- Hello Jeff -
-
- It would seem that there is now an endless
supply of false bird flu information circulating the internet, and many
posts which include ad hominem attacks on me. The lastest is a post titled
'Bird Flu Fiction.' As the primary article is fowarded around the internet
via email it has picked up even more slanderous accusations about me.
Most importantly, the article, itself, is fatally-flawed. I attach it
at the end bottom of this page.
-
- First and for those who are either clueless
or prone to buying into the trash on the net without checking to verify...
-
- Although I have taken yearly USAMRIID
Ft. Deterick seminars on chemical and biological terrorism preparedness,
as have many other health professionals, I am NOT a government agent, have
never been a CIA agent, NSA agent or a zionist backed 'infiltrator.' I
am, however, an American citizen doing her best to stay current on all
the data and inform honestly and accurately in this age of internet insanity
-- which is precisely what genuine infiltrators and agents are trained
to do.
-
- As you know, I took these seminars to
learn about preparing for a chemical/biological/nuclear event on our soil.
I used the Army's information I obtained from the seminars for one reason:
to help inform the American public to the very best of my ability on such
events. I have spent the better part of a decade sharing information on
this subject as well as emerging infectious diseases on your program and
site, and my own emerging diseases message board. I firmly believe a well-informed
public will be one that does NOT panic when an event, whether man-made
or naturally-occurring, takes place. We all need to be armed with information.
I have spent this time, even though quite ill, doing radio interviews
and either authoring articles or fowarding articles written by others to
you for your wonderful site.
-
- I reprint below the latest article to
arrive in my email box. The article entitled "Bird Flu Fiction"
which has been circulating via email, and as it runs through the net grist
mills, like a snowball, it has picked up various remarks accusing me of
being a "zionist-backed disinformation agent," a "CIA agent
and infiltrator" and other such mindless and contrived drivel.
-
- Let us examine the article, on its merits
or lack thereof, without the ad hominem reparte. The article, in my opinion
is flawed.
-
- I have stated over the past few years,
that resurrecting H1N1 Spanish Flu was and is dangerous. I have also written
commentary on and have vocalized on many of our programs, that:
-
- 1. There is a danger of escape of the
1918 pathogen from one of the countries often poorly-secured and operated
bio labs, and, or danger of a release by a bioterrorist.
-
- 2. The BSL 4 level should be maintained
- and it should NOT be downgraded to BSL3 simply because people think Tamiflu
will 'save us.' It won't. My argument is that tamiflu and other antivirals
are not paneceas for Spanish Flu or bird flu because, as we saw in Vietnam,
influenza viruses DO mutate and develop antiviral resistant strains. And
in the case of bird flu, can do so very quickly. We have already had both
tamiflu and amantadine-resistant strains develop. I have warned about
misuse, overuse and abuse of Tamiflu. I have also read aloud the ingredients
in Tamiflu on your program.
-
- Both Dr. Henry Niman and myself have
spoken out firmly and repeatedly against the current research of a Bird
Flu H5N1 vaccine. This research is based on the 2004 Vietnamese strain
of bird flu. If the virus does mutate i.e. develop genes that enable it
to spread easily between humans, via recombination and/or reassortment,
it would be a VERY different virus than the 2004 Vietnamese strain. We
could possibly have a recombination of H3N2 or H1N1 and H5N1. There could
possibly be, in addition, an incorporation of genes that have reassorted
or even genes from other influenza viruses. Note - Dr. Niman discovered
WSN 33 genes in swine sequences in S. Korea...a major, serious discovery
which went virtually unnoticed except on his site and your program.
-
- AS BIRD FLU SPREADS IT PICKS UP MORE
AND MORE MAMMALIAN GENES
-
- Please refer to recombinomics.com and
click on the "What's New" section where you will see various
articles and commentary on the changes in the bird flu viral sequence.
Also of interest, Astrakhan Mute Swan
- (http://www.recombinomics.com/News/0226060
1/H5N1_Astrakhan_Human.html)
- H5N1 Acquisiton of human sequences.
-
- Normally, the first avian flu virus strains
do not infect humans, but over time, and as the virus travels widely now
and is on an unprecedented three continents, it picks up pieces of genetic
material from other flu viruses, some of which may be human influenza.
It then begins to infect a few people. As it further spreads and begins
to pick up more and more material, it then infects more people. And on
and on it goes. There is a legimate worry that the avian flu will infect
the key intermediary animal species: swine. Swine are perfect mixing
vessels. It is widely believed that H1N1 Spanish Flu was initially avian
and jumped to swine. It is further theorized that the Spanish Flu jumped
to humans from swine.
-
- If you read some of the articles regarding
the changes in the H5N1 virus on recombinomics.com "What's New"
section, you will see that Henry discusses changes in the hemaglutinin
(Ha.)
-
- I would hope that the ugly remarks will
cease and that open discussion on the issue of bird flu will continue.
This is America where the individual is allowed absolute Freedom of Speech.
It is far better to discuss the topic and not resort to name-calling and
false accusations...which usually come from people who have little dignity
or grace. It has also a given that people who have a weak arguments quickly
and immediately resort to defamation and slander in debates. Unfortunately,
this has become the standard fare. It would be far better for all of
us if debaters simply stick to the issues and focus on the topic at hand.
-
- Again, Jeff, and I don't need to tell
you but let me again state for those who may have been duped and deceived
by the misinformation pros and others who seem to be emotionally troubled
that I am not in any government organizations, a zionist agent or dupe,
nor am I an asset in any way shape or form of any US or foreign government
intelligence or globalist organization. Further, I have never profited
in any way from my ten years of work covering Bird Flu, Mad Cow, Foot and
Mouth or any other disease issue on your program, site, or any other media
outlet. Or, for presenting information on infectious or emerging diseases
of any kind or the subject of bioterrorism itself. I have no books, videos,
DVDs or audio materials to sell. I do this work because it is an honor
to be a citizen of our nation and I am trying to repay my country for the
wonderful life it has provided me and so many others. I am profoundly
privileged to have earned the trust of so many people...citizens and health
professionals and scientists alike. I am more than grateful for this.
-
- Patricia Doyle, nee DOYLE
-
-
- 1918 Killer Flu 'Came From
Birds'
-
- BBC News
- 10-6-5
-
- The Spanish flu virus that killed 50
million people in 1918-19 was probably a strain that originated in birds,
research has shown. US scientists have found the 1918 virus shares genetic
mutations with the bird flu virus now circulating in Asia.
-
- Writing in Nature, they say their work
underlines the threat the current strain poses to humans worldwide. A second
paper in Science reveals another US team has successfully recreated the
1918 virus in mice. The virus is contained at the US Centers for Disease
Control and Prevention [CDC] under stringent safety conditions. It is hoped
to carry out experiments to further understand the biological properties
that made the virus so virulent.
-
- http://www.nature.com/news/2005/051003/full/437794a.html
-
- The virus was recreated from data produced
by painstaking research by a team from the US Armed Forces Institute of
Pathology. Working on virus samples from the remains of victims of the
1918 pandemic, the researchers were able to piece together the entire genetic
sequence of the virus. They found the virus contained elements that were
new to humans of the time, making it highly virulent. Analysis of the final
3 pieces of the virus' genetic code has revealed mutations that have striking
similarities to those found in flu viruses found only in birds, such as
the H5N1 strain currently found in south east Asia.
-
- Many experts believe it is only a matter
of time before H5N1, or a similar virus, causes many deaths in humans --
possibly after combining [reassorting genome segments] with a human flu
strain. Crucially, the mutations identified by the US researchers were
found in genes which control the virus' ability to replicate in host cells.
The researchers say these mutations may have helped the 1918 virus replicate
more efficiently.
-
- At this stage, they say the H5N1 strain
shares only some, and not all, of these mutations. But these mutations
may be enough to increase the virulence of the virus, and give it the potential
to cause serious human infection without first combining [reassorting genome
segments] with a known human flu strain. The researchers believe the 2
other major flu pandemics of the 20th century -- in 1957 and 1968 -- were
caused by human flu viruses which acquired 2 or 3 key genes from bird flu
virus strains. But they believe the 1918 strain was probably entirely a
bird flu virus that adapted to function in humans.
-
- Julie Gerberding, director of the US
Centers for Disease Control & Prevention (CDC), said: "By unmasking
the 1918 virus we are revealing some of the secrets that will help us predict
and prepare for the next pandemic." Dr Jeffery Taubenberger, lead
researcher of the Nature study, said: "Determining whether pandemic
influenza virus strains can emerge via different pathways will affect the
scope and focus of surveillance and prevention efforts."
-
- Warning
-
- Professor John Oxford, an expert in virology
at Queen Mary College, London, said the suggestion that the virus had the
potential to jump between humans without first combining [reassorting]
with a human virus made it even more of a threat. "This study gives
us an extra warning that H5N1 needs to be taken even more seriously than
it has been up to now," he said. Dr Terrence Tumpey, of the US CDC,
defended the decision to recreate the 1918 flu virus. He said: "We
felt we had to recreate the virus and run these experiments to understand
the biological properties that made the 1918 virus so exceptionally deadly.
"We wanted to identify the specific genes responsible for its virulence,
with the hope of designing antivirals or other interventions that would
work against virulent pandemic or epidemic influenza viruses."
-
- http://www.nature.com/news/2005/051003/full/437794a.html
-
- ProMED-mail promed@promedmail.org
-
- The Nature paper is published in the
5 Oct 2005 online edition and is entitled: "Large-scale sequencing
of human influenza reveals the dynamic nature of viral genome evolution.
The authors are: Elodie Ghedin1, Naomi A. Sengamalay1, Martin Shumway1,
Jennifer Zaborsky1, Tamara Feldblyum1, Vik Subbu1, David J. Spiro1, Jeff
Sitz1, Hean Koo1, Pavel Bolotov2, Dmitry Dernovoy2, Tatiana Tatusova2,
Yiming Bao2, Kirsten St George3, Jill Taylor3, David J. Lipman2, Claire
M. Fraser1, Jeffery K. Taubenberger4 and Steven L. Salzberg1,5. (At 1 The
Institute for Genomic Research, 9712 Medical Center Dr., Rockville, Maryland
20850, USA ; 2 National Center for Biotechnology Information, National
Library of Medicine, National Institutes of Health, Bethesda, Maryland
20894, USA2; 3 Wadsworth Center, New York State Department of Health, Albany,
New York 12201, USA ; 4 Department of Molecular Pathology, Armed Forces
Institute of Pathology, Rockville, Maryland 20850, USA 5 Center for Bioinformatics
and Computational Biology, University of Maryland Institute for Advanced
Computer Studies, College Park, Maryland 20742, USA.)
-
- The Introduction reads as follows: "Influenza
viruses are remarkably adept at surviving in the human population over
a long time-scale. The human influenza A virus continues to thrive even
among populations with widespread access to vaccines, and continues to
be a major cause of morbidity and mortality. The virus mutates from year
to year, making the existing vaccines ineffective on a regular basis, and
requiring that new strains be chosen for a new vaccine. Less-frequent major
changes, known as antigenic shift, create new strains against which the
human population has little protective immunity, thereby causing worldwide
pandemics. The most recent pandemics include the 1918 'Spanish' flu, one
of the most deadly outbreaks in recorded history, which killed 30-50 million
people worldwide, the 1957 'Asian' flu, and the 1968 'Hong Kong' flu (3).
-
- Motivated by the need for a better understanding
of influenza evolution, we have developed flexible protocols that make
it possible to apply large-scale sequencing techniques to the highly variable
influenza genome. Here we report the results of sequencing 209 complete
genomes of the human influenza A virus, encompassing a total of 2 821 103
nucleotides. In addition to increasing markedly the number of publicly
available, complete influenza virus genomes, we have discovered several
anomalies in these first 209 genomes that demonstrate the dynamic nature
of influenza transmission and evolution. This new, large-scale sequencing
effort promises to provide a more comprehensive picture of the evolution
of influenza viruses and of their pattern of transmission through human
and animal populations. All data from this project are being deposited,
without delay, in public archives." - Mod.CP]
-
-
- For Your Information:
- EXCHANGE OF GENETIC MATERIAL
-
- RECOMBINATION
-
- Exchange of genetic information between
two genomes.
-
- REASSORTMENT
-
- If a virus has a segmented genome and
if two variants of that virus infect a single cell, progeny virions can
result with some segments from one parent, some from the other.
-
- "CLASSIC" RECOMBINATION
-
- This involves breaking of covalent bonds
within the nucleic acid, exchange of genetic information, and reforming
of covalent bonds.
-
- This kind of break/join recombination
is common in DNA viruses or those RNA viruses which have a DNA phase (retroviruses).
The host cell has recombination systems for DNA.
-
- Recombination of this type is very rare
in RNA viruses (there are probably no host enzymes for RNA recombination).
Picornaviruses show a form of very low efficiency recombination. The mechanism
is not identical to the standard DNA mechanism, and is probably a "copy
choice" kind of mechanism (figure 1) in which the polymerase switches
templates while copying the RNA.
-
- Figure 2 Marker rescue Recombination
is also common in the coronaviruses - again the mechanism is different
from the situation with DNA and probably is a consequence of the unusual
way in which RNA is synthesized in this virus.
-
- So far, there is no evidence for recombination
in the negative stranded RNA viruses giving rise to viable viruses (In
these viruses, the genomic RNA is packaged in nucleocapsids and is not
readily available for base pairing).
-
- Various uses for recombination techniques
-
- a) Mapping genomes (the further apart
two genes are, the more likely it is that there will be a recombination
event between them).
-
- b) Marker rescue - DNA fragments from
wild type virus can recombine with mutant virus to generate wild type virus
- this provides a means to assign a gene function to a particular region
of the genome. This also provides a means to insert foreign material into
a gene (figure 2).
-
- Recombination enables a virus to pick
up genetic information from viruses of the same type and occasionally from
unrelated viruses or even the host genome (as occurs in some retroviruses
-
- REASSORTMENT
-
- If a virus has a segmented genome and
if two variants of that virus infect a single cell, progeny virions can
result with some segments from one parent, some from the other.
-
- This is an efficient process - but is
limited to viruses with segmented genomes - so far the only human viruses
characterized with segmented genomes are RNA viruses e.g. orthomyxoviruses,
reoviruses, arenaviruses, bunya viruses.
-
- Reassortment may play an important role
in nature in generating novel reassortants and has also been useful in
laboratory experiments (figure 3). It has also been exploited in assigning
functions to different segments of the genome. For example, in a reassorted
virus if one segment comes from virus A and the rest from virus B, we
can see which properties resemble virus A and which virus B.
-
- Reassortment is a non-classical kind
of recombination
-
- PHENOTYPIC MIXING
-
- If two different viruses infect a cell,
progeny viruses may contain coat components derived from both parents and
so they will have coat properties of both parents. This is called phenotypic
mixing (figure 5). IT INVOLVES NO ALTERATION IN GENETIC MATERIAL, the progeny
of such virions will be determined by which parental genome is packaged
and not by the nature of the envelope.
-
- Phenotypic mixing may occur between related
viruses, e.g. different members of the Picornavirus family, or between
genetically unrelated viruses, e.g. Rhabdo- and Paramyxo- viruses. In the
latter case the two viruses involved are usually enveloped since it seems
there are fewer restraints on packaging nucleocapsids in other viruses'
envelopes than on packaging nucleic acids in other viruses' icosahedral
capsids.
-
-
- Figure 6 Phenotypic mixing to form a
pseudotype We can also get the situation where a coat is entirely that
of another virus, e.g. a retrovirus nucleocapsid in a rhabdovirus envelope.
This kind of phenotypic mixing is sometimes referred to as pseudotype (pseudovirion)
formation (figure 6). The pseudotype described above will show the adsorption-penetration-surface
antigenicity characteristics of the rhabdovirus and will then, upon infection,
behave as a retrovirus and produce progeny retroviruses. This results in
pseudotypes having an altered host range/tissue tropism on a temporary
basis
-
- Reassortant Viruses
-
- Description - Viruses containing two
or more pieces of nucleic acid (segmented genome) from different parents.
Such viruses are produced in cells coinfected with different strains of
a given virus.
-
- ANTIGENIC DRIFT AND ANTIGENIC SHIFT
-
- Influenza viruses can change in two different
ways.
-
- One is called "antigenic drift."
These are small changes in the virus that happen continually over time.
Antigenic drift produces new virus strains that may not be recognized by
the body's immune system. This process works as follows: a person infected
with a particular flu virus strain develops antibody against that virus.
As newer virus strains appear, the antibodies against the older strains
no longer recognize the "newer" virus, and reinfection can occur.
This is one of the main reasons why people can get the flu more than one
time. In most years, one or two of the three virus strains in the influenza
vaccine are updated to keep up with the changes in the circulating flu
viruses. So, people who want to be protected from flu need to get a flu
shot every year.
-
- The other type of change is called "antigenic
shift." Antigenic shift is an abrupt, major change in the influenza
A viruses, resulting in new hemagglutinin and/or new hemagglutinin and
neuraminidase proteins in influenza viruses that infect humans. Shift results
in a new influenza A subtype. When shift happens, most people have little
or no protection against the new virus. While influenza viruses are changing
by antigenic drift all the time, antigenic shift happens only occasionally.
Type A viruses undergo both kinds of changes; influenza type B viruses
change only by the more gradual process of antigenic drift.
-
- Flu is a difficult disease to prevent
and control because the virus is able to disguise itself and fool the body,s
immune system into thinking that it has never encountered the infection
before. The virus mutates quickly and regularly to produce new strains
through antigenic shift and drift.1.
-
- Genetic Re-assortment of Influenza A
Viruses
-
- Immunity against Influenza viruses
-
- A host is infected with a particular
influenza virus strain. Antibodies are formed against that strain. The
antibodies formed protect the host against re-infection by the same virus
strain. The Emergence of "New Viruses through Antigenic Shift and
Drift
-
- On the influenza virus, the surface proteins
haemagglutinin and neuraminidase are important in inducing the formation
of antibodies.
-
- Changes in the surface proteins result
in antigenic changes in the virus. The immune system no longer recognizes
the virus strain and the host is susceptible to re-infection.
-
- Influenza viruses can change in two different
ways.
-
- Antigenic Drift
-
- Gradual changes in an already circulating
virus Eventually the virus changes enough so that most of the population
is susceptible to re-infection. There is then an influenza epidemic. Size
and severity of the epidemic is dependent on the degree to which the virus
is different from those already experienced by the population. Influenza
viruses are constantly changing by antigenic drift Type A and Type B influenza
viruses undergo changes by antigenic drift. The WHO Global Influenza Programme
monitors antigenic changes and the adjustments required in influenza vaccines
-
- Antigenic Shift
-
- The sudden emergence of new antigenically
different influenza A sub-type. The host population has no immunity against
the new sub-type and an influenza pandemic follows. Antigenic shift only
occurs occasionally Only Type A Influenza viruses change by antigenic shift
Antigenic shift is of public health concern as subtypes from different
species may then be able to infect humans. Mechanisms of Antigenic shift
-
- Antigenic shift in man probably occurs
through one of these mechanisms:
-
- Direct transfer of a virus from another
species.
-
-
- Genetic re-assortment of avian and human
influenza viruses infecting the same host. Believed to take place in pigs.
See swine influenza. New evidence indicates that it may also take place
in humans. The new virus that emerges may be an avian virus containing
enough human influenza genes to allow human to human transmission.
-
-
- Re-emergence of a virus that may have
caused an epidemic years earlier. For more information see: The Center
for Disease control and prevention, Influenza information.
-
-
- The term antigenic variation refers to
the mechanism in which an infectious organism alters its surface proteins
in order to evade a host immune response. This change in antigenic profile
may occur as the pathogen passes through a host population (also called
"antigenic diversity") or may take place in the originally infected
host.
-
- Antigenic variation can occur through
three broadly defined genetic processes: gene mutation, recombination,
and switching. In all cases, antigenic variation results in pathogens that
are immunologically distinct from the parental strains.
-
- Viruses
-
- The process of antigenic variation occurring
in viruses is categorized as either antigenic drift or antigenic shift.
Antigenic drift, which is exhibited by a wide range of viruses, is a result
of genetic point mutations accumulated by the viral genome over an extended
period of time. This drift produces small antigenic changes in the pathogen
population which ultimately reduce the efficacy of B and T cell memory
during the host immune response.
-
- Antigenic drift has been well characterized
in the influenza virus, and is becoming more and more evident in the rapid
evolution of rhinoviruses and enteroviruses. The Human Immunodeficiency
Virus (HIV) exhibits antigenic drift within the particular host due to
its high rate of replication.
-
- Antigenic shift refers to a more immediate
and extensive change in genetic information. This can occur when two strains
of the pathogen recombine, a process exemplified by Influenza A. In this
instance of genetic recombination, whole segments of the virus genomes
are swapped when human and avian strains dually infect a single host. The
immunological challenges posed by the newly produced influenza strain are
the cause for widespread influenza epidemics.
-
-
- Question: How exactly does influenza
evolve into new strains so often?
- http://www.madsci.org/posts/archives/jan2000/947803959.Vi.r.html
-
- Influenza virus has a number of factors
going for it in regards to its ability to evolve into new strains.
-
-
- Historical Background Influenza viruses
were probably a major cause of disease in ancient times; retrospective
tracing has dated the occurrence of influenza epidemics back to at least
1173. There is a nearly continuous record of epidemics, which are periodically
interspersed with extensive pandemics (i.e. world-wide epidemics). During
the past century, serologic testing of samples from elderly persons has
permitted a more certain assessment of epidemic disease. In 1889, a pandemic
occurred with a type A virus containing an H3-like hemagglutinin and an
equine-like neuraminidase. Little is known of influenza in the intervening
years preceding the devastating pandemic of 1918, which was caused by a
H1N1 (formerly called swine flu) virus. During that epidemic about 20 million
people died worldwide with approx. 500,000 people dying in the United States.
-
- The modern history of influenza began
with its isolation from humans in 1933. This virus was later shown to be
antigenically related to a virus isolated in swine two years earlier. In
1940, a second antigenically distinct human virus was isolated and it was
designated influenza B, to distinguish it from the earlier virus which
was then designated influenza A. Finally, a third antigenically distinct
virus, influenza C virus, was isolated in 1949. We will concentrate on
influenza A & B viruses in this lecture.
-
- Structure
-
-
- The influenza viruses are characterized
by a segmented genome, that is located within a helical nucleocapsid. The
nucleocapsid and matrix proteins are surrounded by an envelope that is
composed of a lipid bilayer. Protruding from the envelope are the antigenic
viral surface glycoproteins: the hemaglutinin (HA) and neuraminidase (NA).
The genome of the influenza A & B viruses is composed of 8 segments
of RNA. Each of the segments code for at least one polypeptide. The structural
proteins of the virion are encoded by separate gene segments and include:
3 viral RNA polymerases, nucleoprotein, matrix, and the HA and NA surface
glycoproteins. Another segment codes for 2 non-structural proteins, whose
functions are not well known.
-
- Classification
-
- Influenza viruses are placed within their
proper type (A, B, or C) by antigenic similarities among their internal
nucleocapsid and matrix proteins. Within the type A viruses, subtypes can
be distinguished by antigenic differences among their HA & NA glycoproteins.
New influenza subtypes are detected by major antigenic changes within the
HA and/or NA glycoprotein subtypes ("antigenic shift). These changes
are believed to occur due to re-assortment with animal influenza A viruses.
Finally, within the type A subtypes, variants can be detected by antigenic
divergence of the HA & NA proteins ("antigenic drift). These new
variants are generated by an accumulation of point mutations in these proteins.
Viral subtypes have not been seen in type B virus, but antigenic variants
have been detected. The lack of major antigenic change in type B is probably
due to the lack of its circulation in animal species.
-
- Generation of new influenza viruses infectious
for humans
-
- As mentioned above, the influenza viruses
are divided into three types (A, B, and C) based on reactogenicity of their
internal antigens. I will limit the remainder of my answer to influenza
type A viruses, since they show the most genetic variation.
-
- Influenza A viruses are classified and
divided into subtypes based on their surface glycoprotein antigens: 14
subtypes of hemagglutinin (HA or H) H1-H14 and 9 types of neuraminidase
(NA or N) N1-N9. These influenza type A viruses are able to infect a number
of different species including: humans, swine, horses birds, and aquatic
mammals. All 14 subtypes of HA have been isolated from birds, 3 of them
in humans, two in pigs, horses, seals and whales, and one in mink. The
NA antigens show a similar species distribution. Therefore, a large number
of non-crossreactive influenza antigens are always circulating in nature.
Antibodies produced against HA and NA antigens are responsible for protection
against re-infection by the identical virus subtype.
-
- Major evolutionary changes (emergence
of new viruses) in the influenza type A viruses occur by the mixing or
re-assorting of their genetic material causing changes in their external
surface HA and NA antigens. This phenomenon is known as "antigenic
shift. The genetic material or genomes of influenza viruses occur in eight
separate molecules or segments. If two different subtypes of influenza
A virus infect the same cell, their genetic segments are able to reassort
and produce a new influenza virus with segments from both infecting viruses.
As an example, if a H3N5 virus and a H2N2 virus infect the same cell the
following offspring viruses can be produced: H3N5, H2N2, H3N2, and H2N5.
This re- assortment can occur between human and animal isolates. Therefore,
new viruses can be produced which can replicate in humans, but have new
subtypes of animal HA and NA antigens. There are no protective antibodies
to these antigens in the human population, so the new virus can spread
very rapidly around the world.
-
- The virus subtypes that have been so
far been known to infect humans are H1N1, H2N2, and H3N2. The H1N1 viruses
circulated from the beginning of the century through the 1950,s. In 1957,
a new H2N2 virus appeared, known as the "Asian Flu, and rapidly spread
around the world. This virus had both a new HA and a new NA. In 1968, another
new virus appeared a H3N2 virus, known as the "Hong Kong Flu. This
virus was not as severe as the H2N2 virus, since it only varied in the
HA antigen. The H1N1 virus also reappeared in 1977. Currently, both the
H3N2 and H1N1 viruses are circulating through the human population. The
major question is what new virus (H?N?) will emerge in the future and cause
the next major world-wide epidemic.
-
- You may then ask, "Why then do people
get sick with the flu every couple of years, when there has been no major
change in the HA or NA antigens?
-
- Well, between major changes in the HA
and NA antigens, point mutations can occur on the HA and NA molecules and
these mutations may help the virus to avoid the protective antibodies and
produce an illness. This phenomenon is known as "antigenic drift.
The H3N2 virus has been able to successfully drift from its initial appearance
in 1968 and still produce infections in 1999.
-
- Additional information about influenza
viruses and their evolution can be found at the following websites:
-
- Flu Viruses at the Centers for Disease
Control
- Influenza (National Foundation for Infectious
Diseases)
- Influenza Information at the World Health
Organization
- Flu News and Info
- Influenzanews
- Flu101
- Ed Balkovic, PhD
- The views and opinions expressed here
are my own and may not reflect those of my employer.
-
- -----------------------
-
- A protein which forms a rod-shaped spike
on the surface of influenza virus. The name haemagglutinin is given because
the spikes are capable of adhering to red blood cells, causing them to
be agglutinated (clumped). Definitions of haemagglutinin on the Web:
-
- A protein which forms a rod-shaped spike
on the surface of influenza virus. The name haemagglutinin is given because
the spikes are capable of adhering to red blood cells, causing them to
be agglutinated (clumped).
- www.science.org.au/nova/014/014glo.htm
-
- Hemagglutinin (HA) is an antigenic glycoprotein
found on the surface of the Influenza virus and is responsible for binding
the virus to the cell that is being infected. en.wikipedia.org/wiki/Haemagglutinin
-
- Suggest this website:
-
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&
db=PubMed&list_uids=7464906&dopt=Citation
- Definitions of neuraminidase on the Web:
-
- An enzyme which forms a mushroom-shaped
projection on the surface of an influenza virus particle. The enzyme assists
in the release of newly-formed virus particles from the surface of an infected
cell.
- www.science.org.au/nova/014/014glo.htm
|
