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References 1 through 126 were used in the Medical Hypotheses Article. References 127 and higher are additional articles supporting the Institute's research or claims made in this website.

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"If there is one word ... that pinpoints the lasting message of this conference in basic science, it is immunology."

- Dr. Jay A. Levy, AIDS researcher, University of California-San Francisco, said of the 12th World AIDS Conference, June 1998.

"These studies demonstrate that gp120 situated on the [T4] cell surface can serve as an effective target for immune destruction by patient antibodies and effector lymphocytes."

- H. Lyerly, et. al., Ref. 62.





"It has been observed that cross-linking of gp120 with anti-gp120 antibodies by itself is sufficient to induce apoptosis in peripheral blood lymphocytes of normal individuals. It has been suggested that circulating anti-gp120 antibodies in HIV-1-infected individuals may crosslink gp120 bound to [T4] cells and prime them for apoptosis in vivo. This hypothesis has been experimentally confirmed with human CD4-transgenic mice given injections of gp120 and sera from HIV-1-infected patients."

- N. Chirmule and S. Pahwa, review article, Ref. 89.





"It appears conceivable that gp120 disseminated by HIV-replicating cells forms bloodborne complexes with anti-gp120 [antibody], thus exposing noninfected [T4] cells to continuous down-regulatory signals. ... The exquisite efficacy of gp120-anti-gp120 complexes in inhibiting T cell receptor-mediated calcium flux may also be viewed as favorable to a gp120-mediated autoimmune mechanism. It places this regulatory phenomenon in a dose range of ... gp120 and anti-gp120 that can reasonably be expected to occur in HIV-infected individuals."

- R. Mittler and M. Hoffmann, Ref. 96.





"We show here that an ongoing humoral immune response [antibody production] to HIV gp120 can sensitize non-infected cells towards apoptosis. ... Our data, as well as those of others, suggest that endogenous anti-gp120 antibody in AIDS patients' serum may actually serve as a contributing rather than neutralizing factor during HIV pathogenesis. ... Under appropriate circumstances, huCD4 crosslinking per se is enough to transduce death signals in vivo."

- Y. Kang, E. Mello, and D. Scott, Ref. 128.





"Several reports have suggested the cross-linking of CD4 by gp120 and anti-gp120 ... renders T cells susceptible to apoptosis.... The results presented here support these findings.... Two factors would be necessary for such a mechanism to contribute to the decline in [T4] cells seen in HIV-infected individuals. The first is that there should be activation of lymphocytes, which has been well documented in seropositive individuals, and the second is the presence of gp120 and anti-gp120 antibodies: both have indeed been detected. Interestingly, higher levels of anti-gp120 antibodies may be associated with a poor prognosis. We conclude that this mechanism of apoptosis ... may contribute the decline in [T4] cells in HIV-infected patients."

- S. Foster, P. Beverley, and R. Aspinall, Ref. 108.





"These studies focus our attention on the ways that HIV infection might stop the production of new T cells. To treat the disease ... we may also need additional therapies to ensure that T-cell production starts anew."

- Dr. Joseph McCune, Gladstone Institute of Virology and Immunology, University of California, San Francisco.





"In conclusion, ... our results support the view that interaction between CD4/gp120 complexes on the surface of [T4] cells and ... anti-gp120 antibodies has an important role in the depletion of uninfected T cells in HIV pathology."

- O. Finco, et. al., Ref. 127.