Archive for the ‘Virus behavior’ Category
Flu has been with humans for thousands of years, but the rise of arboviruses sparks an era of desperate disease, a battle we are losing. These arboviruses—named after the arthropod mosquitoes, fleas and ticks bearing them—have skipped the virus trademark of preserving a human host. The arboviruses prefer reservoir hosts, birds which don’t catch the virus and only carry it. They enter the bird, whose blood kicks up the virulence a notch. The bird then offers up a more deadly virus to the bug’s next vector, the mosquito. Once a human is infected, the virulence is turned up beyond our natural immunity. This is one spark that heats up the world of 2018, when the trouble begins in Viral Times.
Todd Rider, a scientist at defense-funded Lincoln Laboratories, has moved on from detecting viruses to destroying them. It will be 10 years, by some estimates, before a human version is ready to sell. But a viral pandemic might accelerate that process. Right now he’s testing it on mice. From BusinessWeek:
He describes in the recent journal article a new drug, still under development, which he has successfully used to destroy 15 viral strains, including dengue fever, a stomach virus, and a polio virus. To create it, Rider combined two proteins commonly found in the human body. One binds to viral double-stranded ribonucleic acid, a type of molecule found in all viruses. The other induces apoptosis, which is essentially programmed cell suicide. The drug acts like a homing missile that seeks out and kills cells infected by a virus. It appears to have few negative consequences and works against all diseases, even as they mutate. “Most viruses kill the host cells anyway. They are like aliens in a movie,” says Rider.
Even while a vaccine for H1N1 becomes far more available, doctors are discovering the virus creates infections far deeper in the lungs than seasonal flus.
The pattern of infection among the tiny percentage of people who have died from the virus mirrors the infection methods in the Spanish Flu pandemic of 1918, according to a report on CNN. The story also describes how someone dies from H1N1 infection. Their lungs cease to function well enough to give the victim sufficient air.
“Generally, flu stays in the upper airways,” said Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. “What this shows is clearly this virus has capability of infecting and causing inflammation and destruction of cells from the trachea, all the way down into smaller cells of the lungs. “The cells of the lung get directly attacked by the virus,” said Fauci.”
Nine out of every 10 people who have died from H1N1 have “underlying conditions” that are pushed into critical status by losing respiratory function. Like a profiler on a CSI episode, the medical community is trying to match conditions to deaths. 72 percent of those who have died had obesity in their profile.
Vanderbilt University researcher Dr. William Schaffner, professor in the Division of Infectious Diseases at the university’s School of Medicine, was surprised by the H1N1 fatality-obesity connection.
“That was a striking finding,” said Schaffner. “It contributes in a very material way to what we know about risks for a severe outcome with H1N1 infection. We are keeping an eye on obesity as a risk factor for H1N1 death.”
There’s nothing like discovering that a sub-microscopic organism is smarter than pharmaceutical science. TV news reported this week that the H1N1 virus is probably already evading the Swine Flu Vaccine (SFV) which the government has rushed to anxious, uninfected people in the US.
The SFV never had a chance of stopping the flu. Scientists are talking about antigenic drift, now that people are interested in how viruses evolve. The drift takes place as a virus moves through hosts (that’s you and me), changing its proteins to evade antibodies that could kill it. At least that’s what scientists think happens. They’re not sure.
“No one is sure exactly how the antigenic drift of flu viruses happens in people,” says Dr. Jonathan Yewdell. He wrote a paper with two other experts that was published in Science, but at the moment the only hard evidence comes from testing mice with a virus from 1934. The National Institute of Health reports on the leading theory at its Web site.
According to the prevailing theory, drift occurs as the virus is passed from person to person and is exposed to differing antibody attacks at each stop. With varying success, antibodies recognize one or more of the four antigenic regions in hemagglutinin, the major outer coat protein of the flu virus. Antibodies in person A, for example, may mount an attack in which antibodies focus on a single antigenic region. Mutant viruses that arise in person A can escape antibodies by replacing one critical amino acid in this antigen region. These mutant viruses survive, multiply and are passed to person B, where the process is repeated.
These escape artists have been drifting for thousands of years. Pharmaceutical research creates a flu vaccine every year before the drift occurs. If enough people catch and then transmit a flu, the virus is well on its way to changing its shape — so only your natural immunity can hope to neutralize an organism that makes you ill once you breathe it in.