INTERFERENCE OF VIRUSES (Latin the inter-prefix between; death, destruction + ferens, ferentis bearing, transferring; viruses) — antagonistic, or inhibitory, action of one virus or its components on a reproduction of other virus and the course of the infectious process caused by the last. The first virus causing a phenomenon call interfering, and the second — applying or interfered. At simultaneous introduction of viruses the bilateral interference is possible. Phenomenon And. it is used at laboratory diagnosis and vaccinal prevention of some viral infections century. The interference can influence the course of a disease, promoting recovery or, on the contrary, emergence hron, patol, states (in case of an incomplete interference), and also to change terms of emergence and distribution of epidemics.
The interference phenomenon is used also in medical practice. So, virusol. laboratories apply the methods based on an interference to detection, allocation and titration of not cytopathic viruses, and also antibodies to them (e.g., at allocation and studying of a virus of a rubella). In practice of immunization action of live virus vaccines on the incidence caused by both homologous, and heterological agents is revealed positive, caused by an interference. However the interference phenomenon can play also a negative role at immunization, napr, existence of enteroviruses in intestines of the person reduces a prizhivlyaemost of vaccinal strains of a poliomyelitis virus and, therefore, efficiency of vaccination. Besides, the possibility of manifestation of an interference shall be considered by drawing up polyvalent vaccines, and also schemes of vaccination.
Early pilot studies And. century of animals and the person were Hoskins's works (M. Hoskins, 1935) and Magrassi (F. Magrassi, 1935), plants — the Tung tree (T. H. Thung, 1931) and Salamana (R. N. Salaman, 1933), bacteriophages — Whyte (R. V. of White, 1937), S. E. Luria and M. Delbryuk (1942). The term «virus interference» was entered by Findlay and Mack-Kallem (S. M. of Findlay, F. Lake of McCallum, 1937) who repeated experiments of Hoskins who observed inhibitory action (see. Inhibitors ) neurotropic a strain of yellow fever on the infection of monkeys caused by a pantropny strain of this virus. Authors described also an interference between viruses of fever of the valley the Rift and yellow fever. Existence of an interference between viruses with various antigenic structure, and also a possibility of its reproduction in cultures of cells confirm lack of a role of antibodies in this phenomenon.
The interference can arise between strains of the same virus (a homologous interference), and also between viruses, various in immunol. relation (heterological interference); can interfere the viruses similar on morfol, and biochemical, to structure, the mechanism and the place of a reproduction and biol, to properties, and also the viruses differing from each other on all these signs. Interfering activity, and also sensitivity to interfering action practically all infectious viruses have. Besides, infectious viruses can interfere from onkovirusa and with nek-ry intracellular microorganisms (e.g., with causative agents of trachoma, with nek-ry rickettsiae), and this interference can be mutual. Onkovirusa are also capable to interfere among themselves, and this interference is expressed not only in an ingibition of a virus reproduction, but also in reduction of transformation and oncogenicity.
Interfering activity is shown also partially or completely inactivated viruses, defective noninfectious virus particles and infectious virus RNA. However at some viruses (e.g., at enteroviruses) the inactivation reduces or completely suppresses interfering activity. Defective virus particles play an important role in a homologous interference, and also in an autointerferention, edges are represented by the special type of an interference which is expressed in reduction of a reproduction of a virus during the use for infection of animal or fabric cultures of its big concentration (e.g., influenza viruses and vesicular stomatitis).
The interference, as a rule, is a short phenomenon. The exception is made by cases of long presence of an interfering virus at an organism or cultures of cells. E.g., the cellular cultures latentno infected during many passages are steadier against infection hetero - or homologous viruses. In certain cases (entero-and onkovirusa) this stability is more expressed to superinfection by a homologous virus. Treatment of cultures from latent infection returns them former sensitivity to infection with viruses.
Intensity of an interference depends on a number of conditions: 1) biol, properties of viruses (viruses and even strains of one virus differ but interfering activity and on sensitivity to interfering action); 2) pluralities of infection (use of an interfering virus in big, and interfered — in a small dose is optimum); 3) a time slice between introduction of viruses and an order of introduction (introduction of an interfering virus till interfered is more effective); 4) a method of introduction of viruses (in most cases the interference is more expressed during the use of the same way of introduction of both viruses); 5) an object, on Krom researches are made (cellular cultures or animals shall have a certain sensitivity to both interacting viruses, napr, enteroviruses do not interfere in insensitive cellular cultures). Depending on these conditions the full interference (a full ingibition of a reproduction of the interfered virus) or incomplete is observed (decrease in a reproduction of the interfered virus). These conditions also define intensity and duration of a phenomenon — what of the interacting viruses plays a role interfering and what — interfered.
Interfering activity of viruses in animal experiments decreases or is completely inhibited by effect of some hormones (a cortisone, estrones), colchicine and immunodepressive factors (immunodeprossant, a splenectomy, X-ray), and also fall of temperature (see. Inhibitors of viruses ). Some of these influences (the lowered temperature, colchicine, a cortisone) influence also an interference in culture of fabrics.
The interference can be determined by decrease in a reproduction of the interfered virus and synthesis of its components (e.g., RNA, hemagglutinin, a neuraminidase), and also by reduction of weight of the damages caused by this virus in cells and in an organism of animals.
The mechanisms which are the cornerstone of an interference completely are not clear. Discovery of interferon which is formed in cells at contact with viruses substantially cleared the inhibitory mechanism of an interference (see. Interferon ). However a number of the facts relating hl. obr. to a homologous interference, and also to an interference between onkovirusa, it cannot be explained with effect of interferon. Treat these facts: impossibility of detection of interferon in some cases homologous interference; low sensitivity of some viruses (e.g., a virus of the Newcastle disease) to interferon and high — to a homologous interfering virus; existence of an interference in the conditions of suppression of formation of interferon inhibitors of synthesis of cellular RNA and protein; the high specificity of a homologous interference allowing to define the subgroups of some viruses differing in the antigenic relation (e.g., viruses of a leukosis of cats, a virus of vesicular stomatitis). Besides, Markus and Carver (P. Marcus, D. Carver, 1967) described a special type of the heterological interference caused by a number of viruses and which is shown only concerning viruses of the Newcastle disease and Sendai. This interference called by them «internal» (intrinsic interference) was not caused by interferon. Analyzing cases of the interference which is not connected with interferon, Portner and Kingsberi (A. Portner, D. W. Kingsbury, 1971) at least 5 mechanisms causing it suggested about existence: 1) competition for cellular receptors or destruction by their interfering virus; 2) products of the protein coded by an interfering virus and capable to destroy heterological polyribosomes; 3) formation of nonfunctional units with the proteins specific to an interfering virus; 4) blocking of the RNA function of the interfered virus; 5) competition for intracellular substrates and places of replication.
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L. M. Mentkevich, T. G. Orlova.