Rhiza Labs FluTracker Forum

Fatal Ukraine lung patients had D225G on the HA from swine H1N1. This change is also now reported in Norway. The change was also seen in lung samples from 1918 and 1919.

This change allows the virus to bind to cells with alpha 2,6 and alpha 2,3 receptors. Alpha 2,3 receptors are on type II aveolar cells in the lungs, which keep the lungs inflated and fend off invaders by eliciting a cytokine response.
A modified virus that binds to these lung cells is a major concern.

For the two 1918 HA variants, the South Carolina (SC) HA (with Asp190, Asp225) bound exclusively alpha2-6 receptors, while the New York (NY) variant, which differed only by one residue (Gly225), had mixed alpha2-6/alpha2-3 specificity, especially for sulfated oligosaccharides.

http://www.ncbi.nlm.nih.gov/pubmed/1634 ... nalpos=112

using in vitro human and mouse airway epithelial cell models and in vivo mouse infection, we found that the alpha2,3-linked SA receptor was expressed in ciliated airway and type II alveolar epithelial cells

http://www.ncbi.nlm.nih.gov/pubmed/16840327

In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
http://www.doaj.org/doaj?func=abstract&id=80022

CDC has issued an alert (in Sept)

Physicians Asked to be on the Lookout for Possible “Hemorrhagic Pneumonia Cases”
Among Influenza Patients
The CDC says that there have been some anecdotal reports of possible "hemorrhagic
pneumonia" cases among influenza patients who have died or been hospitalized for
severe illness. The phrase "hemorrhagic pneumonia" is somewhat outdated, and most
clinicians will not use the term to describe this condition, which can be a very rare
complication of viral respiratory infection. Some other terms that can be used to
describe this include diffuse alveolar hemorrhage (DAH), which can be caused by
infections but doesn't have to be, and hemorrhagic pneumonitis. In any event, it's a
serious complication that will sometimes lead to acute respiratory distress syndrome
(ARDS). It occurs very rarely as a complication of seasonal influenza, and there is some
concern that it might be more common in H1N1 infections.
The CDC is asking state health officials to look out for possible cases that may involve
clusters of patients who might have these symptoms, or a large proportion of cases with
these symptoms (e.g., 4 of 5 deaths). They will invariably be among the most severely ill
influenza patients (i.e., deaths, ICU patients).
This is a hard diagnosis to make, and the most telling symptom may be hemoptysis
(bloody sputum, frothy bloody cough), although not all cases will have it.
• Acute onset of rather more severe respiratory infection (dyspnea‐‐ difficulty
breathing‐‐ is common)
• Hemoptysis is often seen on initial presentation (~70% of cases)
• CXR and physical exam will suggest alveolar infiltrates (radiographic opacities)
• Diagnosis is usually made by BAL (brochoalveolar lavage) and pathology testing
(increasingly more hemorrhagic fluid/secretions from sequential BAL
Email sent by the Regional Liaison Officer, Region IV, H1N1 Response Surveillance and
Epidemiology Team, Centers for Disease Control and Prevention
Questions concerning possible cases or this email may be directed to Medical Epidemiologist
Zach Moore, MD, at the North Carolina Division of Public health at zach.moore@dhhs.nc.gov

http://www.ncmedsoc.org/blog/wp-content ... umonia.pdf

Betsy McKay: I just wanted to follow-up on the question about the mutation in norway. I wondered if you could talk a little bit more about is it possible that this mutation has produced a more virulent form and what has CDC uncovered through its own work?

Anne Schuchat: this mutation has been seen sporadically here and there around the world. Sometimes it's been seen in patients who had very mild disease and sometimes it's been seen in people who had more severe or fatal disease. And, of course, lots of virus without this mutation has been seen in the fatal as well as the milder forms of H1N1 influenza. There's some theoretical reasons why this particular mutation might lead an influenza virus to live easier in the deep part of the lungs and cause lower respiratory infections, but we've actually seen lower respiratory infections in a severe viral pneumonia without this mutation. So I think it's too soon to say what this will mean long term. It's an important finding and they're looking into it, but I don't think it has the public health implications that we would wonder about. Did you have a second question? Oh, what have we seen so far? I believe it's been seen in the U.S. But associated with mild disease. I believe. I might need to verify that. Do we have another from the room? Okay. We'll go back to the phone.

http://www.cdc.gov/media/transcripts/2009/t091120.htm

Commentary

http://www.recombinomics.com/News/11230 ... 18_US.html

Yup. Spinmeister Schuchat doin' her shuckin' and jivin'.

Excerpt from the definition of shuckin' and jivin' from Wikipedia: Shuckin' and jivin' (or shucking and jiving) is a slang term primarily used by African Americans. It refers to the speech and behavioral mechanisms adopted in the presence of an authoritative figure [1]. Shuckin' and jivin' usually involves clever lies and impromptu storytelling, used to one-up an opponent.....

So we've heard from WHO or Shucky the following: Yawn. "We've seen that since April. We've seen that in very mild cases as well as more serious ones. It spontaneously arises from time to time. There's no evidence of any transmisability. We've seen this is milder cases in the US I think (but I need to verify that). Blah blah blah blah blah."

It's good to know there are no public health implications whatsoever. I feel such a sense of relief.

I'm a soon-to-be 57-year-old female with adult-diagnosed cystic fibrosis. Although I have minimal lung involvement, this disease has primarily resulted in chronic pancreatitis.

My doctor is almost DEMANDING that I receive the "swine flu" vaccine because he said "people like me" could die very easily from it.

I have not received one of these vaccines because I have almost an instinctive, inherent distrust of the vaccine and don't believe all the hype that this vaccine could actually help.

I live with my dog and seldom leave my apartment (other than to take her outside a few times a day). I maybe go to the doctor's/grocery stores 4 times a month, but other than that, I'm in my apartment. (I have a problem with agorophobia.)

What's the REAL scoop here? Do I really need this vaccine, or is there any merit to my inherent distrust of the vaccine "system?"

Thanks in advance for any response you can provide.