthermore, preliminary studies investigating the serum cytokines in patients receiving transfer factor treatment indicate that the latter activates the Th1 secretion pattern, which has a prognostic value (E. Raise et al., Biotherapy, 9[1-3]:49-54, 1996).
Thus, evidence obtained by our group, as well as by Fudenberg and others (A.A. Gottlieb et al., Biotherapy, 9[1-3]:27-31, 1996), suggests that transfer factor has a beneficial effect on HIV-infected patients, as has proved to be the case in other viral infections. As a matter of fact, the literature abounds with reports confirming the extraordinary efficacy of specific transfer factor, be it for subacute viral infections (such as cytomegalovirus and herpes simplex virus) or chronic, secondary manifestations of viral diseases (hepatitis B, Burkitt's lymphoma, nasopharyngeal carcinoma).
The HIV infection can, in some cases, be controlled by the patient's immune system. Cytotoxic T lymphocytes play a key role in this effect (S. Rowland-Jones et al., Nature Medicine, 1[1]:59-64, 1995). Since one of the postulated activities of transfer factor is the increase in the cytotoxic T lymphocytes recognizing cells displaying "foreign" antigens, be they viral or tumor-associated, and proceeding with their destruction, it is plausible to speculate that it can also generate HIV-specific cytotoxic lymphocytes and thus contribute to arresting the progression of the syndrome.
However, if these observations and speculations had even the slightest probability of being confirmed, considering what is at stake, one should be already asking the "obvious" question: Why, after two decades of prominence, has transfer factor sunk into limbo?
It is true that its molecular structure has not yet been elucidated, but hundreds of papers have been published on this moiety, and the clinical results achieved so far have not been challenged. A recent example of striking clinical efficacy is the work of T. Fujisawa and Y. Yamaguchi at the Chiba University School of Medicine, Japan (T. Fujisawa, Y. Yamaguchi, Cancer, 78[9]: 1892-8, 1996).
In an interesting review of the work of Sigmund Freud, John Horgan (Scientific American, 275[6]:106-11, December 1996) refers to University of Pennsylvania psychologist Lester B. Luborsky's "allegiance effect," which can be redefined as "the tendency of researchers to find evidence favoring the ideas they cherish and ignore evidence favoring the ideas they don't." This has certainly played an important role in the overt or implicit rejection of transfer factor, resulting in the curtailing of funding for further fundamental research into the subject.
Be that as it may, a second question also arises: cui bono? Who is the principal beneficiary of such attitudes? Pharmaceutical companies, commercializing profitably on sometimes highly toxic drugs, are the first to benefit from transfer factor's oblivion, since the latter could be offered at a fraction of the price of the former. And to the "cui malo" question, the obvious answer is "the patient."