In viruses, the role of chromosomes is performed by a nucleic acid thread (DNA or RNA), in some it is whole, in others (influenza, reoarenovirus) it is fragmented. Separate sections of the nucleic acid responsible (determining) for the synthesis of a particular protein are called genes. The simplest known viruses contain three to five genes (for example, the DNA-containing polyoma virus; picornaviruses have 6-8 genes). However, in a more complex virus (for example, the large T4 bacteriophage), more than 30 genes control the synthesis of envelope proteins and at least 15 genes control the synthesis of nucleotide precursors; This phage requires about a hundred genes to reproduce.

The gene is not indivisible. It has smaller sections (mutons, recons) that carry certain functions. As you know, a gene is a carrier of three properties at the same time:

1) controls one or another sign of the organism (function),

2) is exchanged in crosses (recombination) and

3) changes (mutation).

The concept of cistron corresponds to the concept of a gene - a unit of function, that is, it corresponds to information about one protein.

The synthesis of enzymes in viruses is encoded in the genes. Any enzyme (protein) can be synthesized only if the nucleic acid contains the corresponding gene encoding the synthesis of this enzyme. The sequence of work of cistrons is determined by induction or repression.

The genome of a virus is understood as the totality of all the genes of a given virus. In some viruses, the genome is formed by a single nucleic acid molecule (DNA or RNA), in others, by several molecules (influenza viruses, reo- and arenaviruses).

The phenotype is the totality of all external and internal features and functions of a given virus. The genotype is determined only by the structure of the hereditary material - DNA or RNA, i.e., the sequence of nuileotides in their molecules or the code of protein synthesis. The phenotype of a virus is not a permanent property. The genotype, on the other hand, is a constant property of the virus, and it changes as a result of mutations that occur in the genome. Mutational changes in the genome of the virus entail changes in its phenotype.

Ways to increase the information capacity of the viral genome. Unlike polycistronic prokaryotic mRNAs, eukaryotic mRNAs are monocistronic, i.e. the principle of "one gene - one mRNA molecule - one protein" is implemented. However, in some cellular mRNAs, and often in viral mRNAs, this principle is violated, and the mRNA can direct the synthesis of two polypeptides.

Ways to increase information are:

1) double reading of the same mRNA, but from another codon initiated;

mRNA usually contains several start codons. mRNA usually contains several start codons. According to the currently accepted “scanning model” hypothesis, the small ribosomal subunit binds to the mRNA near the 5¢ end and slides down until it encounters the initiation codon. However, in most cases, initiation occurs not from the first initiating codon, but from the subsequent AUG - codons. The “correct” functioning AUG codon is recognized by the ribosome due to its surrounding sequences (“flanking” nucleotides). In the event that the first initiation codon is in a less favorable environment than subsequent AUG codons, most small ribosomal subunits will pass this codon and start translation initiation from subsequent AUG codons, however, some subunits will start initiation from the first AUG codon. In this case, one mRNA can direct the synthesis of two proteins of different lengths. Such mRNAs are present in many viruses.

2) translation frame shift;

Translation can occur without a frame shift and with a frame shift. The genetic code is triplet, which means that the three nucleotides that make up a triplet or codon code for one amino acid. In the event that the triplets are preserved and the genetic code has not changed, during translation from two different initiating codons, polypeptides will be synthesized that are a shortened section of the first polypeptide (translation without frameshift).

In the event that a shift has occurred by one or two nucleotides, the meaning of all codons (triplets) behind the shift site changes. In this case, one mRNA molecule can be translated into two unique proteins, i.e. those that do not have identical amino acid sequences.

Thus, the total number of triplets in a nucleic acid molecule may be less than the sum of the number of triplets that make up all genes. More accurate ideas about the number of genes can be obtained by biochemical and genetic analyzes.

4) splicing;

5) frameshift splicing is widespread in a number of viruses. As a result of splicing and frameshift, mRNA genes are translated to form two proteins

One way to conserve genetic material is to cut the precursor polypeptide into sections of different lengths, resulting in different polypeptides with overlapping amino acid sequences.

4) transcription from overlapping regions of DNA, etc.

As a result of overlapping genes and a shift in the frame of translation, the boundaries of genes “open up”, and the concept of “gene” in a certain sense loses its original meaning as a discrete fragment of the genome and acquires rather a functional meaning.

Heredity in viruses

Heredity is a property of organisms to ensure material and functional continuity between generations, as well as to determine the specific nature of individual development. Variation is a property opposite to heredity. The variability of viruses may be due to gene mutation.

Mutations in viruses

Two processes can underlie the hereditary change in the properties of viruses:

1) mutation, i.e., a change in the nucleotide sequence in a certain region of the virus genome, leading to a phenotypically pronounced change in property, and

2) recombination, i.e., the exchange of genetic material between two viruses that are close, but differ in hereditary properties.

Mutation - variability associated with a change in the genes themselves. It can be intermittent, spasmodic in nature and leads to persistent changes in the hereditary properties of viruses.

All mutations of viruses are divided into two groups:

Spontaneous and

induced;

According to their length, they are divided into:

Point and

Aberrational (changes affecting a significant part of the genome).

Point mutations are caused by the replacement of one nucleotide (for RNA-containing viruses) or one pair of complementary nucleotides (for DNA-containing viruses). Such mutations can sometimes reverse, restoring the original genome structure.

However, mutational changes are also capable of capturing larger regions of nucleic acid molecules, i.e., several nucleotides. In this case, dropouts, insertions and displacements (translocations) of entire sections and even turns of sections by 180° (the so-called inversions) can also occur. These will be larger rearrangements in the structure of nucleic acids, and, consequently, violations of genetic information.

It should be noted that point mutations are not always realized. There are a number of reasons why such mutations may not show up. One of them is the degeneracy of the genetic code. As already mentioned, the protein synthesis code is degenerate, that is, some amino acids can be encoded by several triplets (codons). For example, the amino acid leucine can be coded for by six triplets. That is why if in the RNA molecule, due to some influences, the triplet CCU was replaced by CUC, CUA by CUC, then the amino acid leucine will still be included in the synthesized protein molecule. Therefore, neither the structure of the protein nor its biological properties will be violated.

Another thing is when some amino acid is encoded by only one triplet, for example, the synthesis of tryptophan is encoded by only one UGG triplet and has no substitution, i.e., a synonym. In this case, some other amino acid is included in the protein, which can lead to the appearance of a mutant trait.

Both spontaneous and induced mutations are also divided into direct and reverse (reversion). Forward mutations change the phenotype, while reverse mutations restore it.

Spontaneous Mutations

Spontaneous mutations in viruses occur in a population without artificial intervention by the experimenter. There cannot be absolutely homogeneous populations. Homogeneity is relative, therefore, in the course of its development, spontaneous mutants appear with a certain probability in the viral population.

The frequency of mutations of the same trait may be different depending on the strain. Thus, the frequency of mutations on the basis of rct 40° in the W-Fox strain of the polio virus was 2.4´10 -5 , while in the .Ch-AT strain it was an order of magnitude lower - 2.0´10 -6 .

What are the causes and mechanisms of spontaneous mutations? According to Watson and Crick, spontaneous mutations can occur as a result of tautomeric (tautomerism is one of the types of isomerism in which isomers easily pass into each other) transformation of the bases that make up DNA. So, for example, a tautomeric shift in the position of the hydrogen atom of adenine leads to the fact that during replication adenine pairs not with thymine, but with guanine. Such an error in base pairing leads to the replacement of the AT and GC pair during subsequent replications.

Spontaneous mutations that have arisen in the same gene are distributed unevenly along its length. Some sections of the gene mutate frequently, they are called "hot" spots, while others rarely. In addition, spontaneous mutations during replication may be due to errors in the work of enzymes - DNA - or RNA polymerases.

The study of the mutational variability of a particular virus consists in determining the physicochemical and biological properties of the mutant. (virulence, reactogenicity, immunogenicity, the ability to reproduce in a particular system, thermoresistance, hemagglutinating, hemolyzing and other properties).

Mutations in viruses can also occur as a result of their adaptation to unusual biological systems in vitro (cell cultures) and in vivo (animals, chicken embryos).

Mutations at passages on animals. Stable highly immunogenic strains of viruses are obtained by long-term adaptation to laboratory, naturally susceptible or non-susceptible animals. Thus, a vaccine strain (virus fixe) of rabies was obtained.

When adapting viruses to naturally non-susceptible animal species or to heterogeneous tissues of experimentally susceptible animals, the type and age of the animal, the method of introduction of the virus and its properties, as well as the properties of the strain, are of decisive importance.

For the success of the adaptation of viruses to the body of laboratory animals, the weakening of their resistance by exposure to cortisone, temperature, irradiation with g-rays, etc. is essential.

Mutations at passages in cell cultures. Many viruses are successfully grown and attenuated in cell and tissue cultures.

Causes of mutations in the process of adaptation. The change in the properties of the virus during the passages occurs in steps. In the first passages, mainly virions are found that have changed any one genetic trait; with an increase in passages in the population, virions are detected that have changed two or more genetic traits; as the passage progresses, the number of such particles constantly increases, and in the future, the vast majority of viral particles show a change in many genetic traits.

The mechanism of hereditary variability of the viral population during passages is based on two processes: mutation and selection, and in both processes an important role is played by the external environment, which is both a mutation inducer and a selective factor.

If a heterogeneous viral population containing altered and original viral particles is cultivated under normal conditions, this leads to its reversion.

Finally, a large number of facts have accumulated about the variability of the virus caused by the host (host-controlled variation). These changes lie in the fact that the cell affects the nature of the components of the virus synthesizing in it. Such modifications do not affect the nucleotide sequence of the viral genome.

Thus, the host cell can significantly influence the phenotype of the virus or block (partially or completely) its reproduction.

induced mutations

They arise when a virus (its vegetative or dormant form) is exposed to various chemical and physical mutagens, as well as in the process of its adaptation to unusual biological systems (with adaptive variability).

The use of artificial mutagens has two advantages. Firstly, they cause mutations tens and hundreds of times more efficiently than natural factors, and secondly, the action of some artificial mutagens has a known direction, which makes it possible to foresee in advance which elements of the structure of nucleic acids and how one or another mutagen and what changes it will cause.

chemical mutagens. It is proposed to divide mutagens into two main groups:

1) mutagens that react with nucleic acid only during its replication (analogues of purine and pyrimidine bases);

2) mutagens that react with a resting nucleic acid molecule, but require its subsequent replications for the formation of mutations (nitrous acid, hydroxylamine, alkylating compounds).

In recent years, a number of chemical compounds have been synthesized and studied - supermutagens (nitroso derivatives of urea - nitrosoguanidine and its derivatives)

Molecular mechanisms of mutagenic action of chemical compounds. Molecular changes in a viral nucleic acid leading to mutation are based on two main processes, base substitution and base deletion or insertion. There are two types of base substitutions that make up the viral nucleic acid: simple (transition) and complex (transversion). With a simple replacement, one purine base is replaced by another (for example, instead of adenine - guanine) or instead of one pyrimidine base - another pyrimidine base (instead of cytosine - uracil).

With a complex substitution - transversion, instead of a purine base, a pyrimidine base appears or a pyrimidine base is replaced by a purine base.

Another process - deletion (deletion) or insertion of bases - leads to deeper changes in the genetic code than a simple one - base replacement. Mutational damage in one region of the genome often leads to changes in several genetic traits that have different phenotypic manifestations (pleiotropy).

Mutagenic action of analogues of nitrogenous bases (5-bromouracil, 5-fluorouracil, 5-ioduracil, 2-aminopurine, 2,6-diaminopurine). Base analogs induce mutations only when exposed to replicating DNA and RNA molecules. Of this group of compounds, 5-bromouracil and 2-aminopurine are the most well studied. Thymine (T) is uracil (U) in which the hydrogen atom (H) in one of the CH - groups is replaced by a methyl group (CH 3). In other words, thymine is methyluracil. However, in uracil, this hydrogen atom can be replaced by another atom, such as bromine (Br). As a result of such a replacement, a new compound is obtained - bromuracil (BU), which is an analog of thymine, since the structure of the main core (ring) of both compounds is exactly the same, and the difference is only in one group (Br instead of CH 3).

Mutations Indicated by Alkating Compounds. Substances under the action of which bases are removed from nucleic acids include alky compounds - mustard gas and its analogs, ethyleneimine and its analogs - ethyl methanesulfonate and ethyl ethane sulfonate, etc. They directly interact with nucleic acids, purines and mainly with guanine, causing simple (transitions ) and complex (transversion) substitutions; purines (mainly guanine) are removed from DNA and, depending on which nucleotide is found opposite the gap during replication, either a substitution type mutation occurs or it does not occur at all.

In addition to simple substitutions (purine to purine), alkylating agents are able to induce complex substitutions - purine to pyrimidine.

Mutagenic effect of hydroxylamine. Hydroxylamine induces mutations in the form of simple base substitutions in the nucleic acid, the direction of which depends on the type of nucleic acid that the virus contains. In DNA-containing viruses, this mutagen reacts exclusively with cytosine. When exposed to RNA-containing viruses, it reacts with both cytosine and uracil, which causes the replacement of cytosine with uracil and vice versa.

Mutagenic action of nitrous acid. Among substances that chemically change bases in a resting nucleic acid molecule, nitrous acid and hydroxylamine are the most well studied. The mechanism of action of nitrous acid (HNO 2) as a mutagen on the nucleic acids of viruses consists in the deamination of organic bases, i.e., the elimination of the amino group (NH 2) from their molecules. As a result of the action of nitrous acid, adenine (A) is converted into hypoxanthine (Gk), guanine (G) into xanthine (K), and cytosine (C) into uracil (U). As a result of this reaction, new properties appear in deaminated organic bases.

Mutagenic effect of high temperature. The influence of elevated temperature (40-50 °C) was discovered by Freese in experiments with the T4 phage and Yu. 3. Gendon during the processing of RNA of the poliomyelitis virus. Temperature promotes the removal of purines (mainly guanine) from DNA. When such DNA is replicated against the gap caused by the loss of purine, any nucleotides can be included in the replicating strand. If a new type of base is included, which was not previously in this region, a mutation (transition or transversion) can occur.

Mutagenic effect of ultraviolet rays. The action of ultraviolet rays (UV) as mutagens is that they interact with nucleic acid molecules and are absorbed by them, especially rays with a wavelength of 260-280 nm. Once in the nucleic acid molecule, they are absorbed by its constituent organic bases. It turned out that thymine (T), uracil (U) and cytosine-(C) are more sensitive to ultraviolet rays than adenine (A) and guanine (G). As a result of irradiation, the structure of these pyrimidines changes. When irradiated with UV rays, two neighboring thymine molecules combine with each other in pairs, forming the so-called dimers.

Reparations

It has been established that in the cells of organisms there are some kind of correctors, they are the so-called repair enzymes, the task of which is to correct errors in genetic information, correct individual damage in the structure of nucleic acids. Repair enzymes use very subtle techniques of “repair microsurgery” to correct errors and damage in the structure of nucleic acids. They somehow recognize abnormal codons and damaged areas in nucleic acid molecules and try to fix them as quickly as possible. Repairing enzymes tend to correct any error in genetic information before the start of nucleic acid replication, since otherwise this error will pass to the daughter molecules of nucleic acids, be passed on to offspring and become hereditary by the matrix mechanism of copying.

One of the enzymes involved in the restoration of the primary structure of DNA (endonuclease) “cuts off” the damaged nucleotide from the neighboring nucleotide on the left, and the other enzyme on the right. The excised abnormal nucleotide (or region of the molecule) is discarded into the environment. Then another enzyme (an exonuclease) takes over to widen the gap left in the DNA strand. Further, the enzyme DNA polymerase restores the missing sections of damage to the strand according to the law of complementarity, i.e., in accordance with the second strand. At the last stage, the newly synthesized sections are “crosslinked” into a strong single chain with the help of a ligase enzyme, due to which the original DNA molecule is restored, which does not have structural flaws.

Instruction

Among scientists, interest in influenza is caused, first of all, by the fact that, despite all the progressiveness of modern medicine, an absolutely effective cure for this disease has not been found. Like many years ago, people during the period of illness use various "grandmother's" remedies, such as drinking a large amount of liquid, honey, various herbal infusions, etc. Yes, today there are many drugs that can improve the immune system and general well-being of a person who has contracted the flu, however, they are not an absolute panacea. Even with the help of vaccinations, it is not always possible to avoid infection. Ironically, the flu is still "uncharted territory" for medical scientists.

Perhaps the most effective drug has not yet been found due to the constant mutation of the influenza virus. But is this happening? It is impossible to answer this question with accuracy, but the virus, like any other living organism in nature, is trying to survive, to adapt to new conditions of existence. Most likely, it is this desire that causes the influenza virus to change, to acquire other forms that are more resistant to various influences.

Today, scientists identify two paths that the influenza virus can take in its mutation processes, they are called “antigenic drift” and “antigenic shift”. Any organism that tries to capture the influenza virus will begin to resist it in every possible way. At the same time, special antibodies are produced, their task is to eliminate the influenza virus and release the body. However, the influenza virus begins to resist such an attack, it is able to change its structure in order to resist antibodies. As a result of this struggle, new, previously unknown forms of influenza are formed. That is why these mutational processes are “antigenic”. After the mutation, the antibodies produced by the body no longer pose any threat to the new form of the virus. Thanks to this, the flu easily overcomes the barriers of the immune system and begins its destructive activity in the body.

The first type of influenza mutation - “drift” does not occur immediately, the virus changes gradually, therefore it does not pose a particular danger to the body, usually the immune system still copes with the disease. However, the second type of mutation - "shift" is very serious. The virus in the shortest possible time is able to significantly change its structure, forming new genetic combinations. It is because of the second type of mutation that such frightening varieties of influenza as "bird" and "swine" appeared. With such a sharp shift in the structure of the virus, the immune system has practically no chance in the fight, since antibodies simply do not have time to be produced. In this case, the virus can spread very quickly, an epidemic begins that can take a lot of human lives.

Introduction

Improving the safety and productivity of farm animals is impossible without further improvement of veterinary services for animal husbandry. Among the veterinary disciplines, an important place belongs to virology. A modern veterinarian should know not only the clinical and pathological side of the disease, but also have a clear understanding of viruses, their properties, laboratory diagnostic methods and features of post-infection and post-vaccination immunity.

Viruses change their properties both in natural conditions of reproduction and in experiment. Two processes can underlie the hereditary change in the properties of viruses: 1) mutation, i.e., a change in the nucleotide sequence in a certain part of the virus genome, leading to a phenotypically pronounced change in the property; 2) recombination, i.e., the exchange of genetic material between two viruses that are close, but differ in hereditary properties.

Mutation in viruses

Mutation - variability associated with a change in the genes themselves. It can be intermittent, spasmodic and lead to persistent changes in the hereditary properties of viruses. All mutations of viruses are divided into two groups:

· spontaneous;

· induced;

According to their length, they are divided into point and aberration (changes affecting a significant part of the genome). Point mutations are caused by the replacement of one nucleotide (for RNA-containing viruses). Such mutations can sometimes reverse, restoring the original genome structure.

However, mutational changes are also capable of capturing larger regions of nucleic acid molecules, i.e., several nucleotides. In this case, dropouts, insertions and displacements (translocation) of entire sections and even turns of sections by 180 ° (the so-called inversions), reading frame shifts can also occur - larger rearrangements in the structure of nucleic acids, and consequently, violations of genetic information.

But not always point mutations lead to a change in the phenotype. There are a number of reasons why such mutations may not show up. One of them is the degeneracy of the genetic code. The protein synthesis code is degenerate, i.e., some amino acids can be encoded by several triplets (codons). For example, the amino acid leucine can be coded for by six triplets. That is why, if in the RNA molecule, due to some influences, the triplet of CUU was replaced by CUC, CUA by CUG, then the amino acid leucine will still be included in the synthesized protein molecule. Therefore, neither the structure of the protein nor its biological properties will be violated.

Nature uses a peculiar language of synonyms and, replacing one codon with another, puts the same concept (amino acid) into them, thus preserving its natural structure and function in the synthesized protein.

Another thing is when some amino acid is encoded by only one triplet, for example, the synthesis of tryptophan is encoded by only one UGG triplet and there is no substitution, i.e., a synonym. In this case, some other amino acid is included in the protein, which can lead to the appearance of a mutant trait.

Aberration in phages is caused by deletions (dropouts) of various numbers of nucleotides, from one pair to a sequence that determines one or more functions of the virus. Both spontaneous and induced mutations are also divided into forward and reverse.

Mutations can have different consequences. In some cases, they lead to a change in phenotypic manifestations under normal conditions. For example, the size of the plaques under the agar coating increases or decreases; increases or decreases neurovirulence for a particular animal species; the virus becomes more sensitive to the action of a chemotherapeutic agent, etc.

In other cases, the mutation is lethal because it disrupts the synthesis or function of a vital virus-specific protein, such as viral polymerase.

In some cases, mutations are conditionally lethal, since the virus-specific protein retains its functions under certain conditions and loses this ability under nonpermissive (nonpermissive) conditions. A typical example of such mutations are temperature-sensitive - ts-mutations, in which the virus loses the ability to multiply at elevated temperatures (39 - 42°C), while retaining this ability at normal growing temperatures (36 - 37°C).

Morphological or structural mutations may relate to the size of the virion, the primary structure of viral proteins, changes in genes that determine early and late virus-specific enzymes that ensure the reproduction of the virus.

According to their mechanism, mutations can also be different. In some cases, a deletion occurs, i.e., the loss of one or more nucleotides, in others, one or more nucleotides are inserted, and in some cases, one nucleotide is replaced by another.

Mutations can be direct and reverse. Direct mutations change the phenotype, and reverse (reversions) restore it. True reversions are possible when a reverse mutation occurs along with the primary damage, and pseudo-reversions if the mutation occurs in another part of the defective gene (intragenous mutation suppression) or in another gene (extragenic mutation suppression). Reversion is not an uncommon event, as revertants are usually more adapted to a given cellular system. Therefore, when obtaining mutants with desired properties, for example, vaccine strains, one has to take into account their possible reversion to the wild type.

Viruses differ from other representatives of the living world not only in their small size, selective ability to reproduce in living cells, structural features of the hereditary substance, but also in significant variability. Changes may relate to the size, shape, pathogenicity, antigenic structure, tissue tropism, resistance to physical and chemical influences and other properties of viruses. The significance of the causes, mechanisms and nature of the change is of great importance in obtaining the necessary vaccine strains of viruses, as well as in developing effective measures to combat viral epizootics, during which, as is known, the properties of viruses can significantly change one of the reasons for the relatively high ability of viruses to change their properties. is that the hereditary substance of these microorganisms is less protected from the effects of the external environment.

Mutation of viruses can occur as a result of chemical changes in cistrons or a violation of the sequence of their location in the structure of the viral nucleic acid molecule.

Depending on the conditions, the natural variability of viruses, observed under normal conditions of reproduction, and artificial, obtained in the process of numerous special passages or by exposing viruses to special physical or chemical factors (mutagens), are distinguished.

Under natural conditions, variability does not manifest itself in all viruses in the same way. This feature is most pronounced in the influenza virus. The pangolin virus is subject to significant variability. This is evidenced by the presence of a large number of variants in different types of these viruses, and significant changes in its antigenic properties at the end of almost every epizootic.

Causes of suffering Seklitova Larisa Aleksandrovna

Why do viruses mutate?

Why do viruses mutate?

But let's ask another interesting question. Why do some diseases change over time? For example, before it was simple: runny nose, colds, flu, jaundice, and now there are varieties: bird flu, swine flu, various allergies. AIDS appeared, varieties of hepatitis A, B, C and some new diseases previously unknown to medicine.

Due to the fact that a person develops, moves from one Level to another, and these are all different energy ranges, his body, at the moment of transition from Level to Level, begins to work with new energy frequencies. Therefore, he may not give the Cosmos already other types of energies. Hence, the Medical System has to make its own corrections to the work of microorganisms. They redesign the function of microorganisms, orienting them to stimulate production other types of energies. Therefore, there are all sorts of hepatitis and influenza.

At the same time, the emergence of new diseases forces earthly medicine to look for new methods of dealing with them, new medicines, and this contributes to the overall development of mankind. So any minus is converted into a plus.

Let's turn to another problem related to microorganisms - to the topic of cancer.

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Influenza virus. Why does he mutate.

Influenza is carried by every six out of ten sick children and four out of ten adults registered in the clinic (it is clear that these data are far from complete: after all, not everyone goes to the doctor!). Not only that, the flu "whips up" cardiovascular and pulmonary diseases. Severe damage to human health makes the problem extremely acute.

Viruses cause hundreds of diseases in animals, plants, and even bacteria. They account for most of the infectious diseases of modern man, and among them are such formidable as smallpox, rabies, poliomyelitis.

The virus is highly variable and adapts to its environment. The essence of this variability has been deciphered relatively recently. The "top dress" of the virus - its "output", or rather, "input" suit is extremely practical. It could also be called a "hunting" suit: it is perfectly adapted for hunting a cage. The suit is "sewn" from two main protein materials - hemagglutinins (with their help the virus attaches to the surface of the cell - the victim) and neuraminidase (whose enzymes remove the guard at the fortress gates when the virus needs to enter the cell, and then exit it).

But the body also meets the virus "by clothes": it is the protein coat that is the sphere of application of protective forces. It is worth changing at least some part of the protein coat of the virus, and the previously produced antibodies are no longer valid.

So why does the flu virus mutate?
There are two opposing points of view on the nature of the variability of the influenza virus.

Here is the first one.

In laboratory experiments, sensitive cells were infected with influenza virus with different neuraminidase. As a result, not only exact copies of the original viruses were obtained, but also viruses with rearranged fragments. The mechanism of such rearrangement (recombination) is more or less clear.

The nucleic acid strand of the influenza virus consists of eight separate fragments. Each of them is relatively easy to replace... A fragment of a nucleic acid changes, and the corresponding protein in the virus envelope immediately changes as well.

But where do these new fragments come from? It would seem that they have nowhere to come from.

This question puzzled the researchers. He seemed to lead to a dead end. Until they began to study the flu of animals and birds. It turned out that among domestic and wild animals, viruses resembling the causative agent of human influenza circulate. Especially a lot of them were isolated from birds, including migratory ones. Hybrids of influenza viruses of various types have been isolated, for example, from ducks, a human-like influenza virus has been found in whales.

Please note: in avian viruses, all types of neuraminidase are found in humans and other mammals. For example, the neuraminidase of viruses that circulated from 1933 to 1957, as well as the neuraminidase of the so-called "Asian" flu that appeared after 1957.

Thus, an assumption arose: the mutation of the influenza virus is associated with the relationship of organisms in nature and the exchange of influenza viruses in humans and animals. This hypothesis is also supported by the fact that variants of currently circulating human influenza viruses have been isolated in humans and birds.

Still, this is nothing more than a guess. Although recombinations of human and animal viruses are obtained in laboratory experiments, no one has observed such phenomena in nature. It is not clear how new variants of viruses, if they originate in animals, can infect humans. It will take a lot of effort to find out.

This hypothesis looks logical, harmonious and therefore very attractive. She has many supporters. However, other scientists believe that it is impossible to look for the causes of flu variability in interaction with the animal world. Yes, hybrids of human and animal viruses can be found in nature and in a laboratory test tube. But they are not viable and not so aggressive.

Proponents of the second point of view refer to the human body. Everyone seeks where he expects to find. And, what is most surprising, he finds! Special studies have confirmed: in the blood of older people there are antibodies against influenza pathogens that have been circulating for a long time or are not circulating yet!

But after all, studies of whales, ducks, pigs and many other representatives of the animal world seem to convince that the same influenza virus (meaning its nucleic acid - the pathogenic principle) is found in different kingdoms of the living? ..

In addition to large, noticeable shifts in the protein appearance of the virus (they are associated with the replacement of one of the fragments of the hereditary apparatus), there are also less noticeable, but progressive changes in hemagglutinins from year to year. The scientists' proposed explanations for this protein "drift" are being tested experimentally.

What about truth? She, as usual, is somewhere in the middle. As soon as at the crossroads of modern sciences it is possible to erect a harmonious and harmonious building of a well-founded theory of influenza, then all observations will acquire in our minds the only true meaning and take their rightful place among other factors. Most likely, extreme points of view will converge. This has happened more than once when passionate seekers of truth argued.