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[2] Some questions
Date: 15 Mar 2008
From: Allen Lenoir
re: Seasonal influenza, child - China (HK SAR) 20080315.1027
- ------------------------------------------------------------
[Dr Allen Lenoir has posed the following questions. Answers or additional
comments would be welcomed. - Mod.CP]
The statement that H1N1 and H3N2 viruses were found in the victim would
indicate viral isolation and coinfection rather than seropositivity, if
taken literally. Of course, the media may have misunderstood. Can we have a
clarification on this issue?
If it was coinfection, do we know whether or not the victim had been
treated with a neuraminidase inhibitor? A recent report from Harvard has
indicated that neuraminidase inhibitors can increase the possibility of
dual influenza infection.
If the reporter actually meant seropositivity, was the victim ever vaccinated?
- --
Allen Lenoir, MD
Miami, FL
-
(1.5): J Virol. 2008 Mar 5 [Epub ahead of print]
Influenza A virus neuraminidase limits viral superinfection.
Huang IC, Li W, Sui J, Marasco W, Choe H, Farzan M.
Department of Microbiology and Molecular Genetics, Harvard Medical School, Southborough, Massachusetts 01772; Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115; Department of Pediatrics, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Critical Care | Full text | Update of Avian Influenza A Infections ::
Avian influenza A virus (H7N7) associated with human conjunctivitis and a fatal . Risk of influenza A (H5N1) infection among poultry workers, Hong Kong,
http://ccforum.com/content/11/2/209HOME |
AVIAN INFLUENZA A (H5N1): A PRELIMINARY REVIEW::
File Format: PDF/Adobe Acrobat - View as HTMLof six people by H5N1 bird flu, Hongkong conducted a. mass slaughter of chickens . human influenza virus and the ensuing virus would then
http://medind.nic.in/iau/t04/i3/iaut04i3p143.pdfHOME |
Enveloped viruses use multiple mechanisms to inhibit infection of a target cell by more than one virion.
These mechanisms may be of particular importance for the evolution of segmented viruses, because superinfection exclusion may limit the frequency of reassortment of viral genes.
Here we show that cellular expression of influenza A virus neuraminidase (NA), but not hemagglutinin (HA) or the M2 proton pump, inhibits entry of HA-pseudotyped retroviruses.
Cells infected with H1N1 or H3N2 influenza A virus were similarly refractory to HA-mediated infection and to superinfection with a second influenza A virus.
Both HA-mediated entry and viral superinfection were rescued by the neuraminidase inhibitors oseltamivir carboxylate and zanamivir.
These inhibitors also prevented the removal of alpha-2,3- and alpha-2,6-linked sialic acid (SA) observed in cells expressing NA or infected with influenza A viruses.
Our data indicate that NA alone among viral proteins limits influenza A virus superinfection.
PMID: 18321971 [PubMed - as supplied by publisher]
-------
I think the abstract refers to single cell virion entry: a virion can infect only a cell at time, and prevents other virion to attach to the same cell by NA activity. If NA is inhibited by a drug, then the machinery doesn't work.
Perhaps, when a highly replication capable virus (with human receptors affinity) enters in the host, the vast majority of susceptible cells are 'occupied' by virions and thus confers to the virus a competitive advantage versus less replication-capable virus in human receptor suitable cells. In other thread of this forum a study highlight the human / avian influenza viruses coinfection in an Indonesian patient (where H3N2 seems to be the dominant and H5N1 less virulent, with a clinical course milder than single H5N1 infection patients).
中国科学院上海巴斯德研究所::
Flu is caused by influenza virus. A virus is a microorganism that requires between human and avian viruses during co-infection of a human or pig.
http://www.shanghaipasteur.ac.cn/dknow1.aspHOME |
Excuse me for the inevitable uncorrectness. But I think these findings may be important.
Co-infections are common. Just look at data from wild birds. The sero-type of isolates frequently does not match the serotype of the uncloned parental sample.
Look at OSU samples at
http://www.ncbi.nlm.nih.gov/genomes/FLU/Database/shipment.cgi
why does the virus want to prevent double-infection ?
and if the virus doesn't want it, why don't we want it either ?
I'm speculating that it depends on the type of cell
and that later, when uninfected cells in the area of virus production
become rare, then it would cause double infections anyway.
Also, how long does it take to build up double-infection-protection ?
In the meantime the new 2nd virus may have entered
Co-infections are common. ...
Does diferent individual virus swap genetic material between, like individual bacteria (harmful, and non) can do?
Thank You (dr.N., or anybody of sci.).
usually the coinfection-preventing mechanism should address
viruses of the same type, the same infection, maybe even produced
in the same neighbor-cell.
These viruses compete with each other and coinfection-prevention
gives an advantage by better fighting other competing viruses.
The host can be happy, if his enemies waste some energy
by fighting each other.
It could also be a direct advantage. Two or more viruses of initial infection
of a cell could somehow disturb each other and the whole replication process
is less effective then or even may fail.
Well, suppose the virus recognizes that the other virus is just better,
but related, wouldn't it be evolutionary reasonable to suicide and let the
field to the other virus ?
OTOH the virus "wants" to examine the genetical material of those other
viruses and maybe steal from it by reassortment.
while this coinfection may be destructive per single cell (from the virus'
point of view), it's still one of the important driving forces of virus evolution and adaption.
influenza viruses have 8 segments, when there are coinfections
they can mix their segments.
On virus entry the 8 segments are released into the cell, transported
to the nucleus where they are replicated.
The copies are packed outside the nucleus, probably in a way
to ensure exactly one copy of each segment.
You can see such events maybe roughly once per 50 viruses.
When a duck has a 5% chance of having a flu-virus,
then it could have 2 different ones with 0.25%, just multiplicating.
1:20 that a positive duck has another virus.
Most reassortants are not viable but those who are often
induce dramatical changes.
There could also be two different viruses clumbed together in one
drop, and then you get both, but apparantly this is not so
frequent. Usually one dominates.
Please. If there is a co-infection with 8 gene segments each, how many combinations can theoretically come out? How many or found?
Putting an imaginary number on an outcome doesn't lend credibility to the "prediction".
why does the virus want to prevent double-infection ?
and if the virus doesn't want it, why don't we want it either ?
I'm speculating that it depends on the type of cell
and that later, when uninfected cells in the area of virus production
become rare, then it would cause double infections anyway.
Also, how long does it take to build up double-infection-protection ?
In the meantime the new 2nd virus may have entered
I think the abstract refers to single cell virion entry: a virion can infect only a cell at time, and prevents other virion to attach to the same cell by NA activity. If NA is inhibited by a drug, then the machinery doesn't work.
Perhaps, when a highly replication capable virus (with human receptors affinity) enters in the host, the vast majority of susceptible cells are 'occupied' by virions and thus confers to the virus a competitive advantage versus less replication-capable virus in human receptor suitable cells. In other thread of this forum a study highlight the human / avian influenza viruses coinfection in an Indonesian patient (where H3N2 seems to be the dominant and H5N1 less virulent, with a clinical course milder than single H5N1 infection patients).
Excuse me for the inevitable uncorrectness. But I think these findings may be important.
Does diferent individual virus swap genetic material between, like individual bacteria (harmful, and non) can do?
Thank You (dr.N., or anybody of sci.).
Lots of swapping. Many polymorphisms in high path H5N1 can be found in low path.
influenza viruses have 8 segments, when there are coinfections
they can mix their segments.
On virus entry the 8 segments are released into the cell, transported
to the nucleus where they are replicated.
The copies are packed outside the nucleus, probably in a way
to ensure exactly one copy of each segment.
You can see such events maybe roughly once per 50 viruses.
When a duck has a 5% chance of having a flu-virus,
then it could have 2 different ones with 0.25%, just multiplicating.
1:20 that a positive duck has another virus.
Most reassortants are not viable but those who are often
induce dramatical changes.
There could also be two different viruses clumbed together in one
drop, and then you get both, but apparantly this is not so
frequent. Usually one dominates.
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