Destruction of antigenicity in vitro of human serum albumin and of tobacco mosaic virus by ultraviolet radiation

Ultraviolet irradiation first makes human serum albumin unable to precipitate with antibody to the original albumin and then destroys its ability to combine with the antibody. With tobacco mosaic virus both the ability to precipitate and to combine with antibody to the original virus are destroyed simultaneously or nearly so. A rough estimate shows that about 5 J of radiation energy (at λ= 2537 Å) must be absorbed by each milligram of human serum albumin or of the protein of the virus to reduce their capacity to combine with antibodies to half. The structure of the two antigens is very considerably altered before their specific combining capacity is destroyed, which contrasts with relatively slight alterations in the structure of typical enzymes or antibodies when their specific activities are destroyed or in the virus when its infectivity is destroyed

Clinical course of classic Kaposi's sarcoma in HIV-negative patients treated with the HIV protease inhibitor indinavir

HIV protease inhibitors have been shown to exert antiangiogenic and antitumor actions independently from their antiretroviral effect. Based on these studies, HIV-seronegative patients with classic Kaposi's sarcoma were treated with indinavir and followed for clinical evolution, drug pharmacokinetics and Kaposi's sarcoma biomarkers. A favorable clinical course was associated with high drug plasma levels, reduced production of basic fibroblast growth factor, lower numbers of circulating endothelial cells, and a decrease in antibody titers against human herpesvirus 8

Clinical corse of classic Kaposi’s sarcoma in HIV-negative patients treated with the HIV protease inhibitor indinavir.

HIV protease inhibitors (HIV-PI) have been shown to exert anti-angiogenic and anti-tumor actions independently from their antiretroviral effect. Based on these studies, HIV-seronegative patients with classic Kaposi’s sarcoma were treated with Indinavir and followed for clinical evolution, drug pharmacokinetics and KS biomarkers. A favorable clinical course was associated with high drug plasma levels, reduced production of basic fibroblast growth factor, lower numbers of circulating endothelial cell numbers, and a decrease of antibody titers against HHV8