So confusing, some articles say serious, this one minimizes!!

Transmission studies suggest H1N1 is here to stay

http://toronto.ctv.ca/servlet/an/local/CTVNews/20090702/h1n1_studies_090702/20090702/?hub=TorontoNewHome

There are many scientists studying this virus. Helen Branswell has written a good summary on what they are finding, and what it means. This is not the same study as in your post, oramar. I hope this helps. She does a good job of explaining this kind of information clearly.

H1N1 viruses are missing at least two key features seen in all flu viruses present and past that transmit well among people and yet the viruses are spreading quite efficiently, two new studies suggest. The research groups which produced the work differ slightly in their views of the degree to which the novel H1N1 virus is spreading, with one finding transmission isn't yet as efficient as with human flu viruses while the other finding transmission rates are in lockstep with those of seasonal flu cousins.

There is no disputing the evidence, though -- the virus is spreading around the globe, claiming at least 332 lives so far. And it is doing this without all the tools scientists would expect a flu virus to need to become a successful human pathogen.

"The take-home message is that a virus that does not have some of the features that we have previously recognized as hallmarks of adaptation of flu in humans was able to establish itself in humans and cause disease," said Dr. Daniel Perez, an influenza virologist with the University of Maryland. "Regardless of what the virus might do, I believe it is here to stay either as a whole virus or with some of its gene. It may be able to outcompete and-or co-circulate with seasonal flu strains."

Perez was not involved in the studies, both of which will be published Friday in the journal Science. He is, however, familiar with the work; his lab has completed a similar study.

The transmission studies were done by research groups at the U.S. Centers for Disease Control with colleagues from the Massachusetts Institute of Technology and at Erasmus Medical Center in Rotterdam, the Netherlands. Both groups tested spread in ferrets, which are considered an excellent model for flu infection in humans.

The CDC's work suggests the virus isn't yet completely adapted to spread among humans. When healthy ferrets were housed in cages adjacent to and sharing feeding dishes with experimentally infected animals, only two-thirds of the healthy animals became infected in the CDC research. By contrast, the group in the Netherlands found all healthy ferrets caught the new virus when housed next to animals infected with the virus. Perez's work also saw this 100 per cent transmission rate.

In both the CDC and Erasmus studies, ferrets that were infected with human flu viruses transmitted infection to all their healthy neighbours.

Dr. Terrence Tumpey, senior author of the CDC study, said variation in the air flow setups between the CDC's ferret cages and those used in the other studies may explain the differing findings. But based on what they saw, his team believes this virus may still be getting used to its new human host. A key piece of evidence supporting their conclusion relates to the virus's ability to infect cells in the human respiratory tract. The CDC-MIT scientists showed the novel H1N1 virus's hemagglutinin -- the surface protein that locks onto a cell it is about to invade -- currently makes a connection that is weaker or less efficient than that made by regular flu viruses. That suggests the virus has room for improvement. And if it mutates to bind more efficiently, it would become even more adept at spreading from person to person. "I mean, it's transmitting. But we think it could potentially transmit even better," Tumpey said from Atlanta. He suggested with better transmission could come more severe disease -- not just in sheer numbers, but in the proportion of infected people who develop serious illness. "A lot of cases have been mild. But if it was adapted more towards humans, it could be more severe. More consistently severe," Tumpey said.

His counterpart on the Dutch paper, Dr. Ron Fouchier, shares his concerns. "I do agree that the virus might still pick up mutations to improve infection and transmission in humans. But in our opinion, it is already good enough to beat the seasonal flu viruses," he said via email.

The CDC scientists also reported that the virus is missing a feature in an internal gene called PB2 that is known to relate to transmissibility. All seasonal flu viruses and the past three pandemic viruses -- in other words, all flu viruses which have successfully made the jump from other species into humans -- have had this feature. The H1N1 virus does not. They don't know how the virus achieved transmissibility without this mutation or how likely it is to acquire it. But Tumpey said the mutation is also linked to increased virulence or disease severity and the flu community is watching closely for this change.

Both groups studied tissues from the infected ferrets. They found H1N1 viruses triggered infections that went deep into the lungs of the animals. Human flu strains infect the animals' upper airways. That ability of the virus to spread to and proliferate deep in the lungs could help explain what doctors caring for severely ill H1N1 patients are seeing: aggressive viral pneumonias that incapacitate the lungs.

"Certainly, the lesions we noted in our ferrets are consistent with the disease in humans," Fouchier said. "It seems that due to more extensive virus replication, the virus does more damage, and spreads deeper down the airways as compared to seasonal viruses."

Those findings are concerning, suggested Dr. Malik Peiris, a virologist and flu expert at the University of Hong Kong. Peiris, who was not involved in the studies, said that while the H1N1 virus is not as virulent as H5N1 avian influenza or the virus that caused the 1918 Spanish flu, its ability to infect the lower respiratory tract "is clearly cause for caution in regard to the pathogenic potential of this virus in humans." Both H5N1 and the Spanish flu virus infect tissues deep in the lungs.

Fouchier said he is concerned the novel H1N1's ability to invade deep lung tissue could lead to more severe disease when the virus is spreading in true winter conditions, which are better suited to spread of flu.

A study in guinea pigs -- also a good animal model for flu -- published a couple of years ago found that at lower temperatures flu viruses replicate more and for longer durations. If that holds true for humans and for this virus, the severity of H1N1 infections in winter could be greater, Fouchier warned.

Reformatted

(hat tip Avian Flu Diary)

http://scienceblogs.com/effectmeasure/2009/07/swine_flu_animal_experiments.php.

The Reveres remark on the same experiments that I posted on yesterday. They also note the absence of the E627K mutation in these isolates. None of the swine flu isolates in these studies had the E627K mutation in PB2 which was thought to be characteristic of human adapted viruses.

I would just like to to point out that initially, H5N1 bird flu did not have this mutation either, but at some point it acquired it. All human adapted viruses have this trait, and it is likely that swine influenza also will pick this up while co-infecting a host with seasonal flu. The virus is still adapting to humans. This polymorphism has already been found in one isolate, A/Shanghai/71T/2009 from a young Chinese national who was a student in the US. She flew from New York to Hong Kong, and then on to Shanghai. Scientists in mainland Chinese published the sequence. It was not a lab error. Acquisition of E627K is a concern because it allows for optimal replication at 33 C, the temperature of a human nose in the winter. This is the only known case so far. There are likely to be others.

... Two teams, one in The Netherlands and one in the US, have infected ferrets and mice with pandemic H1N1 isolates from Europe, the US and Mexico and compared transmissibility, virulence and pathology with seasonal H1N1 strains. The two papers were published yesterday in the journal, Science (papers here and here).

There were four different pandemic isolates tested in ferrets. The group in Holland used virus from the first Dutch case, a three year old child who had traveled with family to Mexico and had an uncomplicated case that resolved with full recovery. The US isolates were from another uncomplicated pediatric case in California, a seriously ill 29 year old female from Mexico who recovered, and a fatal pediatric patient from Texas. Different seasonal H1N1 isolates were compared to these swine flu isolates by each team.

...while more was made of the slightly less facile transmission by the American team, the swine flu virus was plainly transmissible in the ferret model in both cases. The US team also employed sophisticated glycan microarray analysis which seemed to show slightly less avid binding to human receptors for the swine flu. Their interpretation was that their isolates were not fully adapted to humans and one could expect the virus to change to allow better transmissibility and perhaps more virulence. While lab and animal studies may show some difference, the epidemiological evidence seems quite clear. This virus is capable of rapid and efficient spread. It is already fully transmissible.

These studies also hint at a greater virulence for the swine flu virus compared to seasonal flu virus. Examining the pathology in ferrets (and in the US experiments mice were also used), the new virus will infect cells deeper in the lungs. The US team also found it in the intestinal tract, consistent with the clinical observation that nausea and vomiting is a common presenting symptom.

It has been claimed that the genetics of this virus are very stable and that essentially all isolates so far are "essentially" identical. But the three US isolates had differences in 6 different gene segments and the Mexican isolate exhibited lethality for half the animals compared to none for all the other isolates and the seasonal H1N1 (Table 1). None of the swine flu isolates had the E627K mutation in PB2 which was thought to be characteristic of human adapted viruses. Now it is clear that it isn't a necessary condition. The fact is the early isolates do exhibit amino acid differences and we are not yet sufficiently knowledgeable about which ones are important to declare them functionally identical.

There is nothing super alarming about these experiments, but there certainly is nothing reassuring, either. Even if this virus only has the same virulence as a seasonal virus, it can infect more people and younger, healthier people. Epidemiologically it will look very different and have a different impact.

It's unlikely this will be like a 1918 flu virus. But it doesn't have to be to cause a major problem. Constantly comparing it to 1918 isn't the point. The point is that this is an influenza pandemic, and that's bad enough.

The Editors of Effect Measure are senior public health scientists and practitioners. Paul Revere was a member of the first local Board of Health in the United States (Boston, 1799). The Editors sign their posts "Revere" to recognize the public service of a professional forerunner better known for other things.

"the virus is still adapting to humans". Interesting, that means the historic reports of a first wave in 1918 that was milder than the second actually fits the genetic data. My grandma suffered so much from the 1918 outbreak. She has been dead a long time but she would be horrified to know that this thing is menacing her grand children and great grand children. I would say to her "grandma, don't worry, we ain't going down without a fight".

Quote from referrred link by OP:

"...........flu viruses are known to mutate rapidly, the research team noted, so this one must be watched closely in case it changes to become easier to spread.

Even if it doesn't mutate, it's causing plenty of illness here and abroad already — and vaccine makers are working "at full speed" to develop shots for use in the fall if the government deems it enough of a threat, Dr. Anthony Fauci, infectious disease director of the National Institutes of Health, said"

I agree with indigo girl regarding the process of mutation occurring in some, not others. Obviously those who have died from confirmed H1N1 were either hit with the mutated form, or it mutated in their bodies.

Since pregnant women and young children have become more seriously ill and many have died, there's something they have in common, that allows mutation or attracts the mutated form of this H1N1 flu.

There should be no confusion among those with knowledge of these epidemiological happenings. Everything points to very large numbers being infected by H1N1, and very few of those being reported in a forthright manner to the local Health Departments.

Paperwork phobia being what it is, it seems to me that a better method of reporting reportable diseases must be established for computation of reliable figures showing the incidence of infections. If all doctors' offices, EDs, IC nurses in hospitals, etc. had a website available that would easily bring up a short reporting form, that is connected to WHO and CDC, more accurate figures would be reported.........

There will always be those who tend to negate danger, and those who exaggerate it. I'd go with the safest predictors, and get adequate quantities of PPE and vaccine, to use for the largest expected number who will need it. Sometimes those who negate are tight fisted with money, preferring to wait until hospital staff screams for PPE - and when they get it, they're the heroes. If your hospital has a Purchasing Department head who is one of those, you might start lobbying with that person sooner, rather than later. Give kudos earlier, to purchasers, rather than when nursing staff are refusing to care for infected patients without PPE.