Thalidomide may boost immunity to HIV in children, and more..

Thalidomide may boost immunity to HIV in children. Researchers from the United States and South Africa recently completed a study of thalidomide treatment in HIV-infected infants and children. The drug was safe and did not affect virus levels, but did increase the frequency of specific anti-HIV killer T cells in 3 of 4 children tested. This is the first report of an oral drug that may enhance HIV-specific killer T cell function in infected children.

Weakened viruses generated for potential dengue fever vaccine. Dengue virus is an emerging pathogen in many regions of the world, including a current outbreak in Hawaii. In pursuit of a vaccine against dengue infection, NIAID researchers have produced several weakened strains of the virus. The so-called temperature-sensitive mutants cannot replicate effectively, and therefore may be useful as vaccines.

T cells fight HIV in many ways. Helper T cells that recognize a specific HIV protein known as Gag appear to fight HIV infection. But how they do so is largely unknown. Recently, scientists from Massachusetts General Hospital and Harvard Medical School led a study of Gag-specific helper T cells taken from HIV-infected individuals. The researchers discovered that these T cells could recognize multiple regions of the Gag protein. The cells also appear to attack infected cells by releasing proteins that drill holes in their membranes. The research suggests HIV vaccines should include components that stimulate helper T cells and identifies a short protein fragment that might be used to accomplish this goal.

Bacterial vector induces HIV-specific antiviral immunity in mice. Researchers from the Institute of Human Virology in Baltimore have used a weakened form of an intestinal bacterium as part of a novel AIDS vaccine. The scientists added a gene for gp120, a major HIV surface protein, to weakened Shigella bacteria. When injected into mice, the modified bacteria effectively delivered the HIV gene to immune cells, inducing strong anti-HIV killer T cell responses. The research suggests that weakened bacteria can be used as safe and effective shuttles for DNA vaccines.

Tuberculosis helps HIV thrive. Tuberculosis (TB) is one of the most common opportunistic infections in people with HIV. Scientists from the Centers for Disease Control and Prevention and Case Western Reserve University recently studied how TB affects HIV replication in infected cells. Their research showed that viral production was higher in two types of immune cells, T cells and macrophages, when those cells were exposed to the inflammatory fluid from lungs infected with TB bacteria. The results explain how TB might accelerate HIV disease progression.

Finding the immune system’s “on” switch. Little is known about how specific immune cells are switched on when an infectious microbe invades the body. Many believe the innate immune defenses, which recognize general features of many microbes, play a key role. Scientists from Yale University, Howard Hughes Medical Institute, and Osaka University in Japan recently studied molecules called toll-like receptors (TLR) of the innate immune system. The researchers found that these receptors play a critical role in activating certain T cells. Their studies suggest that different pathways of innate immunity can switch on different arms of the body’s specific immune responses.

Blood vessel walls help HIV survive in other cells. Endothelial cells, which line the inner walls of blood vessels and lymph nodes, can help other cells harbor HIV. Researchers from Pennsylvania State University recently identified a molecule, C/EBP?, that assists in the process. Endothelial cells interact with macrophages, specific immune cells that are early targets of HIV and long-term reservoirs of the virus. Those interactions activate C/EBP? in the macrophages, enhancing HIV replication. The study offers new insight into the complex interplay of multiple cells and factors involved in HIV infection.