Waukeshahealthinsurance.com-
–
Avian flu virus from A A teenager admitted to the hospital Scientists in Vancouver say the virus has mutations in key areas that make it easier for people to spread.
There is no indication that the mutated virus has passed this patient. British Columbia's provincial health officer, Dr. Bonnie Henry, said in a written statement that after tracing dozens of possible contacts between the youth's friends, family and health care providers, “no additional cases were found.” That means the mutated virus is not spreading or threatening anyone else.
But scientists say the genetic changes are a reminder of what the virus could do if it continues to spread.
“This is really one of the first times we've really seen this type of adaptive mutation in H5,” said Dr. Jesse Bloom, a computational virologist at the Fred Hutchinson Cancer Center.
The H5N1 bird flu virus that infected the critically ill but stable toddler is not the same as the one transmitted in Dairy cattle In the United States. It is more closely related to the H5N1 strain circulating in wild birds such as geese in the Pacific Northwest. Although both strains are H5N1, they are distinct, in the same way that Delta and Omicron were different versions of the SARS-CoV-2 virus that causes Covid-19.
Pathologists investigating the case do not yet know how the toddler was infected, as there was no contact with wild birds.
The three mutations that Bloom and other scientists determined made it easier to attach to human cells were found in the virus's genome.
“It caught the attention of a lot of flu virologists, including myself, because some of the sequences had evidence of some of the types of mutations that we were concerned about,” he said.
Influenza viruses enter cells by attaching to surface-adhesive sugars called silicic acid. Birds have the most alpha 2,3 form of sialic acid, but humans have mainly alpha 2,6 sialic acids, especially in the nose, throat and lungs.
Dr. Scott Hensley, a microbiologist at the University of Pennsylvania and an expert in the study of influenza viruses, has shown through decades of basic research scientists which mutations to watch out for.
And Hensley said on Saturday morning, when he looked at the Canadian patient's sequence, newly uploaded to the global genome sharing database GISAID, he saw exactly the changes that allowed the virus to switch from choosing alpha 2,3. Alpha 2.6 sialic acids are abundant in human nose, throat and lungs and many receptors in birds.
He said that one place in the human body where alpha 2,3 receptors are located is the eye. Most of the reported cases of human HIV in the United States The eyes are the first sign that the virus entered the body.
The Canadian youth also had red eyes, one of the first symptoms, so Hensley thinks that's how the virus got in. But the patient developed severe breathing problems called acute respiratory distress syndrome, or ARDS, possibly due to genetic changes, Hensley said, as the virus began to replicate itself in the body.
Again, this is not the beginning of the epidemic, he emphasized. It's a start for the virus to better adapt to human cells, but it won't be enough on its own to fuel an outbreak.
“We need to do a lot of research at this point. We need to try to understand whether this particular virus has effective transmission characteristics,” he said.
Each mutation is ambiguous, meaning that when scientists read the sequence of letters that make up the virus's genome, they can't tell which of the two letters, or nucleotides, should be in which position.
Bloom explains that this can happen when the virus evolves in the host and exists in different forms in the body.
“Typically, when you look at sequences of how the virus is mutating in a host, after two weeks of infection, you see different combinations of mutations,” he said.
The Canadian teenager started showing symptoms a week before he was admitted to the hospital, which may be enough time for the virus to infect the cells it wants to enter.
Get Health's weekly newsletter
Ambiguous mutations could also be the result of the sequence itself, but Bloom doesn't think that's likely because mutations don't seem random and instead occur at important sites where the virus needs to change to survive in a human host.
He noted that several H5N1 viruses isolated from infected birds in British Columbia and Washington were closely related to this virus.
Although this appears to be a dead-end infection — meaning it won't spread beyond this person — it's a good reminder that if the virus can do it once, it can do it again.
In the United States, 53 cases of bird flu have been identified in humans, and there are ongoing outbreaks in dairy cattle, sporadic outbreaks in poultry, and widespread infections in wild birds.
“There's a lot of H5N1 influenza, and influenza has a lot of mutations, so if this virus is in the right place in evolution to get these mutations, it's possible — not certain, but possible — that it could get them again in other infections,” Bloom said.