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In the 2009 flu pandemic, the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses � North American Mexican influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe � "an unusually mongrelised mix of genetic sequences." This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1.

Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. The six genes from American swine flu are themselves mixtures of swine flu, bird flu, and human flu viruses. While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S.

On June 11, 2009, the WHO declared an H1N1 pandemic, moving the alert level to phase 6, marking the first global pandemic since the 1968 Hong Kong flu.

The various types of influenza viruses in humans. Solid squares show the appearance of a new strain, causing recurring influenza pandemics. Broken lines indicate uncertain strain identifications.

Influenza A virus strains are categorized according to two proteins found on the surface of the virus: hemagglutinin (H) and neuraminidase (N). All influenza A viruses contain hemagglutinin and neuraminidase, but the structures of these proteins differ from strain to strain, due to rapid genetic mutation in the viral genome.

Structure of the influenza virion. The hemagglutinin (HA) and neuraminidase (NA) proteins are shown on the surface of the particle. The viral RNAs that make up the genome are shown as red coils inside the particle and bound to Ribonuclear Proteins (RNPs).

The virion is pleomorphic, the envelope can occur in spherical and filamentous forms. In general the virus's morphology is spherical with particles 50 to 120 nm in diameter, or filamentous virions 20 nm in diameter and 200 to 300 (-3000) nm long. There are some 500 distinct spike-like surface projections of the envelope each projecting 10 to 14 nm from the surface with some types (i.e. hemagglutinin esterase (HEF)) densely dispersed over the surface, and with others (i.e. hemagglutinin (HA)) spaced widely apart.

The major glycoprotein (HA) is interposed irregularly by clusters of neuraminidase (NA), with a ratio of HA to NA of about 4-5 to 1.

Lipoprotein membranes enclose the nucleocapsids; nucleoproteins of different size classes with a loop at each end; the arrangement within the virion is uncertain. The nucleocapsids are filamentous and fall in the range of 50 to 130 nm long and 9 to 15 nm in diameter. They have a helical symmetry.

Genome

Viruses of this family contain 7 to 8 segments of linear negative-sense single stranded RNA.

The total genome length is 12000-15000 nucleotides (nt). The largest segment 2300-2500 nt; of second largest 2300-2500 nt; of third 2200-2300 nt; of fourth 1700-1800 nt; of fifth 1500-1600 nt; of sixth 1400-1500 nt; of seventh 1000-1100 nt; of eighth 800-900 nt. Genome sequence has terminal repeated sequences; repeated at both ends. Terminal repeats at the 5'-end 12-13 nucleotides long. Nucleotide sequences of 3'-terminus identical; the same in genera of same family; most on RNA (segments), or on all RNA species. Terminal repeats at the 3'-end 9-11 nucleotides long. Encapsidated nucleic acid is solely genomic. Each virion may contain defective interfering copies.

Structure

For an in-depth example, see H5N1 genetic structure.

The following applies for Influenza A viruses, although other influenza strains are very similar in structure:

The influenza A virus particle or virion is 80-120 nm in diameter and usually roughly spherical, although filamentous forms can occur. Unusually for a virus, the influenza A genome is not a single piece of nucleic acid; instead, it contains eight pieces of segmented negative-sense RNA (13.5 kilobases total), which encode 11 proteins (HA, NA, NP, M1, M2, NS1, NEP, PA, PB1, PB1-F2, PB2). The best-characterised of these viral proteins are hemagglutinin and neuraminidase, two large glycoproteins found on the outside of the viral particles. Neuraminidase is an enzyme involved in the release of progeny virus from infected cells, by cleaving sugars that bind the mature viral particles. By contrast, hemagglutinin is a lectin that mediates binding of the virus to target cells and entry of the viral genome into the target cell. The hemagglutinin (H) and neuraminidase (N) proteins are targets for antiviral drugs. These proteins are also recognised by antibodies, i.e. they are antigens. The responses of antibodies to these proteins are used to classify the different serotypes of influenza A viruses, hence the H and N in H5N1.

Invasion and replication of the influenza virus. The steps in this process are discussed in the text.

Typically, influenza is transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings. Influenza can also be transmitted by saliva, nasal secretions, feces and blood. Infections occur through contact with these bodily fluids or with contaminated surfaces. Flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 �C (32 �F), and indefinitely at very low temperatures (such as lakes in northeast Siberia). They can be inactivated easily by disinfectants and detergents.

The viruses bind to a cell through interactions between its hemagglutinin glycoprotein and sialic acid sugars on the surfaces of epithelial cells in the lung and throat (Stage 1 in infection figure). The cell imports the virus by endocytosis. In the acidic endosome, part of the haemagglutinin protein fuses the viral envelope with the vacuole's membrane, releasing the viral RNA (vRNA) molecules, accessory proteins and RNA-dependent RNA polymerase into the cytoplasm (Stage 2). These proteins and vRNA form a complex that is transported into the cell nucleus, where the RNA-dependent RNA transcriptase begins transcribing complementary positive-sense vRNA (Steps 3a and b). The vRNA is either exported into the cytoplasm and translated (step 4), or remains in the nucleus. Newly-synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface (in the case of neuraminidase and hemagglutinin, step 5b) or transported back into the nucleus to bind vRNA and form new viral genome particles (step 5a). Other viral proteins have multiple actions in the host cell, including degrading cellular mRNA and using the released nucleotides for vRNA synthesis and also inhibiting translation of host-cell mRNAs.

Negative-sense vRNAs that form the genomes of future viruses, RNA-dependent RNA transcriptase, and other viral proteins are assembled into a virion. Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane. The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion (step 6). The mature virus buds off from the cell in a sphere of host phospholipid membrane, acquiring hemagglutinin and neuraminidase with this membrane coat (step 7). As before, the viruses adhere to the cell through hemagglutinin; the mature viruses detach once their neuraminidase has cleaved sialic acid residues from the host cell. After the release of new influenza virus, the host cell dies.

Since RNA proofreading enzymes are absent, the RNA-dependent RNA transcriptase makes a single nucleotide insertion error roughly every 10 thousand nucleotides, which is the approximate length of the influenza vRNA. Hence, nearly every newly-manufactured influenza virus will contain a mutation in its genome. The separation of the genome into eight separate segments of vRNA allows mixing (reassortment) of the genes if more than one variety of influenza virus has infected the same cell (superinfection). The resulting alteration in the genome segments packaged in to viral progeny confers new behavior, sometimes the ability to infect new host species or to overcome protective immunity of host populations to its old genome (in which case it is called an antigenic shift).

 Viability and disinfection

Mammalian influenza virus tend to be labile, but can survive several hours in mucus. Avian influenza virus can survive for 100 days in distilled water at room temperature, and 200 days at 17 �C (63 �F). The avian virus is inactivated more quickly in manure, but can survive for up to 2 weeks in feces on cages. Avian influenza viruses can survive indefinitely when frozen. Influenza viruses are susceptible to bleach, 70% ethanol, aldehydes, oxidizing agents, and quaternary ammonium compounds. They are inactivated by heat of 133 �F (56 �C) for minimum of 60 minutes, as well as by low pH <2.

http://www.cikgu.net.my/index.php?option=com_myblog&Itemid=73&id=372&show=Experts-Virgin-Coconut-Oil-can-prevent-swine-flu.html&user=0

http://www.thevirgincoconutoil.com/articleitem.php?articleid=226

Fight the Swine Flu with Virgin Coconut Oil

MICHELLE OROSA, ABS-CBN News | 05/02/2009 5:29 PM

Two experts say there are a lot of cheap, available means to protect oneself from contracting the deadly H1N1 Influenza A strain, such as consuming coconut products, particularly virgin coconut oil (VCO).

Former Agriculture Secretary and President of the Federation of Free Farmers Rep. Leonardo Montemayor says virgin coconut oil has natural properties that boost the immune system to avoid catching the strain.

�There is no drug that has been proven to be effective against the virus. Our best cure is prevention. And VCO helps do that effectively,� he says.

Virgin coconut oil has long been advocated by industry leaders, members of the academe, and loyal consumers as an immune-system boosting product that helps fights several viruses, including even HIV. Aside from stronger immune system, other health benefits of VCO include increase metabolism, prevents weight gain, improves skin and keeps the heart healthy.

Dr. Tess Espino of the University of the Philippines-Los Ba�os says there is scienfitic basis for the claim, since VCO has lauric acid, a natural anti-viral, anti-bacterial, and anti-fungal compound. The statement also said, �Monolaurin, a natural derivative of lauric acid, has been proven to be effective as well. Because coconut oil is made up of predominantly of medium-chain triglycerides, it becomes an efficient and non-fattening source of energy�

�The natural derivative of lauric acid, monolaurin, actually breaks down the barriers surrounding the virus� cells, effectively destroying the virus,� she explains.

Espino says the recommended dosage for VCO to be effective is 3 tablespoons a day. Substituting it as ingredient for cooking would also help.

But Montemayor adds there are also many other ways one can consume VCO or coconut, such as using the oil to cook, or eating directly from a coconut.

�Parang Pacquiao match lang yan, para matalo niya si Hatton, he has to train very well, strengthen himself and his body. Ganun din tayo, we have to strengthen our immune system against this very deadly virus,� says Montemayor.

Both Montemayor and Espino clarify that VCO itself is not a cure, but that if the virus is contracted, then it would still be effective in minimizing the impact of the strain.

�Many regular users of VCO attest to its beneficial effect in terms of decreasing the incidence of sickness. This is consistent with its effects of enhancing the immune system and strengthening the innate capabilities of the body to protect itself against viral attacks. This is precisely the protection that we need against this new flu virus,� they added.

Montemayor plans to ask the World Health Organization to conduct clinical tests to prove the effectiveness of using VCO against epidemics such as swine flu.

http://www.btimes.com.my/Current_News/BTIMES/articles/mvcof/Article/index_html