Virus tropism. The airborne route of transmission, which determines the main features of the epidemic process - the involvement of all age groups The affinity of viruses to tissues

Tropism [of viruses] host range, tropism- range of hosts, tropism [of viruses].

A set of strains of bacteria, cell types or types of unicellular and multicellular organisms on which a virus of a certain type (strain) can multiply; K.h. limited to those cells that express the receptors used by viruses to enter the cell (see<amphotropic virus>, <ectotropic virus>).

(Source: English-Russian Dictionary genetic terms. Arefiev V.A., Lisovenko L.A., Moscow: VNIRO Publishing House, 1995)


Cell surface proteins, on which the specific binding of the virion protein (viral receptor, antireceptor) occurs, followed by the penetration of the virus into the cell. Determine the tissue tropism of viruses. In some cells, R. are absent, in ... ... Dictionary of microbiology

host circle- tropism [of viruses] A set of strains of bacteria, cell types or species of unicellular and multicellular organisms on which a virus of a certain type (strain) can multiply; K.h. limited to those cells that express receptors, ... ... Technical Translator's Handbook

host range. See tropism [of viruses]. (Source: "English Russian Explanatory Dictionary of Genetic Terms". Arefiev V.A., Lisovenko L.A., Moscow: VNIRO Publishing House, 1995) ...

tropism. See tropism [of viruses]. (Source: "English Russian Explanatory Dictionary of Genetic Terms". Arefiev V.A., Lisovenko L.A., Moscow: VNIRO Publishing House, 1995) ... Molecular biology and genetics. Dictionary.

Circle of hosts. See tropism [of viruses]. (Source: "English Russian Explanatory Dictionary of Genetic Terms". Arefiev V.A., Lisovenko L.A., Moscow: VNIRO Publishing House, 1995) ... Molecular biology and genetics. Dictionary.

This term has other meanings, see Tropism (meanings). Tropisms (from the Greek τροπος turn, direction) cell orientation reaction, that is, the direction of cell growth or movement relative to the stimulus (chemical ... Wikipedia

VIRUS- (lat. virus poison), a term in a broad sense used to refer to any living pathogen of infectious b it and replacing the older term "contagium vivum" (Kircher). For example, they say: V. typhoid, V. diphtheria. But more often... Big Medical Encyclopedia

- (Arboviruses) - a class of RNA-containing viruses coated with a shell. Carried by arthropods (mosquitoes, ticks, mosquitoes, etc.). Causative agents of tick-borne encephalitis, yellow fever and other human and animal diseases. (

The penetration of the virus into the cell is due, on the one hand, to the quality of the cell envelope receptors (mucoproteins or lipoproteins), and on the other hand, to the quality of the “penetration enzyme” of the virus. Thus, influenza viruses and adenoviruses containing specific enzymes (neuraminase, mucinase) react with mucoprotein (polysaccharide) receptors and easily penetrate into the cytoplasm and nucleus of epithelial cells of the respiratory tract.

The polio virus reacts with lipoprotein receptors that have an affinity for lipid-rich brain tissue and penetrates into the cytoplasm of the neuron.

Cell enzymes break down proteins- capsomeres of the virus, resulting in the release of viral nucleic acid in the cytoplasm and its inclusion in the ultrastructure of the host cell.

The protein metabolism of the cell is disturbed. There is hyperplasia and destruction of mitochondria, tubules, endoplasmic reticulum, ribosomes, now aimed at the synthesis of the structural components of the virus with the formation of virions. Reproduction of the nucleic acid is provided in the nucleus of RNA and DNA polymerases, and proteins, capsomeres of the virus, are built on the ribosomes of the endoplasmic reticulum. The lamellar apparatus (Golgi) dies, and at the same time, the specific function of the cell ceases.

The described processes lead to a perversion of protein metabolism in the cell, protein dystrophy occurs, accumulation of denatured protein occurs in the cytoplasm of the cell, the process ends with coagulation or collimation necrosis of the cell.

In infectious process of any etiology
- bacterial or viral - antibodies appear directed against the causative agent of infections. Antibodies circulating in the blood are formed in response to antigenic irritation in the cells of the reticuloendothelial system, but mainly in the cells of immunocompetent organs, and then enter the bloodstream.

Compounds of an antigen with an antibody in the presence of complement have an antimicrobial and antitoxic effect, providing long term post-infection humoral immunity. At the same time, repeated intake of a microbial protein antigen can sensitize the body and cause, at the height of sensitization from a small dose, but re-introduced antigen, an allergic reaction and infection begins to occur with delayed or immediate hypersensitivity phenomena up to the development of anaphylaxis.

These facts explain why the human body, being under the influence of environmental factors, including pathogenic microbes, either does not get sick when infected, or gets sick with a very severe form or a very mild, clinically subtle form of infection (erased forms). Apparently, all these differences in the manifestation of infection depend not so much on the characteristics of the microorganism as on the reactivity of the macroorganism and the degree of its sensitization.

Infectious diseases are studied according to a certain classification scheme, which takes into account a number of features of each group of infections and reveals some general patterns in the course of the infectious process.

"Pathological Anatomy", A.I. Strukov

The virus can only be seen with an electron microscope. For most doctors, both the viruses themselves and electron microscopes known only from photographs in medical books. But the diseases caused by viruses have such a characteristic clinical picture that no microscopes or photographs are needed - everything is already clear.

The fundamental and most essential biological feature of any virus is the following: viruses are not able to multiply without the help of host cells!

Viruses have tropism for a certain type of cells, penetrating into which they turn them into a kind of plant for the production of viruses. It is quite clear that the cell cannot work on two fronts (both for the virus and for the body), and, therefore, cannot fulfill its main purpose - this is where very specific symptoms of the disease arise.

For example, the infectious hepatitis virus can exist and multiply only in. liver cells. The mumps virus (mumps) prefers cells of the salivary glands, the influenza virus prefers cells of the mucous membrane of the trachea and bronchi, the encephalitis virus prefers brain cells, etc. - for each virus, you can list certain cells and tissues of the human body that it infects or can infect.

Any cell of the body performs a number of specific functions inherent only to it. After infection with the virus, sooner or later problems begin to arise. The virus has infected liver cells and other signs of liver failure.

The virus penetrated into the cells of the head, there were disorders of consciousness, convulsions, paralysis.

How does the human body react to the penetration of any virus , naturally begins to fight it - first at the level of nonspecific immunity (interferon, etc.), then antibodies appear. Antibodies neutralize the virus and the disease ends. But, everything is not at all as simple as it might seem at first glance.

Those. the virus seems to be there, and it really is inside certain cells, but there is no disease - the virus, for some reason, does not multiply, waiting for a certain moment when the immune system weakens.

If the virus is able to actively multiply, it quickly leads to the death and destruction of the cell it has captured. From a disintegrated cell, viruses enter the bloodstream, and there antibodies are already waiting for them ... So it turns out that active viruses (i.e., cell destroying viruses) cause acute infectious diseases (rubella, measles, mumps, influenza, etc. .), which last exactly as long as the body needs to synthesize antibodies. And the terms for the production of antibodies are quite definite and, as a rule, are small, about 5-10 days. Therefore, you can always say how much a measles patient will be contagious

when the rash disappears. The specific fact that viruses are inside the cells of the human body increases the main difficulties in the treatment of any viral infections.

It is very difficult to destroy the virus and leave the cell itself alive. It is not surprising that there are very few effective antiviral drugs and they are all, as a rule, very specific, i.e. act on a strictly defined virus (for example, rimantadine - only on influenza A virus) or on a strictly defined group of viruses (for example, acyclovir - on herpes group viruses). Traditional antibiotic therapy, prescribed for all acute and chronic inflammatory diseases (without regard to the causative factor), has no effect on viral particles. In most cases, patients with viral pathology have only one way out - to use the active bioresonance technique, as the most effective and safe method therapy.

Adenoviruses(Adenovirus)

Adenovirus infections are transmitted by airborne droplets from person to person. Cause pharyngitis, bronchitis, conjunctivitis, atypical pneumonia, flu-like diseases.

Polio

The causative agent is the polio virus. Target organs and tissues: upper respiratory tract, central and peripheral nervous systems, intestines. Almost every case of the disease ends in a fatal outcome or incapacitation of the patient.

Coxsackie virus(Coxsackie- Virus)

They are the causative agents of diffuse myositis

striated muscles with symptoms of necrosis (sometimes myocardium), high neurotropism is noted - they can cause damage, new degenerations and paralysis), inflammatory damage to the spleen.

It also occurs in various diseases accompanied by fever and meningeal phenomena.

Ethytheia-Barr virus

Primary Epstein-Barr virus infection may occur in childhood, adolescence, or adulthood; Approximately 50% of children are ill before the age of 5, in most of them the infection proceeds subclinically. In adults and adolescents, depending on various factors, it can occur both subclinically and as an obvious clinical syndrome (infectious mononucleosis, chronic fatigue syndrome). Some B-cell neoplasms are associated with the Epstein-Barr virus. In 90% of cases, the infection is asymptomatic. Most people are already infected by early adulthood. After the initial infection, the Epstein-Barr virus remains in the body for life. 15-25% of healthy EBV-positive adults shed the virus from the oropharynx. Transmission of the virus can occur through transfusion of blood products, but most often it occurs through direct contact of the oral mucosa (kissing) between infected and EBV-positive individuals. Incubation

period is 30-50 days. The main clinical form of infection is infectious mononucleosis. With chronic mononucleosis infection, the so-called chronic fatigue syndrome can develop.

In typical cases of infectious mononucleosis, the following tetrad of signs is noted: fatigue, fever, pharyngitis and lymphadenopathy; at the same time at patients both all listed symptoms, and only some of them can be noted. Usually within a few days, patients feel unwell, then the temperature rises, pharyngitis and adenopathy appear. Pharyngitis can be severe, with severe soreness, exudative phenomena, resembling streptococcal pharyngitis. Any group of lymph nodes may be involved; the lesion is usually symmetrical; adenopathy of the anterior and posterior cervical lymph nodes is often expressed.

Sometimes the only clinical manifestation of the disease may be an increase in one lymph node or one of their groups. The peak of fever usually occurs in the afternoon or early evening, the temperature rises to approximately 39.5 ° C, but can reach 40.5 ° C. Weakness is usually most pronounced in the first 2-3 weeks of illness. Often there is an increase in the spleen and liver. Slightly less common are maculopapular rashes, jaundice, periorbital edema, enanthema on the palate. Most patients have moderate leukocytosis, usually in combination with more pronounced absolute and relative lymphocytosis, due to the appearance of morphologically atypical lymphocytes (mononuclear cells). Atypical lymphocytes can make up to 80% of the total number of leukocytes, but may be absent. Infectious mononucleosis usually resolves on its own. The duration of the disease is different; the acute phase usually lasts about 2 weeks. "Chronization" of symptoms is observed in almost all infected people.

Chronic fatigue is characterized by a constant decrease in performance in previously healthy people.

At the same time, high fever, chronic pharyngitis, an increase in phatic nodes, muscle and joint pain, sleep disturbances, memory impairment, depression, rapid changes in body weight, dysfunction of the gastrointestinal tract, decreased appetite, arrhythmias, dysuria, allergy symptoms and hypersensitivity to drugs, insolation, alcohol. This condition lasts up to six months or more and tends to worsen.

Herpes

Herpes is an infectious disease caused by the herpes simplex virus (HSV).

Herpes is the most common viral infection. About 90% of people on earth are infected with herpes, 30 million people of the US adult population suffer from a recurrent disease. Only 5% of those infected show symptoms of the disease, in the rest it proceeds without clinical manifestations. The virus most often infects:

  • skin;
  • eyes - conjunctivitis, keratitis;
  • mucous membranes of the face;
  • mucous membranes of the genital organs;
  • Central nervous system - encephalitis, meningitis.

The disease is transmitted sexually (genito-genital, genital-anal, oral-genital), by contact with a patient or carrier of HSV.

Infection is most likely to occur through contact with a patient during a relapse of the disease, as well as when the virus is shed without clinical symptoms. Infection is possible through oral-genital contact, if the partner has herpes on the face.

Genital herpes is caused by two serotypes of the herpes simplex virus: HSV-1 and HSV-2.

In pregnant women, the virus can cause pregnancy pathology, spontaneous abortions, and premature births. In the process of childbirth, infection with HSV of the fetus is possible.

The likelihood of transmission of infection, as well as the development of neonatal herpes in a child, depends on a number of conditions:

  • the level of neutralizing antibodies in the mother, which passed to the fetus transplacentally;
  • the level of local antibodies that bind the virus in the genital tract;
  • the duration of the waterless period;
  • the presence of damage to the skin of the child in the process of delivery.
  • Infection of the child can also occur after childbirth, it depends on how active herpetic manifestations are in the mother.

Herpes pathogenesis

As a rule, the virus enters the human body through the mucous membranes and skin. Due to getting into the axon of the nerve, it can penetrate into the nerve cells of the dorsal roots of the ganglia, in which the virus is able to exist in a latent state. block the replication of the virus, the blockade can be eliminated over time.

The main properties of HSV are latency and virulence (the ability to replicate in the central nervous system and cause neurological diseases). The herpes simplex virus can exist latently in the human body and cause subsequent reactivations. Latency allows the virus to avoid the impact of the immune response of the human body. Reactivation can lead to both asymptomatic shedding of the virus and multiple recurrences of the disease. Possible lesions of the mucous membranes, skin (the most common manifestations), genital organs and the central nervous system. How latency will manifest itself depends both on the properties of the virus and on the characteristics of the human body.

Another feature of HSV is neuroinvasion, its ability to penetrate from peripheral nerve cells into the CNS. By disrupting the immune system, the virus causes secondary immunodeficiency. Recurrent disease disrupts the normal course of life and can lead to neuropsychiatric disorders.

Clinical picture of herpes

There are several types of herpes infection:

  • primary;
  • non-primary;
  • recurrent.

In a primary infection, there are no antibodies to herpes in the human body yet. The disease may be asymptomatic, but certain symptoms may also appear. Approximately 2-14 days after infection, local and general symptoms characteristic of this infection appear, virus isolation begins, and herpetic eruptions form. The patient complains of headache, malaise, fever is possible. At 2-3 weeks, the symptoms disappear, and in the next few weeks, the damaged epithelium heals.

Non-primary infection occurs in people who already have antibodies to one type of herpes. Asymptomatic isolation of the virus in this case is quite rare. As a rule, clinical manifestations are observed for about 2 weeks and are not as pronounced as with a primary infection. The most common infection of a person who has antibodies to HSV-1 is the HSV-2 type.

Recurrent infection occurs in patients who have antibodies to the reactivated type of virus and symptoms of genital herpes. Diagnosis of this infection requires the use of type-specific serological and fine culture methods. Clinical manifestations in relapses are mild, and the healing period of the epithelium is up to 4 days. About half of patients with recurrent infection complain of itching, burning, and soreness of the lymph nodes.

The following factors contribute to the recurrence of genital herpes:

  • decreased immune status;
  • hypothermia and overheating of the body;
  • a number of mental and physiological conditions;
  • intercurrent diseases;
  • abortion, the introduction of an intrauterine device.

There are three stages of genital herpes lesions:

  • damage to the external genitalia.
  • herpetic urethritis, colpitis, cervicitis.
  • herpetic endometritis, cystitis, salpingitis.

In women, herpetic vesicles usually form on the labia minora and labia majora, clitoris, and cervix. However, the infection can penetrate into the mucous membrane of the uterus, tubes, appendages in an ascending way. In place of the bubbles, sores are formed that do not bleed, and after healing do not leave scars. The appearance of herpes can be triggered by other sexually transmitted infections. Relapses usually occur after menstruation or sexual intercourse.

In men, the foreskin, glans penis, and balanopreputial groove are most often affected. Men are characterized by the recurrent nature of the disease, in which herpetic vesicles and erosion are formed. Infection can cause herpetic urethritis or balanoposthitis.

papillomavirus

Papillomavirus (human papillomavirus - HPV) is an agent responsible for precancerous lesions of the genital organs, and sometimes pericellular cancer.

warts

Genital warts (genital warts) caused by human papillomavirus have recently become much more common than other sexually transmitted diseases (such as genital herpes or gonorrhea). In the US, HPV affects at least 20 million sexually active people, among whom the number of men and women is approximately the same.

Papillomavirus affects the surface epithelium of the skin and mucous membranes. It causes the development of genital warts, including cervical warts and cervical intraepithelial neoplasia. Warts caused by HPV often regress, which, if the squamous epithelium is affected, can lead to malignant tumors.

The size of genital warts usually does not exceed 5-7 mm., However, it can be several centimeters. As a rule, these formations do not occur in the singular, forming a common growth like a cauliflower.

Formations do not appear immediately after infection with the human papillomavirus, since it multiplies in the deep layers of the epithelium and comes out gradually when the layers change. After that, subject to a decrease in the overall resistance of the organism, genital warts appear, and their carrier becomes contagious.

In men, warts are most often localized:

  • foreskin (bridle, inner leaf);
  • glans penis;
  • anus.

and most often condylomas are localized in women:

  • external genitalia;
  • opening of the urethra;
  • vagina; Cervix;
  • anus.

It should be noted that, being benign formations, warts, nevertheless, represent an oncological threat. A connection between these growths and cancer of the genital organs has been revealed; for women, in addition, there is a risk of cervical dysplasia and difficult childbirth. A frequent complaint of patients is pain during intercourse, which can also result in damage to genital warts, that is, the opening of bleeding.

Papillomavirus leads to subclinical infection and rarely to the formation of warts. In more than 50% of couples, papillomavirus is diagnosed in both sexual partners, which requires their simultaneous treatment to achieve lasting results. Quite often, along with HPV, other sexually transmitted diseases (chlamydia, mycoplasmosis, ureaplasmosis, trichomoniasis and others) are also detected.

It is possible to transmit the virus through both direct and indirect contacts, which is characterized by species and tissue specificity.

There are more than 60 different papillomaviruses in humans, and Various types HPV leads to various types defeats.

Types of HPV:

  • low oncogenic risk -6, 11;
  • average oncogenic risk - 31, 33, 35;
  • high oncogenic risk - 16, 18.

Cytomegalovirus

Cytomegalovirus was discovered in 1956. The causative agent (Cytomegalovirus hominis - CVM) belongs to the herpesvirus family (Herpesviridae). The virus has an affinity for the tissue of the salivary glands and, in localized forms, is found only in these glands. CMV persists in the body (remains) for life. It is widely distributed in the population. Antibodies to cytomegalovirus are detected in 10-15% of adolescents. By the age of 35, these antibodies are already detected in 40% of people. CMV is not highly contagious. Infection usually requires prolonged, close contact or repeated contact.

Cytomegalovirus is a disease caused by a virus of the herpes family that can be asymptomatic or affect internal organs and the central nervous system.

The causative agent of cytomegalovirus is Cytomegalovirus hominis, which enters the body once, remains there forever.

Cytomegalovirus infection, which can only live in the human body, contributes to an increase in the size of normal host cells. Once in the body, the virus leads to immune restructuring in the body. In order for the symptoms of the disease to appear, i.e. there was a transition from a latent form to a clinically expressed form, provoking factors are necessary: ​​taking cytostatics or immunosuppressants, intercurrent diseases, HIV infection.

Infection with cytomegalovirus occurs:

  • in everyday life by airborne droplets and by contact - with saliva when kissing;
  • sexually: by contact - with sperm, mucus of the cervical canal;
  • in blood transfusion and transplantation of donor organs;
  • transplacental - intrauterine infection of the fetus;
  • infection of the child during childbirth;
  • infection of the child in the postpartum period through breast milk from a sick mother.

Clinical manifestations of cytomegalovirus infection

The duration of the incubation period is from 20 to 60 days. The acute phase of the disease lasts from 2 to 6 weeks: an increase in body temperature and the appearance of signs of general intoxication, chills, weakness, headache, muscle pain, bronchitis. In response to the primary introduction, an immune restructuring of the body develops. After the acute phase, asthenia persists for many weeks, sometimes vegetative-vascular disorders.

Multiple lesions of internal organs

Most often, CMV infection manifests itself as ARVI (acute respiratory

malaise, fatigue, headaches, coryza, inflammation and enlargement of the salivary glands, with profuse salivation and whitish deposits on the gums and tongue.

Generalized form of CMV infection with damage to the internal (parenchymal) organs. There is inflammation of the liver tissue, adrenal glands, spleen, pancreas, kidneys. This is accompanied by frequent "uncaused" pneumonia, bronchitis, poorly amenable to antibiotic therapy; there is a decrease in the immune status, the number of platelets in the peripheral blood decreases. Damage to the vessels of the eye, intestinal walls, brain and peripheral nerves is not uncommon. Enlargement of the parotid and submandibular salivary glands, inflammation of the joints, skin rash.

Damage to the organs of the genitourinary system in men and women is manifested by symptoms of chronic nonspecific inflammation. If the viral nature of the existing pathology is not established, the diseases do not respond well to antibiotic therapy.

Pathology of pregnancy, fetus and newborn are the most serious complications of CMV infection. The maximum risk of developing this pathology occurs when the fetus is infected during pregnancy. However, it must be remembered that problems often arise in pregnant women with the activation of a latent CMV infection with the development of viruses (the release of the virus into the blood) with subsequent infection of the fetus.

CMV is one of the most common causes of miscarriage! Intrauterine CMV infection of the fetus leads to the development of severe diseases and lesions of the central nervous system (mental retardation, hearing loss). In 20-30% of cases, the child dies.

Antiviral drugs are used to treat cytomegalovirus, which suppress the infection, although they do not kill everything. Sufficiently effective methods of treatment of viral pathology are methods of active bioresonance. The “Helper” and “Lanta-Z” devices used for this purpose, in combination with passive bioresonance techniques, gomso and informal therapeutic methods of treatment, can effectively deal with the entire spectrum of infectious pathology.

Shingles(Herpeszoster) Belongs to the Herpcsviridae family. The disease is characterized by the appearance of vesicular rashes on the skin of the trunk, head, conjunctiva, accompanied by severe pain. The possibility of penetration of the virus through the placenta, leading to fetal pathology, is proposed. Target tissues: intervertebral ganglia, cranial nerve ganglia, skin, CNS, conjunctiva.

Herpes simplex(Herpessimplex)

Type 1 is the causative agent of acute gingivostomatitis and pharyngitis, aphthous stomatitis, herpetic eczema, conjunctivitis, meningoencephalitis. Type 2 causes genital herpes and neonatal herpes. can play certain role in the etiology of cervical cancer.

Target organs and tissues: central and peripheral nervous systems, liver, spleen, conjunctiva, lungs, adrenal glands, genitals.

Chicken pox(Varicella) Target organs and tissues: respiratory tract, lymph nodes, RES, central nervous system, skin, adrenal glands, conjunctiva.

hepatitis virusA (HepatitisA) The route of transmission is fecal-oral. Causes infectious hepatitis - Botkin's disease. The main target is hepatocytes. Extrahepatic manifestations - joints, skin, muscular system, vasculitis, nervous system, kidneys.

Hepatitis B virus (HepatitisIN) Causes serum hepatitis. Ways of transmission - parenteral, sexual, perinatal. Compared to HAV, it is characterized by a more severe course, more high level lethality. The main target organ is the liver. Extrahepatic manifestations: joints, skin, nodular periarteritis, glomerulonephritis. Has a tendency to become chronic. Chronic HBV can lead to cirrhosis of the liver and hepatocellular carcinoma (liver cancer).

Hepatitis C virus (not A or B)(HepatitisWITH) The main route of transmission is blood transfusion, sexually and through the placenta is rarely transmitted. Similar in many respects to HCV. Target organ - liver, hematopoietic cells. The frequency of pathology is more than 80%.

mumps virus

Target organs and tissues: central and peripheral nervous system, upper respiratory tract, conjunctiva, parotid salivary glands.

Therapy of viral diseases

With viral processes, in standard cases , the terms of therapy can increase from 1 month to six months, because. viral particles are intracellular pathogens that have the ability to replicate. In this case, the number of therapy courses can be from 4 to 6, depending on the dynamics of the self-healing process. In some cases, the treatment process requires dynamic monitoring using segmental express diagnostics, a resonance test, or the Voll APC ATM series. Therapy courses of 8-10 sessions according to the standard scheme (7-20-7-20-7) with intervals from 10 to 21 days can be combined with passive BRT, immunomodulatory and homotoxic therapy.

In chronically occurring processes of viral etiology, hepatitis, herpes viruses. Epstein-Barr, cytomegalovirus reaction, it is advisable to gradually increase the intervals between courses, from 10 days between the 1st and 2nd course, to 14 days between the 3rd and 4th, 4th and 5th, and up to 20 days between

Virus classification

Viruses can only develop in certain cells. tropism viruses - these are the predominant systems of organs and tissues of the body, in the cells of which viruses are capable of reproduction.

By tropism, viruses are divided into:

  • 1. Panthropic (in different organs and tissues of the body)
  • 2. Neurotropic (in nerve cells - rabies virus)
  • 3. Dermatotropic (in skin cells - smallpox virus)
  • 4. Epitheliotropic (diarrhea virus. FMD in epithelial cells)
  • 5. Pneumotropic (in cells of the respiratory tract, influenza virus, adenoviruses)
  • 6. Hematotropic (in blood cells, leukemia virus)

The modern classification of viruses is based on the fundamental (basic) properties of virions, the main of which are:

  • 1. type of nucleic acid
  • 2. virion morphology
  • 3. viral genome strategy
  • 4. antigenic properties of virus proteins
  • 1, 2, 4 properties externally noticeable properties. Viral genome strategy (3) (nucleic acid0 is a viral reproduction method determined by the characteristics of the viral genetic material. The reproduction method depends on the viral genome.

On the basis of various features, viruses are divided into: families, subfamilies, genera and types. Moreover, the division into families is based on two features:

  • 1. type of nucleic acid
  • 2. the presence of a supercapsid membrane.

Exist: 7 families DNA containing viruses, 13 families RNA containing viruses.

Names of viruses (Latin terminology)

The family ends with... viridae , the subfamily ends with ... virinae , genus - on ...... virus , type - for each virus. For example: Sem. Paramyxoviridae

Genus Morbilivirus

Viroids they are agents that cause plant diseases. A small RNA molecule closed in a ring (plasmid). RNA can be in plasmids. Plasmids and viroids are the same. Hence the theory that viruses are escaped organelles (plasmids).

tent, chronic and slow, depending on the release of viruses into the environment and the manifestation of symptoms of the disease.

Latent infections are asymptomatic and may be accompanied either by normal reproduction of the virus in an apparently healthy body and its release into the external environment, or by virus carriage, in which the normal cycle of viral reproduction is disrupted, and the virus persists in the body for a long time.

Chronic viral infections are characterized by a long-term pathological process, periodic states of recovery and relapse.

Slow infections are characterized by a long incubation period, a long progressive course of the disease and end in severe disorders or, more often, death. A typical example of slow infections is AIDS. The development of slow infections is based on violations of genetic, immunological and physiological mechanisms that provide long-term persistence of the pathogen in the body.

Several mechanisms are known that determine the long-term survival of the virus in the body:

1. the virus is in a defective state, unable to replicate and induce an effective immune response.

2. the virus is in the cell in the form of a free genomic nucleic acid, inaccessible to the action of antibodies;

3. the genome of the virus is integrated into the chromosome target cells.

PATHOGENESIS OF VIRAL INFECTIONS

The pathogenesis of viral infections is a set of processes that cause a disease and determine its development and outcome. Pathogenesis is determined by the following factors:

1. virus tropism.

2. virus reproduction rate and number of infectious particles

in offspring.

3. cell response to infection.

4. the body's response to infection-induced cellular changes and

Tropism of the virus to certain cells and organs is characteristic of most viral infections. Tropism is based on the sensitivity to the virus of certain cells, tissues and organs of the macroorganism.

The spread of viruses in the body is possible through the lymphatic system (lymphatic pathway), circulatory system (hematogenous pathway)

And nervous system (neurogenic pathway.) Lymphatic vessels are one of the main pathways by which the virus spreads from the site

original localization. The hematogenous pathway of viruses can be associated with cellular elements (macrophages, erythrocytes, leukocytes), or viruses are transported in a free form with blood plasma. The neurogenic pathway is characterized by the spread of viruses along peripheral nerves.

The transmission mechanism of a virus in susceptible host chains is the way the virus moves from an infected organism to a susceptible one. The mechanism of transmission includes a successive change of three stages: removal of the pathogen from the body into the environment, the presence of the pathogen in abiotic or biotic objects of the environment, the introduction of the pathogen into a susceptible organism. Under natural conditions, there are four main mechanisms of transmission of the pathogen between individuals of the same generation (horizontal transmission): fecal-oral, airborne, transmissible and contact. In addition to those listed, there is a fifth way (vertical transmission), which ensures the transition of the virus from one generation to another (from mother to fetus).

Virus transmission factors are elements of the environment that ensure the transmission of an infectious agent from a source to a susceptible host. The main transmission factors are air, water, food, household items, blood-sucking arthropods.

The route of transmission of a virus is a set of factors that ensure the circulation of the virus between infected and susceptible organisms. There are food, water, household, airborne, transmissible, household transmission routes.

Section 9. Viruses - causative agents of infectious diseases in humans

CAUSES OF ACUTE RESPIRATORY DISEASES (ARI)

In terms of frequency, these diseases rank first. There are no effective vaccines against the viruses that cause them, and the airborne route of transmission causes the rapid spread of the virus in the environment. Cells of the mucous membrane of the upper respiratory tract and eyes carry a large number of markers with which virus receptors specifically interact.

Influenza viruses

Family: Orthomyxoviridae

Genus: Influenzavirus A, B; Influenzavirus C.

Type A virus was discovered by V. Smith, S. Andrews and P. Laidlaw in 1933, type B virus was isolated by T. Francis, R. Medgill in 1940, type C virus by R. Taylor in 1949.

Type A virus causes influenza in humans, mammals, and birds, while viruses B and C cause influenza only in humans. Type A virus plays the most important role in epidemiology.

The virion has a spherical shape and a diameter of 80-120 nm, a molecular weight of 250 MDa. The genome is represented by single-stranded fragmented negative RNA. Nucleocapsid with helical symmetry. The supercapsid contains two glycoproteins - hemagglutinin and neuraminidase, which protrude above the membrane in the form of spikes. The main functions of hemagglutinin are:

1. recognition of a cellular receptor - a mucopeptide that has N-acetylneuraminic acid;

2. ensuring the fusion of the virion membrane with the cell membrane;

3. formation of protective properties.

The functions of neuraminidase include:

1. ensuring dissemination of virions by cleavage of neuraminic acid from newly synthesized virions and cell membranes;

2. determination of the epidemic properties of the virus.

Found 10 various options neuraminidase. The source of infection is only a person, a patient or a carrier. Infection occurs by airborne droplets. The incubation period is very short - 1-2 days. The virus multiplies in the epithelial cells of the respiratory mucosa. The decay products of damaged cells enter the bloodstream, causing severe intoxication and fever. The virus has a depressing effect on the hematopoiesis and immune system, which can lead to secondary viral and bacterial diseases. Immunity is the main regulator of influenza epidemics. As the immune layer grows, the epidemic subsides. But at the same time, strains of the virus with a modified antigenic structure are selected, which continue to cause outbreaks.

The high variability of the influenza virus can be explained by the following factors. First, the occurrence of point mutations, which are most susceptible to hemagglutinin and neurominidase genes. Secondly, reassociation of genes between viruses of humans and birds, mammals, which is facilitated by the segmental structure of the viral genome. Antigenic drift allows the virus to overcome the existing immunity in humans. For laboratory diagnostics, nasopharyngeal discharge and blood are used as material. Virological, serological and genetic methods are used. For specific prophylaxis, several types of vaccines are used: live attenuated (from viruses that spontaneously or as a result of selection have lost their virulence, but remain

or immunogenicity), killed whole-virion, subvirion, subunit.

parainfluenza viruses.

Family: Paramyxoviridae

Genus: Paramyxovirus

The first virus isolates were isolated by W. Chanok in 1957.

Virions are spherical, 150–200 nm in diameter. The genome is represented by single-stranded unfragmented RNA. The nucleocapsid has helical symmetry and is surrounded by a shell of matrix protein M. The virion is covered with a supercapsid consisting of a lipid layer and glycosylated proteins with hemagglutinating, neurominidase, hemolytic, and symplast-forming activities. They are very common causative agents of ARI. Often the cells of the larynx are affected. The disease is especially severe in children. For detection, as a rule, immunological methods are used.

Respiratory adenoviruses.

Family: Adenoviridae

Genus: Mastadenovirus

W. Rowe was first identified in 1953 from the tissues of the tonsils and adenoids. No supercapsid. The virion has the shape of an icosahedron with a diameter of 70 - 90 nm. Each of the apical capsomeres bears filamentous protrusions (fibers) ending in a head. Hereditary information is represented by double-stranded DNA. The source of infection is only a sick person. Infection occurs by airborne droplets or household contact. Depending on the serotype of the virus, the disease can affect the upper respiratory tract, the gastrointestinal tract. Adenoviruses cause sporadic diseases and local epidemic outbreaks.

The incubation period lasts 6 - 9 days. Diseases most often occur in the form of tonsillitis, pharyngitis, bronchitis, atypical pneumonia, pharyngo-conjunctival fever. However, the virus can cause a latent (asymptomatic) or chronic infection with long-term persistence in the tissues of the tonsils and adenoids.

ACUTE INTESTINAL DISEASES

Acute intestinal diseases (ACI) are the second most common after acute respiratory diseases. There are many reasons for the ubiquity of ICD, but the main ones are three of them.

1. Low standard of living of the population, poor sanitary and hygienic conditions.

2. Lack of effective vaccines against many intestinal diseases

3. A large number of various pathogens of OKZ.

Polio virus.

Family: Picornaviridae

Genus: Enterovirus

The viral etiology of poliomyelitis was established by K. Landsteiner and G. Popper in 1909.

The virus has a spherical shape, molecular weight 8–9 MDa. The genome is represented by single-stranded unfragmented RNA. Envelope proteins play a role in recognizing the host cell's receptor, attaching the virion to it, and releasing the viral RNA inside the cell. The virion does not possess hemagglutinating properties. The ability of the polio virus to cause paralysis appears to be related to one of the coat proteins. The only source of infection is humans. The main route of infection is fecal-oral. The entrance gates for the virus are the mucous membranes of the pharynx, stomach, and intestines. In them, the primary reproduction of the virus occurs. It then travels to the lymph nodes and blood. These two stages are asymptomatic. Viruses can enter the central nervous system. The death of motor neurons caused by the vital activity of the virus leads to the development of skeletal muscle paralysis. The patient either dies or remains disabled. After the disease (including in a latent form), a strong lifelong immunity remains. There is no specific therapy against the virus. Patients need to maintain an orthopedic regimen and exercise under the supervision of doctors. In the middle of the 20th century, highly effective polio vaccines were created that ensure the creation of herd immunity.

Rotaviruses.

Family: Rotaviridae

Genus: Rotavirus

First identified by R. Bishop in 1973.

The virion has a spherical shape. The genome is represented by a double-stranded fragmented RNA and is surrounded by a capsid consisting of two layers. The core also contains viral RNA polymerase. The outer protein of the capsid ensures the penetration of the virus into the cell and has a hemagglutinating property. The source of infection is a person. Mostly children under four years of age are affected. The virus multiplies in the epithelial cells of the duodenum. The incubation period is from 1 to 7 days. The main early symptom is vomiting, there is also a slight increase in temperature. Treatment has three main goals: stopping dehydration, maintaining normal water-salt metabolism, and ensuring normal nutrition. To detect the virus, immunological (RPGA, ELISA) and genetic (RNA probes) methods are used. There is no vaccine against rotavirus infection.

Viral hepatitis.

A group of diseases with common clinical syndromes. They represent a major global problem. For the first time, infectious hepatitis was isolated as an independent nosological form in 1888 by the Russian doctor P.S. Botkin.

Hepatitis A virus.

Family: Picornaviridae

Genus: Hepatovirus

The virus has a spherical shape (icosahedron), diameter - 27 nm. The genome is represented by single-stranded positive RNA. The supercapsid is absent. The only source of infection is humans. The method of infection is fecal-oral (mainly water), as well as household and food routes. Children under the age of 14 are at particular risk. The disease has an autumn-winter seasonality. The incubation period varies from 15 to 50 days. The virus multiplies in the regional lymph nodes, penetrates into the blood, and then into the liver cells. Reproduction of the virus in hepatocytes leads to a decrease in the detoxification and barrier functions of the liver. The most acceptable way to diagnose hepatitis virus is enzyme immunoassay. Several types of vaccines have been developed to prevent the disease.

Hepatitis B virus.

Family: Hepadnaviridae

Genus: Orthohepadnavirus

The virion is spherical, 42 nm in diameter. The supercapsid is composed of three proteins. The genome is represented by double-stranded circular DNA. The hepatitis B virus does not contain an oncogene, but it has been established that, by invading the cellular genome, viral DNA can induce various genetic rearrangements, which can cause the development of liver cancer. The only source of infection is humans. Infection occurs by parenteral, sexual and vertical (from mother to fetus) route. Hematogenous way the virus is brought into the liver. In pathogenesis, an important role is played by autoimmune reactions provoked by modifications of the cell membrane by viral proteins. The incubation period averages 60-90 days. The disease can occur in latent, typical icteric, malignant forms. In case of recovery, stable immunity is formed. But the disease can go into a chronic form, a person becomes a carrier. The main diagnostic method is the use of the reverse passive hemagglutination reaction. A DNA probe method has also been developed. Two types of vaccines are used to prevent the disease:

1. A vaccine derived from the plasma of a carrier.

2. genetic engineering vaccine.

Hepatitis C virus.

Family: Flaviviridae

Genus: Hepacivirus

The virion is spherical, 60 nm in diameter. The genome is represented by single-stranded unfragmented RNA. There is a supercapsid.

The source of infection is a person. The routes of infection are the same as for the hepatitis B virus, but the clinical course is easier. Up to 70% of diseases occur in a latent form. In addition to hepatocytes, the virus can infect nerve cells. Most effective method diagnostics - polymerase chain reaction. The main pathogenetic treatment is interferon.

Herpesviruses.

Herpes simplex virus.

Family: Herpesviridae

Genus: Simplexvirus

The virion is spherical, 150–210 nm in diameter. The genome is represented by double-stranded linear DNA, consisting of two fragments. Nucleic acid is coated with protein. There is a capsid and a supercapsid. The epidemiology is different for type 1 and type 2 viruses. There is evidence that up to 70-90% of people are infected with type 1 herpes virus. It is transmitted by direct contact through saliva or utensils. The disease proceeds in the form of vesicular or aphthous stomatitis. Herpes simplex virus type 2 is transmitted sexually or during childbirth from a sick mother to her child. It spreads like a typical venereal disease. For diagnosis, virological, virological and serological methods can be used. As a means of specific treatment, chemotherapy drugs are used - modified nucleosides that suppress the replication of the virus. In the case of acute disease, interferon inducers are effective.

VIRUSES - CAUSES OF NATURAL FOCAL INFECTIONS

Tick-borne encephalitis

Family: Flaviviridae

Genus: Flavivirus

The causative agent was isolated by L.A. Zilber, E.N. Levkovich, M.P. Chumakov in

The virion is spherical, 25–45 nm in diameter. The genome is represented by single-stranded positive linear RNA. The nucleic acid is surrounded by a protein capsid. There is a lipid supercapsid permeated with glycosylated spike-forming proteins that generally have a hemagglutinating property. In accordance with the type of carrier, two types of tick-borne encephalitis virus are distinguished: persulcate (carrier Ixodes persulcatus) and ricinus (carrier Ixodes ricinus). Infection occurs in a transmissible way. Incubation period from

1 to 30 days. The onset of the disease is acute: chills, headache, fever, nausea, muscle pain.

Laboratory diagnosis is carried out mainly by virological and serological methods. Treatment is symptomatic. Killed culture vaccine is used to prevent the disease.

Hemorrhagic fever with renal syndrome.

Family: Bunyaviridae

Genus: Hantavirus

The virion is spherical, about 50 nm in diameter. The genome is represented by single-stranded fragmented negative RNA. There is a capsid and a supercapsid.

The main carriers are rodents - field and East Asian mice, voles, gray rats. Infected rodents shed the virus in saliva, urine, and feces. Human infection occurs through the air. The virus, having entered the body, circulates in the blood for 5-7 days and, having a pronounced vasotropic effect, affects the walls of capillaries and small veins. In this case, the most pronounced changes are observed in the renal vessels. The incubation period is 11–23 days. The onset of the disease is acute: chills, fever, muscle pain, photophobia. From the 3-5th day of illness, a hemorrhagic rash appears on the skin. The kidneys are most affected, their function is restored only 2-3 months after recovery. Immunity after the disease is persistent, long-lasting. Immunological methods are used in laboratory diagnostics. Interferon is used for treatment; in acute renal failure, hemodialysis is necessary.

AIDS VIRUS

Family: Retroviridae

Genus: Lentivirus

First isolated by the French virologist L. Montagnier in 1983.

under the name LAV (Lymphoadenopathy associated virus) and by the American virologist R. Gallo in 1984 under the name of human T-lymphotropic virus. After establishing the identity of these two forms, the virus was given the name human immunodeficiency virus (HIV) to avoid confusion.

The virion is spherical, 110 nm in diameter. The genome is represented by a single-stranded unfragmented positive RNA, which has the form of two identical molecules linked by 5'-ends. The envelope of the virus has the shape of a polyhedron and carries 72 glycosylated protein molecules in the form of spikes. Together with the lipid bilayer, these proteins form a supercapsid. In the center of the virion is a cone-shaped capsid, in addition to the structural protein, it contains reverse enzymes (reverse trans-

scriptase; DNA-dependent DNA polymerase; RNAse H), protease and integrase. Having penetrated into the body, the virus, using a surface protein, recognizes cells containing a specific CD4 marker. This receptor has T-helper cells and, to a lesser extent, macrophages. Entering the cell, the nucleic acid of the virus is rearranged from the RNA form to the DNA form and is introduced into the genome of the host cell. The provirus remains inactive until the T-lymphocyte is activated. From the moment the virus enters the cells, the period of HIV infection begins - the virus carrier, which can last up to 10 years. From the moment of activation, the disease begins - AIDS. The virus is highly variable. Even from the body of one patient, strains of the virus can be isolated that differ significantly in antigenic properties. Two large forms of HIV-1 are known: O (Outlier) and M (Major), the latter is divided into 10 subtypes (A - J). The form of HIV-2 is characteristic of West Africa. The source of infection is only a person - a sick person or a virus carrier. The virus is found in blood, semen, cervical fluid, in nursing mothers - in breast milk. Infection occurs sexually, through blood and its preparations, from mother to child. Cases of infection with the virus through food, drink and insect bites are not known.

Features of the pathogenesis of HIV infection:

1. The virus has a very high rate of reproduction.

2. The virus induces the formation of extensive syncytial structures due to the fusion of infected and uninfected T-helpers.

3. Surface protein molecules circulate freely in the blood, bind to healthy T-helpers, changing their antigenic structure, as a result of which they are recognized and destroyed by T-killers as foreign.

4. When the virus replicates T-helpers die as a result of apoptosis, their titer in the blood decreases sharply.

5. Decreased expression of membrane receptors B-cells, the synthesis of various cytokines (IL-2, IL-4, IL-5, IL-6) is disrupted.

6. The function is broken T-killers.

7. The complement system and macrophages are suppressed.

8. Due to the structural and antigenic similarity of the surface protein of the virus with the receptors of some epithelial cells of the macroorganism, autoimmune antibodies with a wide spectrum of action are synthesized.

9. The virus is neurotropic and infects the cells of the nervous system.

10. As a result of impaired functioning of the immune system, there is a risk of opportunistic infections, tumor diseases and damage to the central nervous system.

The main method for diagnosing virus carriers and HIV infection is the enzyme immunoassay method. However, due to the fact that the surface protein of the virus has an affinity for the receptors of some human cells, antibodies related to antibodies against the surface protein may appear in the body. In this case, there may be false-positive ELISA results. Therefore, all positively reacting sera are subjected to additional analysis using immunoblotting.

For the treatment of HIV infection, it is necessary to find or synthesize drugs that effectively suppress the activity of reverse transcriptase or viral protease. For specific prevention, it is necessary to create a vaccine that would ensure the formation of effective cell-mediated immunity based on virus-specific CTLs. Virus-neutralizing antibodies in this case are not effective.

Section 10 Modern methods virological research and diagnosis of viral infections.

USE OF LABORATORY ANIMALS

L. Pasteur was the first to use laboratory animals to study the properties of the rabies virus.

The use of laboratory animals makes it possible to isolate viruses, determine the nature of a viral infection by symptoms, maintain laboratory strains of viruses, preserve the antigenic properties and activity of viruses, and obtain diagnostic and therapeutic and prophylactic viral preparations.

IN as laboratory animals, white mice, hamsters, guinea pigs, rabbits are most often used, less often monkeys; birds - chickens, geese, ducks.

IN In recent years, newborn animals (more susceptible to viruses), "sterile animals" and animals of pure lines with known heredity (inbred, or linear, animals) have been more often used.



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