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Issue No. 2  | January 17, 2014
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Study Demonstrates NIH-Created Toxin Can Kill HIV-Infected Cells That Persist Despite Treatment

“A team including University of North Carolina and NIH scientists has demonstrated in a mouse model that an HIV-specific poison can kill cells in which the virus is actively reproducing despite antiretroviral therapy. According to the researchers, such a targeted poison could complement antiretroviral therapy, which dramatically reduces the replication of HIV in infected cells but does not eliminate them. …

“The immunotoxin, known as 3B3-PE38, was created in 1998 in the laboratories of Edward A. Berger, Ph.D., of the National Institute of Allergy and Infectious Diseases, and Ira Pastan, Ph.D., of the National Cancer Institute, both part of NIH. This genetically modified bacterial toxin targets HIV-infected cells and becomes internalized by them, shutting down protein synthesis and triggering cell death.” 
 
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Study Examines the Effect of 24 Weeks of Statin Therapy on Systemic and Vascular Inflammation in HIV-Infected Participants on ART

“HIV-infected individuals are at increased cardiovascular disease (CVD) risk due in part to inflammation. Statins decrease inflammation in the general population, but their effect in HIV is largely unknown. … This is an on-going randomized, double-blinded, placebo-controlled trial to evaluate the effect of statins on inflammatory markers in HIV. Subjects received rosuvastatin 10 mg daily or placebo for 24 weeks. Subjects were receiving stable antiretroviral therapy with low-density lipoprotein (LDL)-cholesterol ≤130 mg/dL and evidence of heightened immune activation or inflammation. … 147 were enrolled (78% male, 70% black, median age 47 years). By 24 weeks, LDL-cholesterol significantly decreased in the statin group vs. placebo (-28% vs. +3.8%, respectively; P<0.01). … Twenty-four weeks of rosuvastatin significantly decreased Lp-PLA2, a vascular-specific, inflammatory enzyme that predicts cardiovascular events in the general population. Statins may hold promise as a means of attenuating CVD risk in HIV-infected individuals by decreasing Lp-PLA2 levels.”

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ISSN 1558-3228