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Cal/09 : markedly , 5e4pfu, 22.5% weight loss ("wl") by day 8
Bris/59/07 : fewer
Neth/09 , 5e4pfu,C57B/6, more wl than with Cal/09
Cal/09,Neth/09(21d,1e3pfu) all survived
Cal/09,Neth/09(21d,5e4pfu) few wl
no vax,Neth/09 : "endpoint" by day5
Cal/09 6:2,Neth/09 : no deaths, modest wl,no virus in lungs
SW/30,Neth/09 : no deaths , no virus in lungs on day 6, wl=18.2%
NJ/76,Neth/09 : no deaths , no virus in lungs on day 6 , wl=18.2%
Wei/4,Neth/09 : no deaths , high virus in lungs on day 6 , wl >18.2%
1918 VLP,Neth/09 : no deaths, wl similar to {Cal/09 6:2,Neth/09}, no virus in lungs on day 6
USSR/77,Neth/09 : ~40% deaths, extensive wl, titers on day 6 lower as no vax,Neth/09
Hou/84,Neth/09 : similar
Tx/91,Neth/09 : similar
Bris/59/07,Neth/09 : similar
=== page 5 , 10:55
graphs ...
wl and survival strongly depends on initial dose (limit ~5e4pfu)
NT/68 protects a bit, reason unclear
"inactivated vaccines" , I still don't know whether this is whole-virus or only HA or HA+NA
table1, #mouse titers induced by vaccination
cross reactive neutralizing antibodies , I don't fully understand this , skip that part
reason for protection are the epitopes (--> humoral ?)
150mAbs -24h,
=== page 6 , 11:13
graphs...
ahh, why do we need text, when we have graphs
A:wl by day 5 from Neth/09 infection,C57B/6,2*15myg,(14d,14),8e5pfu {do we get that much by breathing ?}
Code:
wl by day 5 in %
% survival by day 5
10*(log(titers in lungs by day 3))
10*(log(titers in lungs by day 6))
10*log(titers from mAbs showing expected protection from CA/09 challenge)
----------------------------------------------------------------------------
04 99 -- -- mock
22 20 65 46 07 USSR/77
22 25 62 36 07 NT/68
22 -- 61 38 07 Hou/84
22 60 60 16 07 Tx/91
22 40 63 40 07 Bris/59/07
24 00 -- -- Bris/10/07
12 99 -- -- 34 Cal/09 6:2
12 99 48 -- 22 1918 VLP
17 99 44 -- 19 Sw/30
17 99 50 -- 16 NJ/76
21 99 65 41 07 Wei/43
27 00 69 55 07 no vax(control)
-- -- -- -- 28 Neth/09
27 00 66 59 07 control mAb
-2 99 38 47 24 29E3(Cal/09)
01 99 52 51 -- 6B9(1918)
06 99 43 56 21 39E4(1918)
13 99 49 31 -- Poly(Cal/09)
-- -- -- -- 16 Cal/09 virus
{I think, this table will be central in my -hopefully better- summary}
brb 6min
specific : 110 titers
polyclonal: 40 titers
results from antibody treatment is hopefully shown later in a similar table, so it can
just be added here. So I skip this part
=== page 7 , 12:22
table 2
I never know in these tables what's horizontal and what vertical
I want protection against potential Cal/09 infection and I take row 10 to measure this
and include it in my above table
3d-picture of HAs
however the yellow escape mutation positions are identical in 1918 and 2009
=== page 11 , 13:47
make a more complete table of antigenic sites of ~50 viruses , human and swine, 1918-2009 (later)
thinks protection from cell-based immunity and NA play a minor rule
good protection by Tx/91 is unexplained (I remember that that particular strain caused
some GB)
what's monoclonal,polyclonal ?
1976 - why do we have no estimates, how many % of ******-infected people had had
the 1976 vax ? (just ask them !)
the protection back to 1943, does it also hold for the 1977-semi-pandemic , which also
mainly infected children ?
so longterm protection (1943 back to 1918 up to 2009 = 116 years
yet the seasonal vaccine is often a bad match (why ?)
H1N1 antigenically frozen in pigs ? -----edit----- yes, see e.g. the antigenic site Sb in the table below
=== page 12 , 14:08
possible future pandemics from frozen viruses {but we can prepare with vaccine}
same study in humans ? ******=CA/09 is not lethal, usually mild, most people will be infected
earlier or later anyway. In USA, where this site is located, they even have death-penalty,
so you could use these people. However, not in the same country since else the judges might
be more willing to speak death penalties. It all depends on _how many_ such experiments
in humans you wanted to do. Probably not reasonable in this case, but when we get
a severe H5N1-pandemic it could be important.
First verify some few of the results in ferrets or swine
brb 3min
=== page 13 , 14:23
references not read
~4.5 hours in total , 2 tables still to be made , the central table still to be studied and
the results comprehended,learned,visualized
the whole paper writing process is ineffective, you need to long to rea it and the abstract
and author summary is not informative enough (IMO)
Why these long papers and no shorter presentations ?
In math you skip the proofs and just read the theorems for a first understanding,
what are the theorems here ?
it took 9 months, too late for wave 1,wave 2,(wave 3 in Mex.)
pdf , no data are given , so I had to estimate the values for my central table
from graphs.
Data would be useful so we can make our own tables, own graphs ,
maybe better presented. I assume this is not in the interest of the authors and that's
why data and computer-readable tables and plain text (easy to quote and discuss in forums)
are usually not provided (?)
Strains of influenza A virus show marked differences in their ability to infect murine macrophages (MPhi) such that strain A/PR/8/34 (PR8; H1N1) infects MPhi poorly while strain BJx109 (H3N2) infects MPhi to high levels. Given the central role of MPhi in initiating and regulating inflammatory respon …
ahh, these K171Q,K171E,K180N were "escape mutants", apparantly
happened after lots of passages and lots of vaccinations
to "escape" the vaccine
The escape mutants that arose in the presence of the 1918 specific mAb 6B9 and 39E4
contained mutations G172E (G158E by H3 numbering) and K171E (K157E by H3 numbering), respectively. The escape mutants generated by selection with the 2009 H1N1 specific mAb (29E3) carried either a K171E or K171Q or K180N mutation (residues K171 and K180 correspond to K157 and K166 in H3 numbering). These results indicate that all the mAbs bind to the conserved antigenic site Sa (Fig. 5 and 6).
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