Editor's note: Science Scan is a roundup of recently published biotechnology-relevant research.
Unrelated pathogenic microorganisms may act together to remove vulnerable human patients after infection. An article in Nature dated April 24, 2003 describes this dynamic model of "ecological interference," and how it might account for the pattern of fatalities seen in some historical epidemics.
The paper is titled "Ecological interference between fatal diseases." Its lead author is epidemiologist and population biologist Pejman Rohani at the University of Georgia in Athens.
"Our principal finding," Rohani told BioWorld Today, "is that infections unrelated to each other may indeed affect each other's epidemics - either through convalescence or infection-induced mortality. In the Nature paper, we show - based on historical data of measles and whooping cough - that big epidemics of these infections don't recur when the outbreaks are biennial. If they come again every two years we tend to find a big flare-up of measles this year, and a big epidemic of whooping cough next year, followed by another big measles outbreak. We don't see major epidemics of the two at the same time. They occur independently. And that is much more striking than if there was no interaction between the two diseases."
Rohani and his co-authors analyzed case-fatality reports for measles and whooping cough from Aberdeen, Scotland, in the late 1800s, and from 32 European cities before and after the first World War - from 1883 to 1932. This was before vaccinations became widely available, and when the diseases were significant killers in Europe. The patterns of disease and death they found suggested that ecological interference may be strong when fatal infections kill off susceptible organisms.
"Ecological interference," Rohani explained, "is a term suggesting competitive antagonistic interaction between pathogenic agents. For example, that infections like measles and whooping cough might interfere with each other. The reason why we're thinking of this rather than a conventional immunological mechanism is that in an ecological setting, each person is a possible host, or a possible site, where the infection can be found. Then attack by other agents might mean the site is not available to be occupied by that specific disease at that time. This process is particularly pronounced when one infection or both indeed cause substantial mortality.
"Measles is currently not deadly to people in developed countries," Rohani continued, "but it still kills some million children in the developing world, by WHO estimates. So both measles and whooping cough remain significant killers, albeit mostly in the developing nations. We tend to think of them as benign but they are still major killers.
"There are a number of possible avenues for exploration that I'd like to pursue," Rohani observed, "whether this mechanism would explain — as we discuss in the paper — how different serotypes of, say, the dengue fever virus interact. There are a number of infections where antigenic polymorphisms are well known. These infections occur immunologically, through the immune system, but we put forward an alternative mechanism whereby they could also be interacting with each other through an ecological process. It would be interesting to see what that kind of analysis would show in an infection like dengue or ECHO viruses. The latter can cause fatal meningitis. The two infections would be comparable to measles and whooping cough.
"Until now it was thought that the dynamics of dengue fever were largely determined by the number of mosquitoes available to transmit the infection, or by some complex immunological interactions between its viral strains - so-called antibody enhancement. What we believe now," Rohani concluded, "is that one strain actually competes with the other for susceptible human hosts."
Malaria Surge Out Of Africa Links Mosquito, Parasite, Human Agricultural Revolution
Genetic sleuthing has confirmed that a massive explosion of malaria parasite populations (Plasmodium species) originated in Africa about 10,000 years ago. This coincided with the rise of human agricultural societies, and the evolution of Anopheles mosquito carriers of Plasmodium.
However, researchers also found evidence that small populations of Plasmodium falciparum appeared in Africa and spread around the world as many as 100,000 years ago, perhaps in step with human migrations at that time. They report their findings in Science dated April 11, 2003, under the title "Early origin and recent expansion of Plasmodium falciparum." The paper's senior author is from the Laboratory of Malaria and Vector Research at the NIAID in Bethesda, Md.
"Understanding the complex interplay between host and parasite populations," the authors pointed out, "is key to disease control efforts." They report that the 10 most recent mutations appear in African parasites, suggesting that populations there continue to grow faster than elsewhere. The team analyzed 100 worldwide Plasmodium samples and estimated regional population ages based on the number of mutations in mitochondrial DNA. A larger-than-expected number of mutations pointed to longstanding populations that have had more time to evolve.
Fruit Flies Stand In as Insect Models Of Vision - Blighting Human Retinal Degeneration Disorders
Potential treatment strategies for human retinal degeneration have emerged from a study on the disease in fruit flies (Drosophila melanogaster) as an in vivo model. The work is reported in Science dated March 14, 2003, titled "Modulating sphingolipid biosynthetic pathway rescues photoreceptor degeneration." Its authors are at the National Cancer Institute in Frederick, Md.
Their research suggests that ceramide, an integral component in fruit fly cell membranes and cell communication, controls the viability of the insects' photoreceptor cells. These are specialized sensory neurons containing a light-sensitive organelle that houses the visual signaling machinery. By engineering these cells to express the enzyme ceramidase, the authors rescued mutant fruit flies that suffer from retinal degeneration. That enzyme converts ceramide to sphingosine, another player in sphingolipid metabolism.
Many diseases of retinal degeneration, such as retinitis pigmentosa, age-related macular degeneration, cone dystrophy and Oguchi's disease are associated in different components of the visual signaling cascade, and all result in the death of photoreceptor cells.