Do HIV-infected blobs run amok in AIDS?

Wreaking destruction as it crawls, a massive amoebalike creature envelops each living thing that it lures close. The creature finally explodes, showering the area around it with deadly viruses that create replicas of the original monster.

A script for a bad horror movie, perhaps a sequel to The Blob? Nope, it's just a new take on how the AIDS virus, HIV, might work within the body.

When researchers infect human immune cells with HIV in laboratory dishes, they often observe the infected cells fusing into massive entities known as syncytia. Most AIDS scientists consider syncytia a laboratory phenomenon with little relevance to the disease, but David R. Soll of the University of Iowa in Iowa City contends that the multicellular masses occur within HIV-infected people.

He also argues that syncytia may explain some of the ravages of AIDS, even accounting, at least in part, for the immune system decline seen in people infected with HIV. "You cannot avoid syncytia anymore. They just have too many capabilities. They're motile, destructive, invasive, infectious, and seductive," says Soll.

In 1996, Sarah S. Frankel of the Armed Forces Institute of Pathology in Washington, D.C., and her colleagues refocused attention on syncytia when they reported that 11 out of 13 people with HIV had virus-containing syncytia in their adenoid tissue. At this week's American Society for Cell Biology meeting in San Francisco, Soll and his colleagues presented evidence that similar syncytia are found in samples of lymph nodes and blood taken from HIV-infected people. Frankel says that her group has also recently found HIV-induced syncytia in tissues other than adenoid, albeit not in lymph nodes.

Using devices designed to visualize moving cells, Soll's group has even observed syncytia crawling out of some samples of lymph node tissue as if a syncytium were a single cell. Syncytia, which can consist of thousands of cells fused together, crawl by extending a footlike growth that may be as large as a hundred cells.

In laboratory experiments by Soll's group, mobile syncytia disrupted membranes made from collagen, a major structural protein in lymph nodes, and punched holes in endothelial tissue, which lines blood vessels. These destructive tendencies, says Soll, may help explain why people with AIDS often have leaky blood vessels and lymph nodes that appear torn apart.

In the lab dishes, HIV-induced syncytia rarely live more than several days. Because syncytia induced by a chemical treatment survive much longer, Soll concludes that the death of the viral syncytia most likely stems from the massive replication of HIV within them.

"Syncytia are short-lived, but they're self-perpetuating. Every time one blows up, so much virus comes out of it that everything around it gets infected and starts fusing," he notes.

Syncytia may also act as sirens, luring immune cells to their doom. A syncytium secretes at least two proteins that attract immune cells to fuse with it. One is an HIV protein called gp120. The second has been identified, says Soll, but his university's lawyers won't allow its disclosure until they file patents. Theoretically, drugs that inhibit the syncytia's attractants might slow the immune system decline that occurs in AIDS, he says.

Other AIDS researchers note that syncytia were a hot topic when HIV was discovered 15 years ago, but a consensus emerged, and still holds, that they are a rarity in the human body. "Convincing people that they're there in abundance is likely to be a mini-war," says Robert C. Gallo of the Institute of Human Virology in Baltimore.