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H5n1


Loftus

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Is H5n1 a new strand of influenza? Sounds interesting!!!! Time for some research! :eek_big::thumbs_up

Oh by the way does any1 have a site that I can get a cheap science journal on biotechnology or genetics??? I have been trying to get a science journal for some time now, but I don't have the money to get one.

 

H5N1 is what your hearing about when they talk about the bird flu. There are many types of Avian/Bird flu. Its been around for a long time. Right now people only catch it via bad hygiene when handling infected birds or their droppings. The worry is it will mutate and spread to people like other flu's do. Right now, if you catch this type of avian flu it kills most of the people who catch it. Theres been other threads here on it, if you want to search around.

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Just a few days ago, The virus hit India, and was about 400-500 Km away from my home.

Later, I had the chance to meet one of those who witnessed the culling operations that were being done on the birds there.

 

He described it as a holocaust of birds, with the waste matter and dead bodies being thrown very unhygenically.:)

 

Me, knowing that he was a big fat bluffer, told him that I did'nt believe that the authorities would let him get there.

He said that he was in a nearby village and did'nt know about the outbreak till he saw the culling, and that he and his pals could easily come and go to the culling site!;)

 

Seriously, I feel that ignorance will be one hell of a help for this virus to survive before it mutates to a better spreading one.

 

:hihi: H5N1 WILL NEVER GIVE UP!!

TAKE US TO YOUR LUNGS!!:lol:

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Well of course, the outbreak of bird flu caused a lot of fear among people.

 

I heard from my friends that a person infected with h5n1 virus can only live for few weeks.

 

Anyway, here, people had stopped taking chicken for few months to prevent the flu from getting transferred from birds to humans. :hihi:

 

So far, everyone is safe and we are safely eating birds now ;)

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I heard from my friends that a person infected with h5n1 virus can only live for few weeks.

That's a lie. A misunderstanding. A misbelief.

H5N1 cases have been cured.

 

Anyway, here, people had stopped taking chicken for few months to prevent the flu from getting transferred from birds to humans.
In those days, the price of chicken reduced at a nearby shop from Rs 60-70 to Rs 20. So I did take one hell of an advantage of the situation...;)
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  • 10 months later...

According to pessimistic forecasts of the UN experts, the spread of the virus from human to human may lead to the death of at least 150 million people, whereas the Russian head sanitary inspector Gennadi Inishenko predicts 50 million and Russian Emergencies Ministry predicts 27 million might die from this virus. To add a little more worry to our strained imaginations, I may just point out that conformation that a 10-year-old Indonesian child contracted the virus from his aunt and it spread to the father and other members of the family, which is currently under investigation by the WHO, which is particularly worried about human-to-human transmission of bird flu, for somewhat obvious reasons. Unfortunately, other people such as, the Health Ministry spokesman Samaye Mammadova, are being a lot less vigilant, and told the APA that no emergency sanitary regime is due to be held in Azerbaijan, but no “state of emergency” is to be declared.

 

Flu virus (H5N1) happens to be a single stranded-RNA type, and viruses that cause influenza in animals are called "Type A" viruses, and there are many different sub-types, mainly because of the variations in the shell of the virus, specifically how the proteins called hemagglutinin [HA] and neuraminidase [NA] differ. Thus far, are 16 known HA subtypes and 9 known NA subtypes of influenza A viruses have evolved, and, seeing as many different combinations of HA and NA proteins are possible more will come soon enough. Each combination is classed as a different subtype. All known subtypes of Type A viruses can be found in birds, and whilst some have only mild effects on the birds, other subtypes are far more virulent and can be fatal. The type of shell is important, because of the lock and key mechanism, which pathogens use to invade a cell.

 

The main problem, besides acquiring the vaccine in sizeable quantities, is keeping up with the species. As I mentioned in a previous post, the inappropriate application of treatment against the wrong sub-species has led to an increased rate of evolution and a resistance against Tamiflu. Apart from these problems, the virus also has been shifting hurriedly for other reasons.

 

Reasons for its rapid evolution include how they can:

 

-Continually and efficiently manifest small changes or antigenic “drift.”

 

-Can swap or “re-assort” genetic materials and merge with other flu viruses.

 

-As someone mentioned earlier, H5N1 viruses are RNA viruses, and RNA viruses generally have very high mutation rates as they lack DNA polymerases, which can find and fix mistakes, and are therefore unable to conduct DNA repair of damaged genetic material. The lower mutation rates we see with the DNA viruses is the result of the abscensce of proof-reading DNA polymerases within the host cell. Retroviruses integrate a DNA intermediate of their RNA genome into the host genome, and therefore have a higher chance of correcting any mistakes in their genome as a result of the action of proof-reading DNA polymerases belonging to the host cell.

 

-Recent research with similair viruses such as SARS and similair types found that many contain a gene that mutates very slowly. Despite this, the gene responsible for this has a complex three-dimensional structure which is hypothesised to provide a chemical function required for viral evolution in the long term. It most likely acts as a ribosome, which would probably make it unsuited for propogation purposes.

 

-Another interesting thing is that this virus has a documented propensity to acquire genes from viruses infecting other animal species…dangerous…

 

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Another aspect involved in the mutation of viruses is RNA editing, but with many negative sense viruses, reverse transcription is what causes the mutations we predict. Not sure exactly how, but I’ll look later on.

It seems to me to be a case of where reverse transcription, rather than RNA editing, is responsible for the acquired leader mutations. Similarly, the preference for G-to-A and C-to-U changes in the vpr gene is a hallmark of error-prone reverse transcription. This was notified some time back by a group who were researching HIV, and it seems to me to be exactly what’s happening here.

 

Findings published when a group of scientists were doing research into HIV virus evolution (HIV is also an RNA virus and so comparing it to this is quite accurate) concluded that transcripts of the human immunodeficiency virus-type 1 (HIV-1) were subject to RNA editing in chronically infected cells, with multiple guanine-to-adenine (G-to-A) and cytosine-to-uracil (C-to-U) changes in several regions of the HIV-1 RNA; commonly, a G-to-A change in the un-translated leader was present exclusively in spliced HIV-1 messenger RNA (mRNA), but not in the unspliced RNA and the proviral DNA genome. Changes in the viral protein R (vpr) gene were at hand in spliced and unspliced HIV-1 RNA extracted from the cell, but not in the unspliced RNA genome that is packaged in virion particles, and so the study proposes that post-transcriptional mRNA-editing events occur for a subset of viral RNAs. I personally suspect that the same thing has happened with Bird Flu, which could elucidate why it’s altering so rapidly. Known editing mechanisms, however, cannot easily explain these changes in the HIV-1 genome. It was therefore proposed an alternative mechanistic model based on HIV-1 reverse transcription to explain some of the nucleotide changes, but with a few modifications.

 

Infected cells represent a population with one proviral genome because re-infection of HIV-producing cells is prevented by super infection interference. Reverse transcribed viral genomes are likely to end up in the DNA of a subset of cells, thereby producing a heterogeneous cell population. All cells could dock the original proviral genome that is transcriptionally impaired, but there may be several subsets of cells with additional proviruses that underwent at least one round of reverse transcription and all the characteristic mutations, but the chronically infected cell system is far too complex to provide evidence for RNA editing based on sequence differences in the viral DNA and RNA. Seeing as the mutations cluster in the region that is copied first during reverse transcription, this probably means that G-to-A mutation is what comes with the reverse transcriptase (RT) complex, and I think that a low deoxycytidine 5'-triphosphate (dCTP) concentration in the virion particle, which can trigger G-T mispairing (resulting in biased G-to-A mutation) is what causes the hypermutation . Subsequently, final phases of reverse transcription will occur in the cytoplasm of infected cells, and the surplus of deoxynucleotide triphosphate (dNTP) building blocks shuts of this run-away mutation effect, allowing for a potentially useful mutations to take place, but not so many that problems start to appear for the virus. It is also my understanding that a preference for mutation of G residues in the NGT trinucleotide sequence is observable, whereas G residues are usually in the NGA sequence context…

 

Now it is possible to see how H5N1 is such a rapidly evolving virus, and why it has the potential to kill 150 million people as estimated. But we still should be looking at how it evolves...

 

We can put viruses into about four different groups, depending on their mode of replication.

 

·There are “positive-sense viruses” where their genome is used like mRNA, which I think then produces a single protein which is modified by host and viral proteins to allow for the formation of the various proteins needed for replication. RNA replicase, copies the viral RNA to form a double-stranded form used for replication, which subsequently directs the formation of new virions.

 

 

·Negative-sense viruses must have their genome copied by a RNA polymerase or transcriptase to form positive-sense RNA, meaning that the virus must bring along with it the RNA-dependent RNA polymerase enzyme. The positive-sense RNA molecule then acts as viral mRNA, which is translated into proteins by the host ribosomes. The resultant protein goes on to direct the synthesis of new virions, such as capsid proteins and RNA replicase, which is used to produce new negative-sense RNA molecules.

 

 

·There are double-stranded reoviruses which contain up to a dozen different RNA molecules which each code for a mRNA, but I don’t really know a lot about these and specifically how they classify. I think that following this, they all pick up proteins to form a single large complex which is copied with virally-encoded replicase to form new virions.

 

 

·Retroviruses are another type, and are single-stranded but most single-stranded RNA viruses would not use DNA intermediates to replicate like this one. Reverse transcriptase, a viral enzyme that comes from the virus itself after it is uncoated, converts the viral RNA into a complementary strand of DNA, which is copied to produce a double stranded molecule of viral DNA. This DNA goes on to direct the formation of new virions.

 

H5N1 has a segmented genome of eight negative sense, single-strands of RNA, abbreviated as PB2, PB1, PA, HA, NP, NA, M and NS. As I said earlier, I’m not sure how this helps it evolve faster, but perhaps someone could clear that last bit up…I think it’s because RNA viruses lack DNA polymerases which can find and fix mistakes, and are therefore unable to conduct DNA repair of damaged genetic material…

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