Research involving scientists at the University of York has provided important new information about transmission of human leishmaniasis, a group of infectious diseases which kills more than 100,000 people a year.
rofessor Deborah Smith of the Centre for Immunology and Infection at York, working with colleagues at the Wellcome Trust Sanger Institute and Charles University in Prague, has shown that “Leishmania” parasites reproduce sexually in the wild.
The research, published in PLOS Genetics, is a significant step forward in understanding how leishmaniasis is spread in endemic regions. Caused by “Leishmania”parasites, human leishmaniasis is a serious public health problem in more than 90 countries worldwide. There are high fatality rates among children and young people and those with suppressed immune systems. Pharmaceutical treatments are limited and there is no vaccine.
These microscopic organisms infect humans through the bite of a female blood-feeding sand fly carrying infective parasites in its gut. People only become infected, therefore, in geographical regions that are well-suited to support sand fly populations — those with suitable habitats, humidity and temperature. But the biology of the parasite in the sandfly is also critically important in determining the outcome of infection in man.
The new research uses DNA sequencing to investigate genetic variation at the highest level of resolution in “Leishmania “parasites isolated from sand flies caught in a defined focus of human leishmaniasis in south-east Turkey. This analysis provides evidence that “Leishmania “parasites can reproduce sexually in wild-caught sand flies, an event only detected previously under specialised laboratory conditions.. It also establishes, for the first time, quantitative estimates of the relative rates of sexual and asexual reproduction during the parasite life cycle.
Cancer patients may view their tumors as parasites taking over their bodies, but this is more than a metaphor for Peter Duesberg, a molecular and cell biology professor at the University of California, Berkeley.
Cancerous tumors are parasitic organisms, he said. Each one is a new species that, like most parasites, depends on its host for food, but otherwise operates independently and often to the detriment of its host.
In a paper published in the July 1 issue of the journal Cell Cycle, Duesberg and UC Berkeley colleagues describe their theory that carcinogenesis — the generation of cancer — is just another form of speciation, the evolution of new species.
A molecular biologists has long believed that cancer results from chromosome disruption rather than a handful of gene mutations, which is the dominant theory today. That idea has led him to propose that cancers have actually evolved new chromosomal karyotypes that qualify them as autonomous species, akin to parasites and much different from their human hosts.
“Cancer is comparable to a bacterial level of complexity, but still autonomous, that is, it doesn’t depend on other cells for survival; it doesn’t follow orders like other cells in the body, and it can grow where, when and how it likes,” said Duesberg. “That’s what species are all about.”
This novel view of cancer could yield new insights into the growth and metastasis of cancer, Duesberg said, and perhaps new approaches to therapy or new drug targets. In addition, because the disrupted chromosomes of newly evolved cancers are visible in a microscope, it may be possible to detect cancers earlier, much as today’s Pap smear relies on changes in the shapes of cervical cells as an indication of chromosomal problems that could lead to cervical cancer.