Read Online A Planet of Viruses by Carl Zimmer - Free Book Online Page B
Authors: Carl Zimmer
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adapted. Within a single host, natural selection can improve the ability of viruses to escape detection of the immune system.
In 2008, Philip Goulder, a medical researcher at Oxford, led an international team of scientists who found evidence for the ongoing evolution of HIV. They studied the immune systems of 2,800 people from all over the world, examining proteins known as human leukocyte antigens, which infected cells use to transport fragments of viruses to their surface. The fragments can then be recognized by immune cells, which destroys the infected cell. Different people carry different variations in the genes for human leukocyte antigens. Goulder and his colleagues found that most of the HIV in each country carried mutations to the most effective human leukocyte antigens in that country’s population. Their findings tell us that HIV is rapidly adapting to the variations in human immune systems around the world. That is sobering news to those who are trying to build HIV vaccines. If a vaccine ever succeeds in boosting an effective immune response in people, HIV might well evolve a way to escape.
It’s possible that vaccine developers could keep HIV from escaping by continually rolling out new vaccines that would stay one step ahead of the virus. Another intriguing possibility is to look back over its history. A team of American scientists compared a wide range of HIV-1 subtype B strains and reconstructed one of the proteins made by their common ancestor. They then used that ancestral protein to make a vaccine. The researchers found that monkeys injected with the vaccine were able to produce an immune response to a much wider range of HIV strains than more conventional vaccines. The future of fighting HIV, perhaps, may lie in its past.
Becoming an American
West Nile Virus
In the summer of 1999, Tracey McNamara got worried. McNamara was the chief pathologist at the Bronx Zoo. When an animal at the zoo died, it was her job to figure out what killed it. She began to see dead crows on the ground near the zoo, and she wondered if they were being killed by some new virus spreading through the city. If the crows were dying, the zoo’s animals might start to die too.
Over Labor Day weekend, her worst fears were realized: three flamingoes died suddenly. So did a pheasant, a bald eagle, and a cormorant. McNamara examined the dead birds and found they had all suffered bleeding in their brains. Their symptoms suggested that they had been killed by the same pathogen. But McNamara couldnot figure out what pathogen was responsible, so she sent tissue samples to government laboratories. The government scientists ran test after test for the various pathogens that might be responsible. For weeks, the tests kept coming up negative.
Meanwhile, doctors in Queens were seeing a worrying number of cases of encephalitis—an inflammation of the brain. The entire city of New York normally only sees nine cases a year, but in August 1999, doctors in Queens found eight cases in one weekend. As the summer waned, more cases came to light. Some patients suffered fevers so dire that they became paralyzed, and by September nine had died. Initial tests pointed to a viral disease called Saint Louis encephalitis, but later tests failed to match the results.
As doctors struggled to make sense of the human outbreak, McNamara was finally getting the answer to her own mystery. The National Veterinary Services Laboratory in Iowa managed to grow viruses from the bird tissue samples she had sent them from the zoo. They bore a resemblance to the Saint Louis encephalitis virus. McNamara wondered now if both humans and birds were succumbing to the same pathogen. She convinced the Centers for Disease Control and Prevention to analyze the genetic material in the viruses. On September 22, the CDC researchers were stunned to find that the birds were not killed by Saint Louis encephalitics. Instead, the culprit was a pathogen
In 2008, Philip Goulder, a medical researcher at Oxford, led an international team of scientists who found evidence for the ongoing evolution of HIV. They studied the immune systems of 2,800 people from all over the world, examining proteins known as human leukocyte antigens, which infected cells use to transport fragments of viruses to their surface. The fragments can then be recognized by immune cells, which destroys the infected cell. Different people carry different variations in the genes for human leukocyte antigens. Goulder and his colleagues found that most of the HIV in each country carried mutations to the most effective human leukocyte antigens in that country’s population. Their findings tell us that HIV is rapidly adapting to the variations in human immune systems around the world. That is sobering news to those who are trying to build HIV vaccines. If a vaccine ever succeeds in boosting an effective immune response in people, HIV might well evolve a way to escape.
It’s possible that vaccine developers could keep HIV from escaping by continually rolling out new vaccines that would stay one step ahead of the virus. Another intriguing possibility is to look back over its history. A team of American scientists compared a wide range of HIV-1 subtype B strains and reconstructed one of the proteins made by their common ancestor. They then used that ancestral protein to make a vaccine. The researchers found that monkeys injected with the vaccine were able to produce an immune response to a much wider range of HIV strains than more conventional vaccines. The future of fighting HIV, perhaps, may lie in its past.
Becoming an American
West Nile Virus
In the summer of 1999, Tracey McNamara got worried. McNamara was the chief pathologist at the Bronx Zoo. When an animal at the zoo died, it was her job to figure out what killed it. She began to see dead crows on the ground near the zoo, and she wondered if they were being killed by some new virus spreading through the city. If the crows were dying, the zoo’s animals might start to die too.
Over Labor Day weekend, her worst fears were realized: three flamingoes died suddenly. So did a pheasant, a bald eagle, and a cormorant. McNamara examined the dead birds and found they had all suffered bleeding in their brains. Their symptoms suggested that they had been killed by the same pathogen. But McNamara couldnot figure out what pathogen was responsible, so she sent tissue samples to government laboratories. The government scientists ran test after test for the various pathogens that might be responsible. For weeks, the tests kept coming up negative.
Meanwhile, doctors in Queens were seeing a worrying number of cases of encephalitis—an inflammation of the brain. The entire city of New York normally only sees nine cases a year, but in August 1999, doctors in Queens found eight cases in one weekend. As the summer waned, more cases came to light. Some patients suffered fevers so dire that they became paralyzed, and by September nine had died. Initial tests pointed to a viral disease called Saint Louis encephalitis, but later tests failed to match the results.
As doctors struggled to make sense of the human outbreak, McNamara was finally getting the answer to her own mystery. The National Veterinary Services Laboratory in Iowa managed to grow viruses from the bird tissue samples she had sent them from the zoo. They bore a resemblance to the Saint Louis encephalitis virus. McNamara wondered now if both humans and birds were succumbing to the same pathogen. She convinced the Centers for Disease Control and Prevention to analyze the genetic material in the viruses. On September 22, the CDC researchers were stunned to find that the birds were not killed by Saint Louis encephalitics. Instead, the culprit was a pathogen
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