The host range of different viruses varies significantly. Some viruses have a wide range of hosts, while others infect only certain cells of one host species. Host range may be limited by species (species-specific viruses) or determined by higher order taxonomic categories. Viruses with a wide host range are common among plant viruses. For example, tobacco mosaic virus and aster yellows virus infect both plants and their insect vector. Arboviruses are examples of animal and human viruses that have multiple hosts. West Nile virus infects humans, mosquitoes, and waterfowl; tick-borne encephalitis virus - humans, animals, ticks. However, no viruses have been found that can simultaneously infect prokaryotic and eukaryotic cells.
Types of virus-cell interaction
There are three types of interaction between the virus and the cell: productive, abortive and integrative.
Productive type- ends with the formation of a new generation of virions and the death (lysis) of infected cells (cytolytic form). Some viruses leave cells without destroying them (non-cytolytic form).
Abortive type - does not end with the formation of new virions, since infectious process in the cell is interrupted at one of the stages.
Integrative type, or virogeny- characterized by the incorporation (integration) of viral DNA in the form of a provirus into the cell chromosome and their joint coexistence (joint replication).
Reproduction of viruses occurs in several stages, successively replacing each other: adsorption of the virus on the cell; penetration of the virus into the cell; “undressing” the virus; biosynthesis of viral components in the cell; formation of viruses; release of viruses from the cell.
Adsorption
The interaction of a virus with a cell begins with the process of adsorption, i.e., the attachment of viruses to the cell surface. This is a highly specific process. The virus is adsorbed on certain areas of the cell membrane - the so-called receptors. Cellular receptors can have different chemical natures, representing proteins, carbohydrate components of proteins and lipids, lipids. The number of specific receptors on the surface of one cell ranges from 10 4 to 10 5. Consequently, tens and even hundreds of viral particles can be adsorbed on the cell.
Penetration into the cell
In order to replicate, the virus must find a susceptible cell. Each virus has so-called tissue tropism - the ability to infect cells of a certain type. Thus, plant viruses infect either leaf tissue, bract tissue, or cells of the root system. Bacterial viruses are species-specific - archbacterial viruses cannot infect an E. coli cell, and many coliphages do not penetrate the Shigella cell. The tissue specificity of animal and human viruses is most pronounced. Thus, hepatitis viruses infect hepatocytes, the Epstein-Barr virus (causes infectious mononucleosis) has tropism for B-lymphocytes, HIV - for T-lymphocytes, intestinal viruses - for enterocytes, Coxsackie B viruses have cardiotropism. A number of viruses have tropism for more than one , but to several cell types. Thus, polioviruses are tropic to cells of the respiratory tract, gastrointestinal tract (GIT), and central nervous system (CNS).
Hepatitis C virus (HCV) is lymphotropic and hepatotropic.
The specific affinity of viruses for cells and tissues is determined by two mechanisms:
- The presence of virus-specific receptors on the cell surface.
- The content in the system of activating enzymes necessary for the proteolytic cleavage of viral surface proteins and the manifestation of the infectious activity of the virus.
There are two ways for animal viruses to enter a cell: viropexys and fusion of the viral envelope with the cell membrane. With viropexis, after the adsorption of viruses, invagination (invagination) of a section of the cell membrane and the formation of an intracellular vacuole, which contains a viral particle, occur. The vacuole with the virus can be transported in any direction to different parts of the cytoplasm or the cell nucleus. The fusion process is carried out by one of the surface viral proteins of the capsid or supercapsid shell. Apparently, both mechanisms of virus penetration into the cell do not exclude, but complement each other.
The penetration of the virus into the host body is solved differently in different biological species.
1. Plant viruses penetrate the host body as wound infections, where they spread through plasmodesmata, xylem and phloem.
2. Bacterial viruses - by introducing nucleic acid into the cell body or by entering the virion.
4. Animal and human viruses go through a more complex path when infecting the host. Some viruses (influenza virus, rotaviruses) replicate and cause disease at the point of entry into the body (entry gate of infection). Other viruses, having entered the host’s body using one or another mechanism, go through the stage of spread. The spread of the virus in the body is accompanied by viremia (viremia) - circulation of the virus in the blood, which indicates the generalization of the infection.
There are several ways viruses spread in the body:
1. Neural pathway (rabies and herpes viruses).
2. Lymphatic route (reoviruses, polyomaviruses).
3. Hematogenous pathway associated with cellular components and blood plasma (rubella virus, hepatitis B and C viruses, cytomegalovirus, enteroviruses).
The preservation of the virus as a biological species is ensured by its susceptible host, which is the main element of the ecological niche of the virus.
The ability of a host cell or organism to become infected is called susceptibility.
"Strip"
The process of “undressing” involves removing the protective viral shells and releasing the internal component of the virus, which can cause an infectious process. “Undressing” of viruses occurs gradually, in several stages, in certain areas of the cytoplasm or nucleus of the cell, for which the cell uses a set of special enzymes. In the case of virus penetration by fusion of the viral envelope with the cell membrane, the process of virus penetration into the cell is combined with the first stage of its “undressing”. The end products of "undressing" are the core, nucleocapsid or nucleic acid of the virus.
Biosynthesis of virus components
The viral nucleic acid that has entered the cell carries genetic information that successfully competes with the genetic information of the cell. It disorganizes the functioning of cellular systems, suppresses the cell’s own metabolism and forces it to synthesize new viral proteins and nucleic acids that are used to build viral offspring. Implementation genetic information
The virus is carried out in accordance with the processes of transcription, translation and replication.
Formation (assembly) of viruses
Synthesized viral nucleic acids and proteins have the ability to specifically “recognize” each other and, if their concentration is sufficient, they spontaneously combine as a result of hydrophobic, salt and hydrogen bonds.
1. The formation of viruses is a multi-stage process with the formation of intermediate forms;
2. Easy to assemble arranged viruses consists in the interaction of viral molecules nucleic acids with capsid proteins and the formation of nucleocapsids (for example, polio viruses). In complex viruses, nucleocapsids are first formed, with which supercapsid shell proteins interact (for example, influenza viruses);
3. The formation of viruses does not occur in the intracellular fluid, but on the nuclear or cytoplasmic membranes of the cell;
4. Complexly organized viruses during the process of formation include components of the host cell (lipids, carbohydrates).
Exit of viruses from the cell
There are two main types of release of viral progeny from the cell. The first type - explosive - is characterized by the simultaneous release of a large number of viruses. In this case, the cell quickly dies. This exit method is typical for viruses that do not have a supercapsid shell. The second type is budding. It is characteristic of viruses that have a supercapsid shell. At the final stage of assembly, the nucleocapsids of complex viruses are fixed on the cell plasma membrane, modified by viral proteins, and gradually protrude it. As a result of protrusion, a “bud” containing a nucleocapsid is formed. The “bud” is then separated from the cell. Thus, the outer shell of these viruses is formed as they exit the cell. With this mechanism, a cell can produce a virus for a long time, maintaining to one degree or another its basic functions.
The time required to complete the full cycle of virus reproduction varies from 5-6 hours (influenza viruses, smallpox, etc.) to several days (measles viruses, adenoviruses, etc.). The resulting viruses are able to infect new cells and undergo the above-mentioned reproduction cycle in them.
Video: Cell life and interaction with the virus.
№ 19 Types of virus-cell interaction. Stages of viral reproduction.
Types of virus-cell interaction.
There are three types of interaction between the virus and the cell: productive, abortive and integrative.
Productive type- ends with the formation of a new generation of virions and the death (lysis) of infected cells (cytolytic form). Some viruses leave cells without destroying them (non-cytolytic form).
Abortive type- does not end with the formation of new virions, since the infectious process in the cell is interrupted at one of the stages.
Integrative type, or virogeny- characterized by the incorporation (integration) of viral DNA in the form of a provirus into the cell chromosome and their joint coexistence (joint replication).
Reproduction of virusescarried out in several stages, successively replacing each other: adsorption of the virus on the cell; penetration of the virus into the cell; “undressing” the virus; biosynthesis of viral components in the cell; formation of viruses; release of viruses from the cell.
Adsorption.The interaction of a virus with a cell begins with the process of adsorption, i.e., the attachment of viruses to the cell surface. This is a highly specific process. The virus is adsorbed on certain areas of the cell membrane - the so-called receptors. Cellular receptors can have a different chemical nature, representing proteins, carbohydrate components of proteins and lipids, lipids. The number of specific receptors on the surface of one cell ranges from 10 4 to 10 5. Consequently, tens and even hundreds of viral particles can be adsorbed on the cell.
Penetration into the cell.
There are two ways for animal viruses to enter a cell: viropexys and fusion of the viral envelope with the cell membrane. With viropexis, after the adsorption of viruses, invagination (invagination) of a section of the cell membrane and the formation of an intracellular vacuole, which contains a viral particle, occur. The vacuole with the virus can be transported in any direction to different parts of the cytoplasm or the cell nucleus. The fusion process is carried out by one of the surface viral proteins of the capsid or supercapsid shell. Apparently, both mechanisms of virus penetration into the cell do not exclude, but complement each other.
"Strip".The process of “undressing” involves removing the protective viral shells and releasing the internal component of the virus, which can cause an infectious process. “Undressing” of viruses occurs gradually, in several stages, in certain areas of the cytoplasm or nucleus of the cell, for which the cell uses a set of special enzymes. In the case of virus penetration by fusion of the viral envelope with the cell membrane, the process of virus penetration into the cell is combined with the first stage of its “undressing”. The end products of "undressing" are the core, nucleocapsid or nucleic acid of the virus.
Biosynthesis of virus components.
The viral nucleic acid that has entered the cell carries genetic information that successfully competes with the genetic information of the cell. It disorganizes the functioning of cellular systems, suppresses the cell’s own metabolism and forces it to synthesize new viral proteins and nucleic acids that are used to build viral offspring.
The implementation of the genetic information of the virus is carried out in accordance with the processes of transcription, translation and replication.
Formation (assembly) of viruses.
Synthesized viral nucleic acids and proteins have the ability to specifically “recognize” each other and, if their concentration is sufficient, they spontaneously combine as a result of hydrophobic, salt and hydrogen bonds.
There are the following general principles for assembling viruses with different structures:
1. The formation of viruses is a multi-stage process with the formation of intermediate forms;
2. The assembly of simply arranged viruses involves the interaction of viral nucleic acid molecules with capsid proteins and the formation of nucleocapsids (for example, polio viruses). In complex viruses, nucleocapsids are first formed, with which supercapsid shell proteins interact (for example, influenza viruses);
3. The formation of viruses does not occur in the intracellular fluid, but on the nuclear or cytoplasmic membranes of the cell;
4. Complexly organized viruses during the process of formation include components of the host cell (lipids, carbohydrates).
Exit of viruses from the cell.
There are two main types of release of viral progeny from the cell. The first type - explosive - is characterized by the simultaneous release of a large number of viruses. In this case, the cell quickly dies. This exit method is typical for viruses that do not have a supercapsid shell. The second type is budding. It is characteristic of viruses that have a supercapsid shell. At the final stage of assembly, the nucleocapsids of complex viruses are fixed on the cell plasma membrane, modified by viral proteins, and gradually protrude it. As a result of protrusion, a “bud” containing a nucleocapsid is formed. The “bud” is then separated from the cell. Thus, the outer shell of these viruses is formed as they exit the cell. With this mechanism, a cell can produce a virus for a long time, maintaining to one degree or another its basic functions.
The time required to complete the full cycle of virus reproduction varies from 5-6 hours (influenza viruses, smallpox, etc.) to several days (measles viruses, adenoviruses, etc.). The resulting viruses are able to infect new cells and undergo the above-mentioned reproduction cycle in them.
Block 1
Features of the biology of viruses. Principles of virus classification.
Features of reproduction (stages of reproduction):
1. Selective adsorption on cellular receptors (attachment)
2. Receptor-mediated endocytosis:
· Clathrin-dependent;
· Caviolin-dependent;
· Clathrin-caviolin-independent;
Interaction with receptors – depolymerization of clathrin – formation of a pinocytosis vesicle – entry into the CP
Early endosome – late endosome
3. Undressing (deproteinization) (in shelled cells + fusion of the cell’s CPM and supercapsid): ECLIPSE
4. Synthesis of macromolecules:
· Synthesis of early mRNA non-structural proteins (polymerases, viral proteases, replication rate regulators);
· Genome replication:
Ø +RNA: in the CP;
Ø -RNA: completion to +RNA;
Ø DNA: in the nucleus;
Ø Retrotranscription: -RNA –DNA.
· Synthesis of structural proteins (capsid and supercapsid proteins, enzymes) and late mRNAs;
· Post-translational modification of protein.
** Possible integration of the genetic material of the virus into the host genome (hepatitis B, herpes, HIV)
Provirus– viral DNA integrated into the cell genome
5. Virion assembly:
· DNA viruses: in the nucleus;
· RNA viruses: in the CPM.
Glycoproteins of complex viruses are transported to the CPM or accumulate in the ER
6. Virion release:
Lytic type of reproduction: polio
Non-lytic type: by budding - hepatitis B
Classification
1. By structure:
2. By type of NK:
· RNA (80% of all viruses) (Retroviruses, Rhabdoviruses, Picornoviruses, Coronaviruses):
Ø +RNA chain: used as mRNA and genome (poliovirus);
Ø -RNA chain: serves as a genome; as mRNA, the complementary +RNA chain is completed (parainfluenza);
Ø Double-stranded
DNA (in many bacteriophages) (Adenoviruses, Herpesviruses, Parvoviruses):
Ø Double-stranded (herpes);
Ø Single-chain (provoviruses);
Ø Double-stranded ring (papillomavirus);
Ø Double-stranded ring with a defect in one chain (geatite B)
3. By virion size:
· Large;
· Average;
· Small.
4. According to the shape of virions:
· Spiral symmetry (Rabies virus);
· Icosahedral symmetry (Human Adenovirus).
Tropicness to tissues and cells.
6. According to the transmission mechanism:
· Aerogenic (flu, rotavirus);
· Fecal-oral (enteroviruses, rotavirus);
· Transmissible (West Nile fever);
· Contact (smallpox, rabies, HIV, CMV, hepatitis).
7. By class of hosts affected:
Zoonoses:
Ø Brucellosis – pigs;
Ø Anthrax – cattle;
Ø Encephalitis - ticks;
Ø Lyme disease;
Ø Leptospirrosis.
· Anthroponoses;
· Anthropozoonoses:
Ø Tuberculosis;
Ø Plague (pneumonic);
Ø Salmonellosis.
Virological method, main stages.
Method for detecting and identifying viruses by cultivation; is the isolation of a virus from pathological material on a susceptible living system.
Identification: Antiviral drugs or serums.
Stages
1. Preparation of material (feces, nasopharyngeal swabs, cerebrospinal fluid, blood, urine, conjunctival swab):
· Filtration through bacterial filters;
· Treatment with antimicrobial and antifungal drugs.
2. Model selection:
Living systems.
· Cell culture (specially cultured media):
There are 2 types of cultures: suspension culture and monolayer of cells, which is placed in a special vessel - “mattress”
*Mattress: a vessel coated with a compound (collagen) to anchor cells to the wall, high purity grades of agar are used.
Classification:
v Primary/non-transplanted: the culture is obtained from the original tissue each time.
v Transplantable: adapted to invitro conditions (Hel culture: cervical carcinoma; Hep – 2 laryngeal cancer): cancer cells capable of unlimited division (“eternal cell cultures”); form multilayer cultures.
v Semi-transplantable (embryonic cells - for the production of vaccines), not capable of malignant degeneration; capable of making up to 50 divisions (Hayflick limit); form a monolayer of cells.
· Bird embryos (uninformative);
· Laboratory animals (observation of clinical manifestations).
3. Infection.
4. Assessment of the phenomena of the presence of viruses:
Salk color test (for suspension cultures):
Dulbenko phenomenon (culture on agar)
· In a monolayer:
Ø Formation of syncytium – measles;
Ø Circles of virions with cavities – poliomyelitis;
Ø Groups of virions between fibroblasts – adenovirus;
Ø Hemadsorption – flu
5. Virus titration
6. Identification:
· Direct detection of antigen virus: RIF, ELISA, RNGA
· Serodiagnosis:
Ø ELISA, RSK, RNGA;
Ø RNCPD (in monolayer)
· Gene diagnostics (PCR);
Cytoscopy:
Ø Taurus Babesha-Negri (hippocampus): rabies;
Ø Owl's eye: CMV;
Ø Empty nucleolus: adenovirus.
Stages of interaction of viruses with sensitive cells and factors that can disrupt them.
1. Adsorption: interaction of specific cell CPM receptors and adhesins on the surface of the virion.
Damaged cells may not have specific receptors
2. Penetration: fusion of the supercapsid with the cell membrane (for complex viruses) or clathrin/caviolin-dependent endocytosis (for simple ones)
3. Undressing (release from the nucleocapsid) and activation of the NK.
4. Synthesis of NA and viral proteins
5. Virion assembly: gene association. material and capsid protein
6. Exit from the cell and acquisition of a supercapsid (for complex ones)
Forms of viral infection.
By localization.
1. Focal: short incubation period, viruses multiply in organs without entering the blood and lymph. Characterized by short and unstable immunity. Mainly respiratory infections.
2. Generalized: long incubation period; Pathogens travel through the blood and lymph throughout the body, affecting susceptible tissues. Immunity is long-lasting and persistent.
By duration.
1. Acute disease (often): pronounced clinical manifestations; As a rule, the body is freed from viruses and recovered, but chronicity is possible if the treatment is incorrect.
2. Inapparent form: atypical acute infection (there are no symptom complexes characteristic of an acute process).
3. Slow infections: a multi-month incubation period, after which symptoms appear, always ends in death (HIV infection, rabies, leprosy).
4. Chronic form (persistence): lasts for several months (brucellosis);
· Remission: improvement of condition, minor manifestation or absence of symptoms;
· Relapse: exacerbation of the pathological process, clear manifestation of the clinic.
According to the number of pathogens.
1.Monoinfection: caused by a pathogen of one species.
2. Mixed form: infection occurs with several viruses; At the same time, their mutual influences are possible, manifested in the suppression or enhancement of the action of pathogens on the body.
The basis of virus taxonomy is the virion, which represents the final phase of virus development. A virion consists of a genomic nucleic acid surrounded by one or two envelopes. Based on their structure, viruses can be divided into four types, which differ in the nature of the packaging of morphological subunits:
1) viruses with helical symmetry;
2) isometric viruses with cubic symmetry;
3) viruses with binary symmetry, for example phages: their head has a cubic type of symmetry, and their tail is spiral;
4) more complexly organized viruses that have a second shell.
The shell in which the genomic nucleic acid is packaged is called the capsid. The most simply organized viruses are nucleocapsids: they consist only of nucleic acid and a protein shell built from identical peptide molecules. Since the number of amino acid residues in a protein molecule is always less than the number of nucleotides in a gene (triplet code), in order to package a genomic nucleic acid, it is required big number identical protein molecules. And repeated repetition of protein-protein interactions is possible only if the subunits are symmetrically arranged. There are only two ways to package identical protein molecules into a capsid in which it would be stable. A polymer will be stable if it meets the lowest free energy level. The process of formation of such a polymer is similar to the crystallization process; it proceeds according to the type of self-assembly. One of the variants of such self-assembly occurs using helical symmetry, the other - cubic symmetry.
With helical symmetry (thread-like viruses have it), the protein subunits are arranged in a spiral, and between them, also in a spiral, the genomic nucleic acid is laid out.
With helical symmetry, the protein sheath better protects the genomic nucleic acid, but it also requires large quantity protein than with cubic symmetry. Most viruses with a closed sheath have cubic symmetry. It is based on various combinations of equilateral triangles formed from a combination of spherical protein subunits. When combined in a certain way with each other, they can form a closed spherical surface. From various combinations of equilateral triangles that form a common vertex and a common axis of symmetry, various options polyhedra: tetrahedrons, octahedra and icosahedrons.
Types of virus-cell interaction. There are three types of interaction between the virus and the cell: productive, abortive and integrative.
Productive type - ends with the formation of a new generation of virions and death (lysis) of infected cells (cytolytic form). Some viruses leave cells without destroying them (non-cytolytic form).
Abortive type - does not end with the formation of new virions, since the infectious process in the cell is interrupted at one of the stages.
Integrative type, or virogeny, is characterized by the incorporation (integration) of viral DNA in the form of a provirus into the cell chromosome and their coexistence (joint replication).
The main stages of interaction between a virus and a cell:
1) adsorption of the virus on the cell;
2) penetration of the virus into the cell;
3) “undressing” the virus;
4) biosynthesis of viral components in the cell;
5) formation of viruses; release of viruses from the cell.
10. Features of antiviral immunity. The role of phagocytosis and humoral factors in immunity. Interferons, characteristics of basic properties, classification. Features of the action of interferons on viruses.
All immune systems are involved in protecting the body from viruses, but antiviral immunity has significant specific features. They are determined by the fact that it is not the complement and macrophage systems that respond first to the penetration of the virus into the body, but the interferon and T-killer cell systems. Another feature of the formation of immunity is associated with the fact that viruses have a weak antigenic effect on B lymphocytes and their activation, proliferation and differentiation requires the participation of T helper cells and, accordingly, the latter’s presentation of processed viral antigen (peptide fragments) with the participation of MHC class II molecules. Therefore, the role of macrophages and other antigen-presenting cells is not so much phagocytosis itself, but rather the processing and presentation of antigen.
The first response to virus penetration is the interferon system, which suppresses the intracellular reproduction of viruses. In addition, a- and b-inhibitors present in the blood serum have an antiviral effect. Alpha inhibitor is a thermostable substrate, part of α-globulins, prevents the adsorption of viruses on the cell, and is destroyed by neuraminidase of ortho- and paramyxoviruses. Beta-inhibitor is a heat-labile mucopeptide, part of b-globulins, suppresses the reproduction of ortho- and paramyxoviruses.
However, interferons and inhibitors were not enough to protect against viruses, so nature created another, very powerful defense mechanism at the body level against viruses. It is represented primarily by T-cytotoxic lymphocytes and other killer cells. These cells recognize all foreign antigens, including viral ones, presented to them by MHC class I molecules. The main biological significance of T-killer cells is the detection and destruction of any cells infected with foreign antigens.
Interferon is a family of glycoprotein proteins that are synthesized by cells of the immune system and connective tissue. Depending on which cells synthesize interferon, three types are distinguished: ?, ? and?-interferons.
Alpha interferon is produced by leukocytes and is called leukocyte; beta interferon is called fibroblastic, since it is synthesized by fibroblasts - connective tissue cells, and gamma interferon is called immune, since it is produced by activated T lymphocytes, macrophages, natural killer cells, i.e. immune cells.
The production of interferon increases sharply during infection with viruses; in addition to the antiviral effect, interferon has antitumor protection, as it delays the proliferation (reproduction) of tumor cells, as well as immunomodulatory activity, stimulating phagocytosis, natural killer cells, regulating antibody production by B cells, activating the expression of the major histocompatibility complex.
Mechanism of action. Interferon does not directly affect the virus outside the cell, but binds to special cell receptors and affects the process of virus reproduction inside the cell at the stage of protein synthesis.
Types of virus-cell interaction. There are three types of interaction between the virus and the cell: productive, abortive and integrative.
Productive type- ends with the formation of a new generation of virions and the death (lysis) of infected cells (cytolytic form). Some viruses leave cells without destroying them (non-cytolytic form).
Abortive type- does not end with the formation of new virions, since the infectious process in the cell is interrupted at one of the stages.
Integrative type, or virogeny- characterized by the incorporation (integration) of viral DNA in the form of a provirus into the cell chromosome and their joint coexistence (joint replication).
Reproduction of viruses carried out in several stages, successively replacing each other: adsorption of the virus on the cell; penetration of the virus into the cell; “undressing” the virus; biosynthesis of viral components in the cell; formation of viruses; release of viruses from the cell.
Adsorption. The interaction of a virus with a cell begins with the process of adsorption, i.e., the attachment of viruses to the cell surface. This is a highly specific process. The virus is adsorbed on certain areas of the cell membrane - the so-called receptors. Cellular receptors can have a different chemical nature, representing proteins, carbohydrate components of proteins and lipids, lipids. The number of specific receptors on the surface of one cell ranges from 10 4 to 10 5. Consequently, tens and even hundreds of viral particles can be adsorbed on the cell.
Penetration into the cell. There are two ways for animal viruses to enter a cell: viropexys and fusion of the viral envelope with the cell membrane. With viropexis, after the adsorption of viruses, invagination (invagination) of a section of the cell membrane and the formation of an intracellular vacuole, which contains a viral particle, occur. The vacuole with the virus can be transported in any direction to different parts of the cytoplasm or the cell nucleus. The fusion process is carried out by one of the surface viral proteins of the capsid or supercapsid shell. Apparently, both mechanisms of virus penetration into the cell do not exclude, but complement each other.
"Strip". The process of “undressing” involves removing the protective viral shells and releasing the internal component of the virus, which can cause an infectious process. “Undressing” of viruses occurs gradually, in several stages, in certain areas of the cytoplasm or nucleus of the cell, for which the cell uses a set of special enzymes. In the case of virus penetration by fusion of the viral envelope with the cell membrane, the process of virus penetration into the cell is combined with the first stage of its “undressing”. The end products of "undressing" are the core, nucleocapsid or nucleic acid of the virus.
Biosynthesis of virus components. The viral nucleic acid that has entered the cell carries genetic information that successfully competes with the genetic information of the cell. It disorganizes the functioning of cellular systems, suppresses the cell’s own metabolism and forces it to synthesize new viral proteins and nucleic acids that are used to build viral offspring.
The implementation of the genetic information of the virus is carried out in accordance with the processes of transcription, translation and replication.
Formation (assembly) of viruses. Synthesized viral nucleic acids and proteins have the ability to specifically “recognize” each other and, if their concentration is sufficient, they spontaneously combine as a result of hydrophobic, salt and hydrogen bonds.
There are the following general principles for assembling viruses with different structures:
1. The formation of viruses is a multi-stage process with the formation of intermediate forms;
2. The assembly of simply arranged viruses involves the interaction of viral nucleic acid molecules with capsid proteins and the formation of nucleocapsids (for example, polio viruses). In complex viruses, nucleocapsids are first formed, with which supercapsid shell proteins interact (for example, influenza viruses);
3. The formation of viruses does not occur in the intracellular fluid, but on the nuclear or cytoplasmic membranes of the cell;
4. Complexly organized viruses during the process of formation include components of the host cell (lipids, carbohydrates).
Exit of viruses from the cell. There are two main types of release of viral progeny from the cell. The first type - explosive - is characterized by the simultaneous release of a large number of viruses. In this case, the cell quickly dies. This exit method is typical for viruses that do not have a supercapsid shell. The second type is budding. It is characteristic of viruses that have a supercapsid shell. At the final stage of assembly, the nucleocapsids of complex viruses are fixed on the cell plasma membrane, modified by viral proteins, and gradually protrude it. As a result of protrusion, a “bud” containing a nucleocapsid is formed. The “bud” is then separated from the cell. Thus, the outer shell of these viruses is formed as they exit the cell. With this mechanism, a cell can produce a virus for a long time, maintaining to one degree or another its basic functions.
The time required to complete the full cycle of virus reproduction varies from 5-6 hours (influenza viruses, smallpox, etc.) to several days (measles viruses, adenoviruses, etc.). The resulting viruses are able to infect new cells and undergo the above-mentioned reproduction cycle in them. Productive viral infection with the formation of daughter populations and characteristic clinical manifestations is possible only if there are sensitive cells in the infected body in which the reproductive cycle of the pathogen is carried out. For example, the polio pathogen can replicate only in the cells of the gastrointestinal tract and central nervous system of primates and humans.
Abortion infection develops when the pathogen penetrates into insensitive cells (for example, when the bovine leukemia virus enters the human body) or into cells that are not capable of providing a full reproductive cycle (for example, those at the G0 stage of the cell cycle). The ability of cells to maintain virus-specific reproductive processes also suppresses IFN, the antiviral effect of which is directed against a wide variety of viruses.
Persistent viral infection occurs during such an interaction between a virus and an infected cell, when the latter continues to carry out its own cellular functions. If infected cells divide, an infected clone is formed. Thus, an increase in the number of infected cells contributes to an increase in the overall population of the pathogen in the body. However, persistent viral infections usually impair cellular functions, eventually leading to clinical manifestations. In humans, the development of persistent infections to a certain extent depends on age. For example, intrauterine infection with rubella measles virus or cytomegalovirus (CMV) leads to time-limited persistence of the pathogen. The appearance of symptoms is associated with the ability of the fetus to develop immune responses to the infectious agent.
Latent (hidden) viral infection. While persistent infections are accompanied by the constant release of daughter viral populations, in latent lesions they are formed sporadically. The reproductive cycle of such pathogens slows down sharply in the later stages and is activated under the influence of various factors. Latent infections are characteristic of most herpesviruses, causing recurrent and usually non-progressive diseases.
Inapparate infections[from lat. in-, negation, + appareo, be] are accompanied by asymptomatic circulation of small amounts of the pathogen in individual organs. In this case, the pathogen can only be identified using special methods. What distinguishes such lesions from asymptomatic carriage is the high likelihood of clinical manifestations. This term is used for a number of infections in which there are no obvious signs of disease. In the practice of viral infections in humans, the alternative term “subclinical infection” is often used. Actually, latent infections can be regarded as chronically occurring in-device infections, in which a balance is established between the body and the pathogen.
Dormant (cryptogenic) viral infection- a form of manifestation of a viral infection in which the pathogen is in an inactive state in separate foci (for example, in the nerve ganglia). Clinically, the infection manifests itself only when the body’s defenses are sharply weakened. For example, type 3 herpes virus, which causes chickenpox during initial infection, persists in the body for life. Recurrence of the disease in the form of herpes zoster is possible only with impaired immune status (most often in old age).
Slow viral infections characterized by a long incubation period (months and years), during which the pathogen multiplies, causing increasingly obvious tissue damage. Initially, the pathogen multiplies in a limited group of cells, but gradually infects an increasing number of them. The diseases end with the development of severe lesions and death of the patient. Slow viral infections include subacute sclerosing panencephalitis, HIV infection, etc.
