Viruses have DNA and RNA. What is hepatitis C virus RNA? breeding site in a cell

Opening viruses, causing malignant tumors in animals, occurred at the turn of the 19th and 20th centuries. In 1910, Peyton Rausch discovered that acellular filtrate from avian sarcoma tissue could cause the development of a similar sarcoma in chickens. Around the same time, the viral nature of avian myeloblastosis was proven. It was later discovered that there is often a very significant latency period between infection with the virus and the development of cancer.

However, until the 1960s there was clear evidence that the incorporation of viral DNA into the cell genome is a necessary condition for the development of malignant transformation, as there have been no cases of isolation of viral DNA from cancer cells.

Currently there are two types of viral oncogenes. Both of these types of oncogenes are inserted into cellular DNA. Viruses of the first type carry oncogenes that cause rapid malignant “transformation” of cells in in vitro cultures and cause the development of tumors in the body. In the second type, the virus acts more slowly and it takes considerable time for the tumor to develop. Viruses of the second type do not cause malignant transformation of cells in in vitro cultures.

RNA viruses cause the development of a number of different tumors in animals, with the most common induction of lymphomas, leukemias and sarcomas by these viruses. The typical structure of such viruses is two identical chains of RNA molecules combined with the reverse transcriptase enzyme, dressed in a glycoprotein shell. When infected with a virus, its reverse transcriptase causes cells to synthesize DNA complementary to the viral RNA.

This DNA then it is integrated into the cellular chromosomes, and on its basis the cell itself begins the synthesis of new viral proteins, viral reverse transcriptases and elements of the glycoprotein shell. Because of their mechanism of action, this type of virus is called retrovirus. They all have a very similar appearance in electron micrographs and are the smallest viruses known.

Some of retroviruses(for example, avian leukemia, feline and murine leukemia viruses) contain only three genes and have a very long incubation period from the moment of infection to the formation of a tumor. Other viruses (eg, Rous sarcoma virus (RSV)) cause very rapid malignant transformation and can be isolated from tumor cell cultures.

Shown, that HRV virus contains a special gene (v-src) that can cause fibroblast transformation in vitro. This gene encodes the production of a protein kinase that phosphorylates tyrosine. Unfortunately, the action of this protein kinase triggers a cascade of different metabolic processes, and it is very difficult to assess which of them leads to malignant transformation.

It is now known that both normal and malignant cells contain in their genotype DNA sections that are similar or identical to a number of sequences of oncogenic RNA-containing viruses. Such regions are called cellular proto-oncogenes (to distinguish them from viral oncogenes). It is postulated that activation of these areas, resulting from carcinogenic exposure, triggers a whole chain of events leading ultimately to malignant transformation of the cell. It is also believed that retroviruses incorporated these cellular regions into their genome during evolution.

We now have a better understanding of the mechanisms of action viral activation products. An example of such a product is protein kinase activated by the sre gene, as well as a number of other virus-induced carcinogens. These are receptors for epidermal growth factor, produced by the v-erb gene, and platelet-derived growth factor (TGF), encoded by fragments of the v-sis gene, and a number of proteins that bind to the cell nucleus, the production of which is caused by the avian leukemia virus.

Viral oncogenic molecules are in most cases structurally different from their cellular counterparts; in addition, they lack introns. For example, the protein encoded by the v-erb gene is homologous to the cellular receptor for epidermal growth factor (EGF), but it lacks part of the extracellular domain, including the EGF-specific site. Since the molecule produced by the virus lacks the plasma region responsible for autophosphorylation, such a viral receptor is always in the “on” state.

Both normal and cancer cells contain sections of DNA sequences homologous to the RNA of oncogenic viruses. If these cellular oncogenes are expressed or activated by carcinogens, this leads to malignant transformation of the cells.

Oncogenic and malignant transformation.
At stage A, a normal cell, which is characterized by low proto-oncogenic activity, produces growth factor (x) or differentiation proteins or receptors (y).
Carcinogens increase the activity of proto-oncogenes, which gives rise to neoplastic transformation.
According to another mechanism: when infected with a retrovirus, viral promoters or oncogenes (B) are introduced into the DNA of the cell, which also leads to an increase in oncogenic activity and subsequent malignant transformation.

Virus can activate processing in cells by introducing special regulatory sequences into them - protein reading promoters, thus disrupting normal transcription processes. The mechanism of introduced mutagenesis triggered in this way can involve a whole complex of different processes. An example is the introduction of a viral sequence of “multiple terminal repeats” (MTR) into the DNA of a cell. When inserted into cellular DNA, this sequence initiates transcription in both directions of the DNA chain, allowing both cellular and viral genes to be transcribed simultaneously. This mechanism of action is characteristic of the cellular leukemia virus, when the viral DNA is integrated into the cellular DNA immediately after the c-myc site, causing its activation.

First retrovirus, which has been clearly demonstrated to be associated with malignancy, was human T-cell leukemia virus (HTCL-1), isolated from chronic cutaneous T-lymphoma cells. This virus is quite widespread and can be transmitted sexually, through blood, especially among drug addicts, and from a pregnant woman to her fetus. Initially, the endemic area of ​​circulation of this virus was mainly represented by tropical countries, but currently in the United States, a seropositive reaction to the virus is found in every 4,000 people in the population. In addition to T-cell leukemia, the virus causes tropical spastic paralysis.

After 20 years of observation for seropositive patients The risk of developing the latter disease is estimated to be about 5%. One of the viral genes, namely the tax gene, causes an increase in the production of cellular interleukin-2 (IL-2) and its receptors, which is the main factor stimulating T-cell division.

Retroviruses can cause tumor diseases not directly, but indirectly, as has been shown for the human immunodeficiency virus (HIV-1), which causes the development of AIDS. Cases of cancer development in HIV-infected people are discussed in one of the reviews. It is noted that HIV-infected people most often develop three types of tumors: immediate or high-grade B-cell lymphoma; Kaposi's sarcoma (KS, which is caused by another virus - herpesvirus GSK, or herpesvirus 8); cervical carcinoma.

Before developing effective methods of treatment for HIV-infected people more than 40% of them developed some type of cancer. Nevertheless, the connection of this virus with the development of cancer is most likely indirect and mediated by the development of general chronic immunosuppression of the body, which allows other carcinogenic viruses to cause cancer. B-cell lymphomas also have a rather complex pathogenesis. Although B cells are not affected by the HIV-1 virus, they can be targeted by other types of viruses, such as Epstein-Barr virus (EBV). Cervical cancer in women also develops on the basis of a secondary viral infection - human papillomavirus (HPV), against the background of general immunosuppression caused by HIV-1. Due to a general decrease in the body's immune responses, all these tumors develop especially quickly and aggressively.

Family Picornaviridae (Picornaviridae) consists of 8 genera:

Enteroviruses(polio)

Rhinoviruses(ARVI)

Afthoviruses(foot and mouth disease)

Hepatoviruses(hepatitis A)

This family belongs to non-enveloped viruses containing single-stranded plus RNA. The diameter of the virus is about 30 nm, the virion consists of an icosahedral capsid surrounding single-stranded RNA with the VPg protein. The capsid consists of 12 pentagons (pentamers), each of which in turn consists of 5 protein subunits-protomers: VP1, VP2, VP3, VP4.

Family Reoviruses (Reoviridae) contains 4 genera:

Orthoviruses(gastrointestinal and respiratory infections)

Arboviruses(arboviral infections: Kemerovo virus is transmitted by ticks, sheep blue tongue virus is transmitted by woodlice)

Coltiviruses(Colorado tick fever virus)

Rotaviruses(diarrhea)

The reovirus virion has a spherical shape (diameter 70-85 nm), a two-layer capsid of the icosahedral type, and no shell. The genome is represented by double-stranded fragmented (10-12 segments) linear RNA. The inner capsid and genomic RNA make up the core of the virion. The internal capsid of reoviruses contains a transcription system: proteins lambda-1, lambda-3, mu-2. Spines, represented by the lambda-2 protein, extend from the core. In rotaviruses, the internal capsid includes proteins VP1, VP2, VP3, VP6. The outer capsid of reoviruses consists of proteins sigma - 1, sigma - 3, mu - 1c, as well as proteins lambda -2, protruding in the form of spikes. The sigma -1 protein is a hemagglutinin and attachment protein, the mu -1c protein has the ability to infect intestinal cells and subsequently affect the central nervous system.

Family Bunyaviruses (Bunyaviridae) includes 5 genera:

Bunyaviruses(California encephalitis, Jamestown Canyon encephalitis, La Crosse encephalitis, Tyaginya, Inco, Guaroa fevers - viruses are carried by mosquitoes, the incidence is endemic in 20 US states)

Phleboviruses(mosquito fever or pappataci fever). The reservoir and carrier of the virus are female mosquitoes. The disease occurs in Europe (Mediterranean), Asia (Iran, Pakistan), North Africa, Italy, Portugal. Outbreaks occurred in Transcaucasia, Crimea, Moldova and Central Asia.

Neuroviruses(Crimea-Congo hemorrhagic fever, the main reservoir of the virus in nature is many types of pasture ticks, infection occurs through tick suction. In Russia, this disease occurs in the Krasnodar, Stavropol territories, Astrakhan, Volgograd and Rostov regions, the republics of Dagestan, Kalmykia and Karachay- Circassia.

Hantaviruses(HFRS-hemorrhagic fever with renal syndrome)

Tospoviruses non-pathogenic for humans and affects plants

Virions are oval or spherical in shape, with a diameter of 80-120 nm. These are complex RNA genome viruses containing three internal nucleocapsids with helical symmetry. Each nucleocapsid consists of a nucleocapsid protein N, single-stranded minus RNA, and a transcriptase enzyme. The three RNA segments associated with the nucleocapsid are designated by size: L (long) - large, M (medium) - medium, S (short) - small. The core of the virion is surrounded by a lipoprotein shell, on the surface of which there are spikes - glycoproteins G1 and G2, which are encoded by the M-segment of RNA. w80-

Family Togaviruses (Togaviridae) consists of 4 genera, 2 of which play a role in human pathology:

Alphavirus(viruses transmitted by arthropods cause diseases in humans accompanied by fever, skin rashes, the development of encephalitis and arthritis, in the Primorsky Territory - Semliki forest fever virus)

Rubivirus(rubella virus)

Their genome consists of a linear single-stranded plus RNA surrounded by a capsid (C-protein) with cubic symmetry and consisting of 32 capsomers. The nucleocapsid is surrounded by an outer two-layer lipoprotein shell, on the surface of which glycoproteins E1, E2, E3 are located, penetrating the lipid layer. The diameter of virions is from 65 to 70 nm.

Family Flaviviruses (Flaviviridae) comes from the Latin flavus - yellow, after the name of the disease yellow fever. Pathogenic for humans are included in 2 genera:

Flavivirus(yellow fever, tick-borne encephalitis virus, Omsk hemorrhagic fever virus, dengue fever virus, Japanese encephalitis virus, West Nile fever virus)

Hepacivirus(hepatitis C virus)

These are complex RNA genomic viruses of spherical shape, their diameter is 40-60 nm. The genome consists of a linear single-stranded plus-strand RNA surrounded by a capsid with cubic symmetry. The nucleocapsid contains one protein – V2. The nucleocapsid is surrounded by a supercapsid, the surface of which contains the V3 glycoprotein. The structural protein V1 is located on the inner side of the supercapsid.

Family Orthomyxoviruses (Orthomyxoviridae) includes the genus:

Influenzavirus(influenza virus, which includes 3 serotypes: A, B, C)

The diameter of the viral particle is 80-120 nm. The virion has a spherical shape. In the center of the virion there is a nucleocapsid, which has a helical type of symmetry. The genome of influenza viruses is a helix of single-stranded segmented minus-strand RNA. The capsid consists mainly of a protein - nucleoprotein (NP), as well as proteins of the polymerase complex (P). The nucleocapsid is surrounded by a layer of matrix and membrane proteins (M), which are involved in the assembly of the viral particle. On top of these structures is a supercapsid - an outer lipoprotein shell, which bears spines on its surface. The spines are formed by two complex glycoprotein proteins: hemagglutinin (H) and neuraminidase (N).

Family Paramyxoviruses (Paramyxoviridae), which includes 2 subfamilies:

Subfamily Paramyxoviruses:

Morbillivirus(measles virus)

Respirovirus(parainfluenza virus)

Rubulavirus(mumps virus, parainfluenza)

Subfamily Pneumoviruses:

Pneumovirus(respiratory syncytial virus (RS))

Metapneumovirus(PC virus)

The paramyxovirus virion has a spherical shape, a diameter of 150-300 nm, surrounded by an envelope with glycoprotein spikes. Under the shell is a helical nucleocapsid consisting of unfragmented linear single-stranded minus RNA bound by proteins: nucleoprotein (NP), polymerase-phosphoprotein (P) and large protein (L). The nucleocapsid is associated with matrix (M) protein located under the virion envelope. The virion envelope contains spikes - two glycoproteins: fusion protein (F), hemagglutinin-neuraminidase (HN) attachment protein, hemagglutinin (H) or (G) protein.

Family Rhabdoviruses (Rhabdoviridae) includes about 80 genera and causes diseases of animals and plants.

Lassavirus(rabies virus)

Vesiculovirus(vesicular stomatitis virus)

Virions have the shape of a cylinder with semicircular and flat ends (bullet shape), the size of virions is 130x300x60x80. They consist of a two-layer lipoprotein shell and a nucleocapsid of helical symmetry. The shell is lined from the inside with M-protein, and the spikes of glycoprotein G extend from it on the outside. The RNP of the nucleocapsid consists of genomic RNA and proteins: N - protein, which covers the RNA as a cover, L - protein and NS - protein, which are the transcriptase of the virus. The genome of rhabdoviruses is represented by single-stranded non-fragmented linear minus RNA.

Family Filoviruses (Filoviridae) contains two genera:

Genus of Marburg-like viruses(African hemorrhagic fever Marburg)

Genus of Ebola-like viruses(African hemorrhagic fever Ebola)

Viruses have the form of long filaments (80-1000 nm) with an envelope and single-stranded minus RNA enclosed in a capsid. Contains polymerase. The symmetry of the capsid is helical. The shell has spines (spicules).

Family Coronaviruses (Coronaviridae), includes 1 genus, uniting more than 10 species that cause diseases in humans and animals.

Coronavirus(causes damage to the respiratory organs, including SARS, gastrointestinal tract, nervous system)

Virions are round in size, 80-220 nm in size. The core of the virion is represented by a helical nucleocapsid containing single-stranded plus RNA. The nucleocapsid is surrounded by a lipid shell, covered on the outside with club-shaped projections - peplomeres. Ash meters give the viral particle the appearance of a solar corona. The virion shell contains glycoproteins E1 and E2, which are responsible for the adsorption of the virus on the cell and penetration into the host cell.

Family Retroviruses (Retroviridae), which includes 7 genera:

Alpharetrovirus(leukemia viruses, avian sarcoma viruses, chicken Rous sarcoma viruses)

Betaretrovirus(mouse mammary cancer virus, human endogenous retrovirus, simian virus)

Gammaretrovirus(sarcoma and leukemia viruses of mice, cats, primates)

Deltaretrovirus(bovine leukemia virus, human T-cell lymphotropic viruses)

Epsiloretrovirus(skin sarcoma virus)

Lentivirus(AIDS virus)

Spumavirus(foaming viruses of humans, monkeys, bovine syncytial virus)

Retroviruses have a spherical shape, size 80-130 nm. The virion has an envelope and a nucleocapsid core. The capsid is icosahedral. Reverse transcriptase is associated with the genome of single-stranded plus RNA. Viruses contain proteins: group antigen (gag), polymerase protein (pol) and envelope proteins (env). About 30 oncoantigens are known.

Family Arenaviruses (Arenaviridae) includes the genus:

Arenavirus(lymphocytic choriomeningitis viruses, Lasa, Junin, Machupo, Guanarito, causing severe hemorrhagic fevers)

The virion has a spherical or oval shape, with a diameter of about 120 nm. Outside, it is surrounded by a shell with club-shaped glycoprotein spikes GP1, GP2. Under the shell there are 12-15 cellular ribosomes, the capsid is spiral. The genome is represented by two segments (L, S) of single-stranded minus RNA, encoded by 5 proteins: L, Z, N, G.

Family Caliciviruses (Caliciviridae) contains Norwalk group gastroenteritis viruses and porcine vesicular exanthema virus.

The virion is non-enveloped, has an icosahedral capsid with 32 cup-shaped depressions (pits). The shape is spherical, diameter 27-38 nm. On the surface of the virion there are 10 protrusions formed by the edges of cup-shaped depressions. The genome is linear, single-stranded plus RNA.

LECTURE

From Lat. "virus" - poison

Viruses are an extracellular form of life that has its own genome and is capable of reproducing only in the cells of living organisms.

A virion (or viral particle) consists of one or more DNA or RNA molecules enclosed in a protein shell (capsid), sometimes also containing lipid and carbohydrate components

The diameter of viral particles (also called virions) is 20-300 nm. Those. they are much smaller than the smallest of prokaryotic cells. Since the sizes of proteins and some amino acids. are in the range of 2-50 nm, then the viral particle could be considered simply a complex of macromolecules. Due to their small size and inability to reproduce themselves, viruses are often classified as “non-living”.

They say “A virus is an intermediate form of life, or non-life,” because outside the host cell it turns into a crystal.

They say: c. this is a transition from chemistry to life

The life cycle of the virus begins

1. from penetration into the cell.

2. To do this, it binds to specific receptors on its surface and

a) either introduces its nucleic acid into the cell, leaving the virion proteins on its surface,

b) or penetrates entirely as a result of endocytosis. In the latter case, after the virus penetrates into the cell, it is “undressed”—the release of genomic nucleic acids from the envelope proteins.

3. As a result of this procedure, the viral genome becomes accessible to cell enzyme systems that ensure the expression of viral genes.

4. It is after the penetration of the viral genomic nucleic acid into the cell that the genetic information contained in it is deciphered by the host’s genetic systems and is used to synthesize the components of viral particles.

Compared to the genomes of other organisms, the viral genome is relatively small and encodes only a limited number of proteins, mainly capsid proteins and one or more proteins involved in viral genome replication and expression. Necessary metabolites and energy are supplied by the host cell.

DNA viruses carry either single- or double-stranded DNA as genetic material, which can be either linear or circular. DNA encodes information about all the proteins of the virus. Viruses are classified depending on whether their DNA is single or double stranded and whether the host cell is pro- or eukaryotic. Viruses that infect bacteria are called bacteriophages.

1 - smallpox viruses; 2 - herpes viruses; 3 - adenoviruses; 4 - papovaviruses; 5 - hepadnaviruses; 6 - parvoviruses;

First group - double-stranded DNA viruses,

- Replication is carried out according to the following scheme: DNA -> RNA -> DNA.

- they got the name retroid viruses.

- P Representatives of this group of viruses are hepatitis B virus and cauliflower mosaic virus.

1. Replication of the DNA genome of these viruses is carried out through intermediate RNA molecules:

2. RNA molecules are formed as a result of transcription of viral DNA in the cell nucleus by the host enzyme DNA-dependent RNA polymerase.

3. Only one of the viral DNA strands is transcribed.

4. DNA synthesis on an RNA template occurs as a result of a reaction catalyzed by reverse transcriptase; first the (-) strand of DNA is synthesized,

5. and then on the newly synthesized (-) DNA strand, the same enzyme builds a (+) strand.

Overall, the general pattern of genome replication of retroid viruses is strikingly similar to that of retroviruses. Apparently, this similarity also has an evolutionary basis, since the primary structure of the reverse transcriptases of these viruses reveals a certain similarity to each other.

Second group - double-stranded DNA viruses,

- Replication is carried out according to the DNA -> DNA scheme.

- from the genome of these viruses in the infected cell, DNA-dependent RNA polymerase transcribes mRNA molecules (i.e. (+) RNA),

mRNA (i.e. (+) RNA) takes part in the synthesis of viral proteins,

Reproduction of the viral genome is carried out by the enzyme DNA-dependent DNA polymerase: (±) dna → (+) RNA

In some cases, cellular enzymes produce both mRNA and DNA; in other cases, viruses use their own enzymes. It happens that both enzymes serve the process of replication and transcription. This group includes herpes viruses, smallpox, etc.

Influenza virus diagram

Influenza virus is an example of a “-”-single-stranded RNA virus. It has a shell and a spiral core. The core consists of eight “-” RNA segments, which, in combination with proteins, form helical structures. Each segment encodes one of the viral proteins. The virus contains the largest amount of matrix protein, which is located on the inner side of the shell and gives it stability. All envelope proteins are encoded by viral RNA, whereas lipids are cellular in origin (see DNA viruses, assembly). The main shell proteins are hemagglutinin and neuraminidase.

Infectious process proceeds according to the scheme (transparent 2 below) begins with the attachment of the virus to the surface of the host cell through hemagglutinin. Then the shell fusion with the cell membrane occurs, the nucleoprotein core (nucleocapsid) enters the cell, and the virus-encoded RNA-dependent RNA polymerase synthesizes + strands of mRNA on the viral “-” strands, after which viral proteins are produced on the ribosomes of the host cell. Some of these proteins play an important role in viral genome replication.

Replication occurs in the nucleus, where, with the help of the same, but probably modified RNA polymerase, “-” RNA chains are formed. After nucleocapsid proteins enter the nucleus, nucleocapsid assembly occurs. The nucleocapsid then passes through the cytoplasm, attaching envelope proteins along the way, and leaves the cell, budding from its plasma membrane. It is believed that neuraminidase is involved in the budding process.

Third group constitute double-stranded genomes, (±) RNA genomes.

Known double-stranded genomes are always segmented (i.e., composed of several different molecules).

This includes reoviruses. Their reproduction proceeds according to a variant close to the previous one. Along with the viral RNA, the viral RNA-dependent RNA polymerase also enters the cell, which ensures the synthesis of (+) RNA molecules. In turn, (+) RNA ensures the production of viral proteins on the ribosomes of the host cell and serves as a template for the synthesis of new (-) RNA chains by the viral RNA polymerase

Chains (+) and (-) RNA, complexing with each other, form a double-stranded (±) An RNA genome that is packaged into a protein shell.

- Reoviruses birds (from the English respiratory respiratory, enteric intestinal, orphan orphan) are icosahedral viruses without an envelope, the protein capsid of which consists of two layers - outer and inner. Inside the capsid are 10 or 11 segments of double-stranded RNA.

Reoviruses infect the respiratory and intestinal tracts of warm-blooded animals (humans, monkeys, cattle, small ruminants, bats,

Infectious process begins with the penetration of RNA into the cell and then proceeds in accordance with the diagram (transparent 2 - below). After partial destruction of the outer capsid by lysosome enzymes, the RNA in the thus formed subviral particle is transcribed, its copies leave the particle and combine with ribosomes. The host cell then produces proteins necessary for the formation of new viral cysts.

Replication RNA viruses occur by a conserved mechanism. One of the strands of each RNA segment serves as a template for the synthesis of a large number of new + strands. On these + chains, - chains are then formed as on a matrix; the + and - chains do not diverge, but remain together in the form of double-chain molecules. the assembly of new viral particles from newly formed + and – segments and capsid proteins is somehow connected with the miotic spindle of the host cell.

This includes viruses in which the genome replication cycle can be divided into two main reactions: RNA synthesis on a DNA template and DNA synthesis on an RNA template.

In this case, the composition of the viral particle as a genome can include either RNA (retroviruses ( Retroviridae- from REversed TRanscription)), or DNA (retroid viruses).

The viral particle contains two molecules of genomic single-stranded (+) RNA.

The viral genome encodes an unusual enzyme (reverse transcriptase, or revertase), which has the properties of both RNA-dependent and DNA-dependent DNA polymerases.

Only in 1970 did American scientists G. Temin and Mitsutani and, independently of them, D. Baltimore solve this riddle. They proved the possibility of transferring genetic information from RNA to DNA. This discovery overturned the central dogma of molecular biology that genetic information can only be transferred in the DNA-RNA-protein direction. It took G. Temin five years to discover the enzyme that transfers information from RNA to DNA - RNA-dependent DNA polymerase. This enzyme was named reverse transcriptase. G. Temin managed not only to obtain DNA fragments complementary to a given RNA chain, but also to prove that DNA copies can be integrated into the DNA of cells and transmitted to offspring.

This enzyme enters the infected cell along with the viral RNA and ensures the synthesis of its DNA copy, first in single-stranded form [(-) DNA], and then in double-stranded form [(±) DNA]:

The viral genome in the form of a normal DNA duplex (the so-called proviral DNA) is integrated into the chromosome of the host cell.

As a result, the double-stranded DNA of the virus is essentially an additional set of genes in the cell that replicates along with the host DNA when it divides.

To form new retroviral particles, proviral genes (virus genes in the host chromosomes) are transcribed in the cell nucleus by the host transcription apparatus into (+) RNA transcripts.

Some of them become the genome of the new “offspring” of retroviruses, while others are processed into mRNA and used to translate proteins necessary for the assembly of viral particles

This group includes

a) human immunodeficiency virus (HIV)

Information about AIDS is in the Old Testament

Our ganome contains genetic marks from previous AIDS pandemics

The study of hepatitis C virus RNA is the most important procedure, which allows us to accurately determine the duration and methods of treatment for patients.

Diagnosis of the disease consists of several different blood tests, such as:

• hepatitis C markers (anti-HCV);
• determination of hepatitis C virus RNA (HCV RNA).

The first study is done at the first suspicion of hepatitis. The second option is the most significant in the treatment of HCV RNA, so we will consider it in more detail.

What is viral hepatitis C?

Hepatitis C virus, or HCV, is an infectious disease that affects the liver. Infection with the virus occurs through blood. You can become infected by giving a blood transfusion when the rules for sterilizing medical instruments are not followed. Less common are cases where the disease is acquired sexually or from a pregnant mother to the fetus. Hepatitis C comes in two types.

Chronic hepatitis C is the most dangerous. This is a form of illness that can last throughout life. It leads to serious liver problems such as cirrhosis or cancer. In 70-90% of infected people, the disease enters the chronic stage.

The most important thing is that it proceeds secretly, without icteric signs. In this case, most often they complain of fever, nausea and vomiting, physical weakness, increased fatigue, loss of appetite and weight. At the same time, against the background of slight compaction of liver tissue, its malignant degeneration quite often occurs. For this reason, viral hepatitis C is often called a “time bomb” or “gentle killer.”

Another feature of the disease is its very slow development, estimated in tens of years.

Typically, those infected do not experience any symptoms and are unaware of their true condition. Often the disease can only be identified when visiting a doctor for another issue.

Risk groups include:

• children who received the hepatitis C virus from their mothers;
• drug addicts;
• people who have pierced body parts or made tattoos with unsterile instruments;
• those who received donated blood or organs (before 1992, when hemodialysis was not carried out);
• persons infected with HIV;
• healthcare workers in contact with infected patients.

Determination of hepatitis C RNA

Determining the RNA of the HCV-RNA virus, also referred to as, is a study of biological material (blood), with which you can determine the direct presence of the hepatitis virus gene material in the body (any single virus is a single particle of RNA).

The main test method is PCR, or the polymerase chain reaction method.

There are two types of blood tests to determine HCV RNA:

• qualitative;
• quantitative.

Qualitative test

Carrying out a qualitative analysis makes it possible to determine whether the virus is in the blood. All patients who are found to have hepatitis C antibodies must undergo this test. Based on its results, you can get 2 answers: “present” or “absent” the virus. A positive test result (detected) indicates that the virus is actively multiplying and infecting healthy cells in the liver.

The qualitative PCR test is set to a specific sensitivity, from 10 to 500 IU/ml. If the hepatitis virus detected in the blood has a specific content of less than 10 IU/ml, then detection of the virus may become impossible. A very low specific viral load is observed among patients prescribed antiviral therapy. Therefore, it is important to know how sensitive the medical system is for diagnosing and producing a high-quality result with polymerase chain reaction.

Often, polymerase chain reaction for hepatitis C is performed immediately after the corresponding antibodies are found. Subsequent tests, while undergoing antiviral therapy, are carried out at 4th, 12th and 24th weeks. And another analysis after stopping AVT is done 24 weeks later. Then - once a year.

Quantitative test

Quantitative RNA PCR analysis, sometimes called viral load, determines the concentration (specific content) of the virus in the blood. In other words, the viral load refers to a certain amount of viral RNA that can be present in a specific amount of blood (it is customary to use 1 ml, equal to 1 cm cubed).

The units of measurement for test results are international (standard) units divided by one milliliter (IU/ml). The content of the virus is sometimes presented differently, depending on the laboratories where the research is carried out. For hepatitis C, quantification sometimes uses values ​​such as copies/ml.

It is necessary to understand that there is no specific dependence in the severity of hepatitis C on the concentration of this strain in the blood.

Checking the “viral load” allows you to determine the degree of infectiousness of the disease. So the risk of infecting another person with the virus increases with increasing concentration of hepatitis in the blood. In addition, high levels of virus reduce the effect of treatment. Therefore, a low viral load is a very favorable factor for successful treatment.

In addition, the hepatitis C test and its determination by PCR play an important role in the application of therapy for the disease and in determining the success of treatment. Based on the test results, the rehabilitation course is planned. For example, if the specific concentration of the hepatitis virus decreases too slowly, antiviral therapy is prolonged, and vice versa.

In modern medicine, it is considered that a load greater than 800,000 IU/ml is high. A load in excess of 10,000,000 ME/ml is considered critical. But to this day, experts from different countries do not have the same opinion about the limits of the viral load.

Quantitative test frequency

In general cases, a quantitative analysis for HCV-RNA hepatitis is done before antiviral therapy and 3 months after the end of treatment procedures to determine the quality of the therapy performed.

The quantitative assessment of the results according to the sample specified above will be considered as the result for the quantitative test. The result will be a verdict of “below the measurable range” or “not detected in the blood” - this is the norm for a healthy person.

The sensitivity parameter of a qualitative test is usually lower than the sensitivity of a quantitative test. The “Absent” designation shows that both types of tests did not find RNA of the virus. If the test value is “below the measured range,” the quantitative type of analysis most likely did not find hepatitis RNA, although this confirms the presence of a virus with a very low specific abundance.

Hepatitis C and its genotypes

Hepatitis C virus RNA genotyping diagnoses the presence of different. Science knows more than 10 types of the virus genome, but for medical practice it is enough to identify several genotypes that have the largest share in the region. Determining the genetic type plays a key role in choosing the timing of treatment, which is very necessary given the wide range of side effects of hepatitis drugs.

Treatment options

The only effective way to cure hepatitis C virus, as a rule, is a combination of 2 medications:

• interferon-alpha together with;

Individually, these medications are not as effective. Recommended dosages of medications and timing of use should be prescribed only by a doctor and individually to each patient. Treatment with these medications can last from 6 to 12 months for the first regimen and from 3 to 6 months for the second and third regimens.

1 - paramyxoviruses; 2 - influenza viruses; 3 - coronaviruses; 4 - arenaviruses; 5 - retroviruses; 6 - reoviruses; 7 - picornaviruses; 8 - capiciviruses; 9 - rhabdoviruses; 10 - togaviruses, flaviviruses; 11 - bunyaviruses

The genomes of almost all known RNA-containing viruses are linear molecules; they can be conveniently divided into 3 groups.

The first group is single-stranded genomes of positive polarity, i.e. with a nucleotide sequence corresponding to that of mRNA.

Such genomes are referred to as (+) RNA.

Viral (+) RNA genomes encode several proteins, including an RNA-dependent RNA polymerase (replicase), capable of synthesizing RNA molecules without the participation of DNA.

With the help of this enzyme, the (-) RNA strands of the phage are first synthesized,

Then, in the presence of a special protein called a “host factor,” the replicase synthesizes the (+) strand of RNA.

At the final stage, virions are formed from accumulated viral proteins and (+) RNA.

A simplified diagram of this process is as follows:

(+) RNA (-) RNA

Single-stranded (+) RNA genome is characteristic of

a) phage Qβ,

b) tobacco mosaic viruses,

Tobacco mosaic virus is an example of a + single-stranded plant virus; the virus does not have an envelope, is helical, contains 2130 identical capsid protein molecules and one strand of RNA. RNA is located in a helical groove surrounded by protein subunits and is held in place by numerous weak bonds.

The infectious process, which occurs according to the diagram (transparent 2 below), consists of the penetration of the virus into the plant cell, followed by the rapid loss of its capsid. Then, as a result of direct translation of +single-stranded viral RNA by the ribosomes of the host cell, several proteins are formed, some of which are necessary for the replication of the viral genome.

Replication is carried out by RNA replicase, which produces copies of RNA for new virions. Synthesis of the capsid protein occurs only after the RNA that has infected the cell has undergone some modification, making it possible for the cell's ribosomes to attach to the portion of the RNA that encodes this protein. Virion assembly begins with the formation of discs from the capsid protein. Two such protein disks, arranged concentrically, form a biscuit-like structure, which, when RNA binds to it, takes on the shape of a helix. Subsequent attachment of protein molecules continues until the RNA is completely covered. In its final form, the virion is a cylinder 300 nm long.

3) polio,

4) tick-borne encephalitis.

The second group is single-stranded genomes with negative polarity, i.e. (-) RNA genomes.

Since (-) RNA cannot perform the functions of mRNA, to form “its” mRNA, the virus introduces into the cell not only the genome, but also an enzyme that can remove complementary copies from this genome according to the following scheme:

(-) RNA (+) RNA

This viral enzyme (RNA-dependent RNA polymerase synthesized in the previous reproduction cycle) is packaged in the virion in a form convenient for delivery into the cell.

The infectious process begins with the viral enzyme copying the viral genome, forming (+) RNA, which acts as a template for the synthesis of viral proteins, including RNA-dependent RNA polymerase, which is part of the resulting virions

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