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HERPES VIRUSES — a sort of viruses which virions consist of a nucleocapsid with ikosaedralny type of symmetry and a lipoproteidny cover. Diameter of virion of 100 — 150 nanometers, a genome is presented to two-filamentous DNA.

The majority of the known viruses of herpes allocated from the person and animals (tab. 1) causes infectious diseases, others induce development of tumors or associate with them (tab. 2).

Viruses of a herpes simplex (VPG — Herpes simplex virus — HSV) — one of the widespread viruses affecting the person. Modern domestic classification of VPG is developed by A. K. Shubladze with sotr. on the basis of an antigenic structure of viruses also includes 6 groups. All viruses pathogens for laboratory animals, chicken embryos; in the infected cells intracellular inclusions form. In cellular cultures show gemadsorbiruyushchy effect, form simp flippers; under an agar covering create plaques, various on morphology. The cytopathic effect is shown generally by strains of the first antigenic group.

Is later on the basis serol, tests of hybridization nucleinic to - you and distinctions in nucleotide structure, and also on biol, to VPG properties are divided into two groups: type 1 and type 2.

Fig. 1 Diffraction pattern of mature virion of a virus of a herpes simplex: 1 — an external cover; 2 — it is central the located nucleocapsid. Negative contrasting; X 150 000.
Fig. 2. Diffraction pattern of two unripe: virions of a virus of a herpes simplex without. an outside cover (are specified by shooters). Negative contrasting; X 200 000.

Virion (fig. 1) consists from is central the located dense body — the nucleoid (75 nanometers) including virus DNA; the proteinaceous capsule — the capsid covering nucleoid (100 nanometers) and the outside, concluding a nucleocapsid cover (145 — 210 nanometers). The capsid is constructed of 162 tubular hollow proteinaceous natures of capsomeres (10 X X 13 nanometers) of five - and a hexagon form, laid on cubic type of symmetry. The outside cover of irregular shape contains proteins, carbohydrates, lipids and other substances; in the antigenic relation shows affinity with antigens of a host cell. In population of a virus there are always incomplete virions: without nucleoid — empty or without outside cover — «naked» and their combinations (fig. 2). The floating density of a virus in solution of chloride of caesium of 1,27 — 1,29 g/ml. Virus DNA makes apprx. 7% of weight of virion, a pier. weight 54 — 92-10 6. The guanine and tsitozin is made by 57 — 74%.

Fig. 3. The diffraction pattern of adsorption of virion (1) of a virus of a herpes simplex on a cell (2). Ultrathin section of a cell; X 100 000.
Fig. 4. The diffraction pattern of formation of a virus of a herpes simplex in a kernel of the infected cell: 1 — nucleocapsids; 2 — empty (without nucleoid) capsids. Ultrathin section of a cell; x 20 000.

Adsorption of viruses on cells of fabric cultures (fig. 3) happens within 2 — 3 hour. The mechanism of process is explained by existence of the ionized groups a surface of a cell and a virus both nonspecific reaction, and specific interaction of receptors of a cell with receptors of a virus.

Penetration of a virus into a cell (viropeksis) is carried out by the mechanisms which are the cornerstone pino-and phagocytosis. Release virus nucleinic to - you from the «dressing» covers comes to the end with deproteinization. The subsequent implementation of information coded in a genome is connected with synthesis of virus components and is carried out by DNA replication, a transcription of DNA in information RNA and broadcasts of RNA in protein at suppression of synthesis of cellular components.

Fig. 5. Diffraction pattern of unripe virions: 1 — nucleocapsids (without cover) a virus of a herpes simplex in a kernel of a cell; 2 — mature virions — nucleocapsids. coated, in perinuclear space. Ultrathin section of a cell; X 50 000.
Fig. 6. The diffraction pattern of an exit of a mature virus (1) from a cell (2). Ultrathin section of a cell; X 150 000.

Assembly of nucleocapsids (unripe virions) happens in a kernel of cells (fig. 4). Formation of a virus comes to an end in the course of escaping of a kernel in cytoplasm by acquisition of an outside cover at the expense of a part of a nuclear membrane (fig. 5). After that the mature virus goes beyond a cell (fig. 6).

In the course of synthesis of a virus there are considerable changes of the mitotic mode of cells and emergence of kolkhitsinopodobny metaphases. Chromosomal damages are expressed generally in chromatid and isochromatid breaks. In kernels there is a regrouping (margination) of chromatin, swelling of kernels to the subsequent lysis and formation of eosinophilic DNA-containing of inclusions. Cells are rounded, among them appear this - layers. Further there is vacuolation of cells, disturbance of structure of cytoplasmatic organoids and finally (in 24 — 72 hours after infection) there occurs destruction of the infected cells.

Are the weak inductor of interferon, are highly sensitive to ether, trypsin, warming up, are steady against X-ray, well remain at low temperatures and in the dried-up state.

At primary infection (is more often in the early childhood) get to blood (virusemia), breed in fabrics ekto-and an endodermal origin and cause various acute clinical manifestations which are most often connected with damage of mucous membranes, skin, corneas, sometimes a liver, a brain and other bodies. In the most part of cases there occurs clinical recovery, however a virus (or its genome) remains in an organism during all life in the latent form in the absence of any symptoms of a disease (apprx. 90% of the population are VPG carriers). Under the influence of some stressful factors (overcooling, various bacterial infections etc.) the virus is periodically reactivated, causing patol. the process reminding primary display of an infection. As a result of the virusemia connected with existence of a virus in all fractions of blood at the time of a disease (it is possible also in the interrecurrent period) the virus can break a placental barrier, get into a fruit and cause various patol, processes. Feature hron, a herpes infection is constant existence in blood of the person of specific virus neutralizing antibodies.

In experiments on cellular cultures it is shown that at hron, a herpes infection synthesis of a virus happens as a productive infection in separate cells.

The long persistention in an organism creates a possibility of the transforming action of a virus on cells. In experimental conditions the phenomenon of transformation is established for animals and the person. Are known Oncogenous, allocated from frogs, birds, rodents, cattle and some species of monkeys. There are data on allocation and gerpesopodobny viruses from tumors of the person. At the same time the intimate association with tumor cells is revealed, however the final role in development of new growths in the person remains unproven.

See also Chicken pox (etiology) , Viruses , Herpes (etiology) .


  • It is dangerous to the person.
    • Strikes also a cattle, sheep, dogs, cats, rats.


Bibliography: Zhdanov V. M. and Gaydamovich of S. Ya. Virusologiya, M., 1966, bibliogr.; Laboratory diagnosis of viral and rickettsial diseases, under the editorship of E. Lennet and N. Schmidt, the lane with English, page 520, M., 1974; Shubladze A. K. and Mayevsky T. M. Gerpes, M., 1971, bibliogr.; The herpesviruses, ed. by A. S. Kaplan, N. Y. - L., 1973; Jok1 i k W. K. The large DNA animal viruses, the poxvirus and herpesvirus group, in book: Molecular basis virol., ed. by H. Fraenkel-Conrat, p. 576, N. Y. a. o., 1968; Klein G. Summary of papers delivered at the conference on herpesvirus and cervical cancer (Key Biscayne, Florida), Cancer Res., v. 33, p. 1557, 1973, bibliogr.

A. F. Bocharov.