In experiments with mice, University of California, San Francisco scientists discovered that the worms develop normally into adults as long as they are in direct contact with a potent class of immune cells in their hosts liver or with products from these cells. If the worms fail to connect with their targets, known as CD4+ T lymphocyte cells, their development slows. The worms will still mature eventually, but will produce far fewer eggs than normal, the research shows.
Other parasites are known to adapt to host signals but the UCSF research is the first to identify a specific host cell that a parasite partners with and to suggest the molecules the parasite may recognize as a signal in this remarkably refined exploitation. Clarifying the molecular mechanisms could aid vaccine development by identifying ways to block the parasites evasion of immune defenses.
The UCSF scientists suggest that the worms dependence on their hosts CD4+ cells evolved as a means for the parasites to gauge their hosts overall health. When a person is weak or sick and the immune cell count is low, the parasitic worms automatically switch to the mode that takes less of a toll on the host, decreasing the chance that the worms meal ticket will die. When the person recovers from malnutrition or whatever infection had dampened the CD4+ count, the worms may sense the increased CD4+ cell levels and switch to their more rapid development rate and robust egg production.
Discovery of the dual-track reproduction strategy may explain reports by researchers in Africa that HIV-positive people with schistosomiasis experience milder infections from the worms than do those who are HIV-
Contact: Wallace Ravven
University of California - San Francisco