Chinese scientists analyzing the genome of the SARS virus have documented the startling rapidity of its evolution from an animal pathogen into one able to infect human cells.
Their analysis, reported yesterday in the journal Science, shows that as the virus perfected its human attack mechanism, its potency soared. Early on, it was able to infect only 3 percent of the people who came in contact with a patient; a few months later, the infectivity rate was 70 percent.
The speed of the transformation indicates the importance of identifying and isolating patients at the earliest possible stage to prevent widespread viral epidemics. Health authorities are now concerned about bird flu, an infection of birds and people, that has spread through Asia.
The new analysis, based on samples of the virus taken from Chinese patients in the early, middle and late stages of the epidemic, affords a rare glimpse of evolution at work at the molecular level.
The Chinese researchers gave special attention to one of the SARS virus' tools for entering a cell, known as the spike protein. They found that the gene that specifies the design of the spike protein changed the units of its genetic material very rapidly in the early stages of the epidemic, producing many new versions of the spike protein. The new versions were maintained, an instance of positive selective pressure.
But in the later stages the sequence of units in the gene stabilized, as if the spike protein had been perfected for attacking human cells. The gene was now under "purifying" or negative selective pressure, meaning that any virus with a different version was discarded from the competition.
The evolution of the spike protein from its animal to human attack mode began in mid-November and was complete by the end of February, a mere 15 weeks later.
Another gene, which the virus needs for the delicate task of making more copies of itself, stayed stable throughout the period that the virus was switching from its animal to human host.
Dr. Hua Tang, an evolutionary biologist at the University of Chicago who helped with the analysis, said the increasing infectivity of the virus during its transition to humans showed that it was "better to control it at a very early stage when the infection rate is lower."
Dr. Kathryn Holmes, an expert on SARS-type viruses at the University of Colorado, said the study was "wonderfully done," because of its speed, the foresight in saving specimens from the critical early stages of the outbreak, and its analysis of epidemiology at the molecular level.
"These things are going to keep happening," Holmes said, referring to other pathogens that have moved from animal to human hosts. "If we could catch the virus before it had a chance to make these mutations you could abort an epidemic."
Though most organisms have DNA as their genetic material, several classes of viruses use RNA instead. These RNA viruses, which include influenza and HIV as well as SARS, have a high rate of mutation, the process of accumulating changes to the units of their genetic material. Though some mutations derange the genes, a few create useful new versions of a protein, allowing the virus to gain some new function.
Holmes said there was great interest in understanding how these highly mutable viruses switched hosts and caused new diseases.
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