2005=H1N1. 2021=COVID19? THE ASSHOLES dug this OUT OF A GRAVE!? (ROFLMAO)

OK, remember when they dug up the virus, H5N1 (aka Spanish or ‘bird’ flu) up in Alaska?  This occurred in 2005 or thereabouts.  Read the first article from today’s WaPo, then read the one from the Guardian from 2005.  Can anybody honestly tell me that they didn’t either let H1N1 loose on purpose?  And given the Bush mafia’s propensity for making money on anything evil, well…it’s not a big stretch to where paranoia becomes good sense, is it?  Honestly, exactly when did people get to be so goddamned STUPID???  At least Hitler had the grace to be honest about eradication of his population instead of allowing  the people to swallow stupidity as an excuse.  Grrrr.  I’ll get off my soapbox now.   

 TheWashington Post

How Time and Mutations Engineered the New H1N1 Strain

By David Brown
Washington Post Staff Writer
Monday, May 11, 2009 

Once Upon a Time there was a little flu virus. It was probably born in Kansas in late 1917 or 1918, although nobody is really sure. Its name was H1N1. It grew up to be very wicked.

The story of the new strain of swine influenza now circling the world actually starts a lot farther back than the 20th century, but the year the "Spanish influenza" appeared is a good place to start.

From the second week in March 1918, when soldiers at an Army camp in Kansas began to get ill, until the final mini-waves of 1920, the Spanish flu infected about 97 percent of the people on Earth and killed at least 50 million of them.

The virus probably came from waterfowl, which carry dozens of different flu viruses. At some point, either before or after it got into human beings, the virus got into pigs, a species that can be infected by avian and human strains. It has stayed in swines ever since, and in people for almost as long.

The swine-origin influenza A (H1N1) virus circulating in Mexico, the United States and Canada, and present in two dozen other countries, is a descendant of the Spanish flu H1N1 virus. In the past 90 years, though, a lot of new blood -- metaphorically speaking -- has entered its lineage. It does not look or act much like its notorious ancestor.

This might be a good place to address this A and H and N business.

Influenza virus is part of a family called Orthomyxoviridae. There are four sub-classifications -- influenza virus A, influenza virus B, influenza virus C and thogotoviruses. It's like citrus fruit, which encompass oranges, lemons, limes, grapefruit, etc.

Influenza A and B cause illness in people; the others almost never do. There are many, many types of influenza A but only one influenza B.

The diversity of influenza A arises from variations in the two proteins on its surface, called hemagglutinin (abbreviated H or HA) and neuraminidase (N or NA). Together, the proteins make up the face that a flu virus presents to the immune system of a bird, a pig or a human being.

In this setting, the face's appearance is no small matter. The immune system's ability to recognize a virus is one of the first steps in stopping it.

One strategy involves antibodies. They attack only if they are tailor-made for the virus, which requires the immune system to get a good look at the surface proteins. The immune system can offer the best protection if it has seen the pathogen before and has the right antibodies ready.

Think of H as hair and N as nose, two features for learning and remembering the identity of a virus. In the world of influenza A, there are 15 subtypes of H (straight blond, wavy red, short black, kinky black, etc.) and nine subtypes of N (Roman, ski jump, flared, long, etc.). Each subtype is numbered -- H1N1, H3N2, H9N2 and so forth.

H1N1 is simply one combination of two of these subtypes that give the virus an appearance recognizable to the immune system -- say, short black hair and a long nose. Within these subtypes, however, there are subtle -- and sometimes not so subtle -- variations. They arise from mutations in the genes governing the H and N proteins.

Over time, an H1N1 influenza A virus can change its appearance significantly through random mutation. It can streak its short black hair and put a gold stud in its long nose one year, and shave its hair into a Mohawk and add a diamond stud in the other nostril the next. Pile up enough of these, and pretty soon the immune system no longer recognizes it as the virus with the short black hair and the long nose it once knew -- even though it still fits that description.

That is why the Spanish flu virus, the new swine flu virus and some of the human flu viruses circulating in recent winters can all be H1N1 viruses and yet look and behave so differently.

Research in the past few years on the Spanish flu virus -- which has been reconstructed from fragments extracted from lung-tissue samples from people who died in 1918 -- has revealed that much but not all of its killing potential resided in the H protein. One of the reassuring things about the new swine flu strain is that it does not have those same "virulence factors," even though it shares the same broad H1N1 features.

Studies done in the past two weeks suggest that people who have received flu shots in the past few years -- shots that protect against the most common human H1N1 strain in circulation -- are not protected against this swine flu strain, even though it also is H1N1. Why? Because it looks so different to the immune system that the virus-killing antibodies do not react.

Such is the importance of looks, immunologically speaking.

The human H1N1 flu virus -- and it's "human" only because it is in us -- that circulates each winter changes a little bit year to year in a phenomenon called "antigenic drift" as mutations creep into the H and N genes. But it can also change much more rapidly through something called "antigenic shift," which happens when entire H or N proteins (or both) are swapped out wholesale for new versions.

This is possible because influenza's genes are on eight separate strands, or "gene segments." One or two or more can be replaced, like cards in draw poker.

That's a rare event, however, and requires that two flu strains invade a single cell, replicate and then get their products mixed up in the packaging. The result is a virus dramatically different in immunological appearance, and sometimes in disease-causing capability, from either parent.

One way or another, a new influenza virus with the identity of H2N2 appeared in 1957. Because it was a new combination, nobody had immunity. It was called "Asian flu," and it spread everywhere, outcompeting H1N1 strains, which disappeared in people but remained in pigs.

In 1968, another strain, an H3N2 combination, appeared on the scene. Nobody had immunity to it either. It had a world's worth of susceptible victims and caused the "Hong Kong flu" pandemic that year and the next.

In 1977, a strange thing happened. The H1N1 virus, absent for years in people, reappeared. Curiously, it was almost exactly like the last strains in the 1950s. It was so close, in fact, that many people suspect it was released into the world by mistake from 1950s samples kept in a lab freezer.

Whatever the source, it spread widely as the "Russian flu," infecting lots of people born after the disappearance of H1N1 two decades earlier.

Since then, H1N1 and H3N2 strains have been circulating, mutating in small ways, and infecting new victims year to year. At the moment, the dominant H1N1 strain is one called A/Brisbane/59/2007. By chance, the dominant H3N2 strain was also found in Brisbane, Australia, in 2007 and is named A/Brisbane/10/2007. Influenza B, which has caused about one-third of infections in the United States this flu season, is dominated by a strain called B/Florida/04/2006.

But now comes a whole new H1N1 virus. It is formally labeled A/California/04/2009 (see graphic), and it was taken from a 10-year-old boy in San Diego who came down with the flu on March 30. It has an H from an H1N2 virus circulating in American pigs and an N from an H1N1 virus found mostly in Eurasian ones.

Our immune systems, familiar with other H's and N's, do not know what to make of it. We have no antibodies against the combination, so we have no protection against it. And we will generate antibodies only if we get infected by the virus or vaccinated with a killed version of it; either way will teach the immune system what it looks like.

This is the swine flu or, as the federal government likes to call it, confusingly but inoffensively, the H1N1 strain.

It's coming soon to a neighborhood near you. But we don't yet know how this tale will end.

©2009 The Washington Post Company

The Guardian U.K.

From frozen Alaska to the lab: a virus 39,000 times more virulent than flu

· Tight security to prevent 'select agent' escaping
· Publication of its genetic code raises fears of misuse

·         Ian Sample, science correspondent

·         The Guardian, Thursday 6 October 2005

Only a handful of scientists have security clearance to access the laboratory at 1600 Clifton Road in Atlanta, Georgia, home to the US government's Centres for Disease Control and Prevention. Before entering, they must pull on a protective hood, don breathing apparatus and pass through electronic fingerprint and retina scanners to prove their identity.

Inside the lab lies a batch of a virus, designated a "select agent", that more than justifies the extreme level of security. Resurrected nearly 90 years after it spread around the globe, leaving an estimated 50 million people dead, it is a replica of the 1918 Spanish flu virus.

The recreation of the virus, which was driven by an urge to unravel why the 1918 pandemic was so devastating, has raised as many fears as it has hopes. While the researchers argue the work will hugely improve protection against natural flu viruses, critics say there is a real danger the virus will escape, with potentially disastrous consequences.

The recreation process was laborious. Scientists collected fragments of the virus from lung tissue taken from victims at the time and preserved in formalin or, in one case, isolated from the lungs of a woman victim whose body had later become frozen in the Alaskan permafrost. Using the fragments, they painstakingly pieced together and read the complete genetic code before using the sequence to rebuild the virus from scratch.

By injecting it into mice, the team led by Dr Jeffery Taubenberger at the Armed Forces Institute of Pathology in Maryland was able to establish just how ferociously effective it was, compared with more common flu strains. All the mice infected died within a few days; all infected with contemporary strains recovered. "I didn't expect it to be as lethal as it was," Dr Terrence Tumpey, a scientist on the project from the US Centres of Disease Control and Prevention, told the journal Nature.

By creating flu strains with only certain parts of the 1918 virus, researchers investigated which of the eight genes that make up the virus were most responsible for its virulence. They discovered that rather than being caused by one or two genes, they all played a part, which suggests that the virus had completely adapted to cause disease in humans, something they say could happen again with avian flu strains.

In a second paper, published in Nature today, Dr Taubenberger and colleagues at the US Centres for Disease Control and Protection analysed the genetic make-up of the recreated virus. Surprisingly, they found it had no similarities to any of the human viruses in circulation, suggesting that the Spanish strain had jumped from birds to humans, and didn't mix with a human virus first, as had been believed.

The finding that Spanish flu came straight from birds has raised concerns among scientists. Previously, a pandemic was only thought likely if an avian strain merged with a human flu virus. "For me, it raises even more concern than I already had about the pending potential of a flu pandemic," said Professor Ronald Atlas, co-director of the centre for the deterrence of biowarfare and bioterrorism at the University of Louisville in Kentucky. "It looks as though an avian strain evolved in 1918 and that led to the deadly outbreak, in much the same way as we're now seeing the Asian avian flu strains evolve."

According to Dr Taubenberger, knowing what mutations gave rise to the 1918 Spanish flu virus will help scientists check viruses to work out which, if any, are evolving to the point where a pandemic is possible. The H5N1 strain of bird flu in Asia is already mutating to make it more suited to humans, he said.

Despite the new insights given by the project, many scientists were alarmed at the recreation itself and particularly that the full genetic sequence was to be made public on an online genetic database.

"Assuming this is a replicant of the 1918 flu strain, if it got out, it could initiate disease in humans and given the work they've done, one had to say it would be infectious," said Prof Atlas.

Viruses have escaped from high-security labs before. During the recent Sars outbreak the virus escaped at least twice, once in Taiwan and once in Singapore, when researchers became contaminated.

Other scientists warned that the 1918 virus's genetic code could easily be misused. Such has been the pace of progress in genetic science that companies now build genes to order for customers who send in details of sequences they want.

"If the genetic sequence is out there on a database, then that is a clear security risk," said Dr John Wood, a virologist at the National Institute for Biological Standards and Control, in Potters Bar.

According to Dr Julie Gerberding, director of the US Centres for Disease Control and Protection, a pandemic is unlikely even if the virus escapes because of most people's natural immunities and the availability of antiviral drugs and flu vaccines.

Publication of the research still raises questions about the powers of academic journals who take ultimate responsibility for publishing the papers, said Dr Wood. "That is some responsibility," he said.

The US National Science Advisory Board for Biosecurity concluded at an emergency meeting last week to discuss the possible publication of the papers that their benefits outweighed their risks.

FAQ: 1918 flu pandemic

Why was the 1918 Spanish flu pandemic so lethal?

The worst pandemic in human history, the 1918 strain killed an estimated 50 million people. Because flu viruses were unknown at the time, no isolates of the pathogen were made, making it impossible for scientists to study. Scientists believe the virus was originally found only in birds but jumped to humans and evolved to become very infectious

Whom did the 1918 flu virus kill?

Most flu viruses kill the very young, the old and the infirm. But the Spanish flu was unusual in striking young, fit people extremely hard. Even with good healthcare, up to one third of those who picked up the infection died, many within days

What is a select agent?

Its designation as a 'select agent' by US Centres for Disease Control and Prevention puts it on a list of controlled pathogens and toxins including ricin, smallpox virus, anthrax and ebola

How secure is the virus?

It is held in a biosafety level 3 enhanced laboratory, kept at a negative pressure to prevent air escaping. Workers must wear protective clothing, breathing apparatus and gain entry via fingerprint and retina scans

·         guardian.co.uk © Guardian News and Media Limited 2009