**11. The mutagenic effect**

nodes). Once in the intestine, adenoviruses asymptomatically replicate in the epithelial cells

Latency creates the possibility of endogenous recurrences of acute infection and chronic hyperplasia (in fact, chronic inflammation) of infected lymphoid tissue. The possibility of activating a viral infection in the tonsils (chronic tonsillitis), mesenteric lymph nodes, and appendix is not excluded. Adenoviruses can be activated on the background of immunosuppressive therapy in AIDS patients. A number of new serotypes (serotypes 43–47 of subgroup D) were first isolated from AIDS patients (from feces), allowing to believe that a persistent infection

The mechanism of persistence of adenoviruses in the lymphoid tissue still remains unclear. Most likely, this is due to the low content of sensitive (permissive) cells and very slow replication of the virus in lymphocytes, that is, with severely limited productive infection. It is significant that in the experiments of W. Rowe et al., who discovered adenoviruses in 1953, it took several weeks for the degeneration of a culture of adenoid tissue associated with the reproduction of latent adenoviruses. The possibility of integrative virogeny with partial expression of the viral genome is not excluded. In approximately 50% of the tonsils in adults,

As mentioned above, adenoviruses are unsusceptible to interferons. The acyclic nucleoside phosphonates HPMPC (cidofovir) [26] exhibit antiadenoviral activity. However, these substances are toxic, so they are applied locally in the form of ointments or by injection directly into the affected organ. The target of HPMPC is adenoviral DNA polymerase. The mechanism of the antiviral effect of this compound is based on its phosphorylation by cell kinases and in the synthesis of DNA by competition with conventional nucleosides. At consecutive inclusion in a thread of two molecules of HPMPC, elongation is blocked. The targeted effect of NM on infected cells is provided by a higher affinity of HPMPC diphosphate for viral DNA polymerase than for host DNA polymerase.

Adenovirus infection is perhaps the only respiratory disease other than influenza, against which specific prevention methods have been developed. Military contingents in the United States since 1971 are vaccinated with live oral adenovirus vaccine against serotypes 7 and 4 which were isolated in the 1950s [27]. Live oral adenovirus vaccine has proven to be safe and highly effective in numerous clinical trials, as well as in clinical observations of acute respiratory infections among US military personnel. However, live oral adenoviral vaccine types 4 and 7 are approved only for use in military teams for adults 17–50 years old. To avoid the virus being thrown into the upper respiratory tract, it is recommended to swallow the tablets whole, without chewing. Adenovirus is extremely stable under natural conditions, and there is the possibility of being

it was possible to detect adenoviral antigens in the absence of an infectious virus.

and/or Peyer's patches, periodically evolving from feces.

**9. Antiadenovirals**

6 Adenoviruses

**10. Adenovirus vaccines**

creates favorable conditions for the evolution of adenoviruses [25].

Representatives of the genus *Mastadenovirus* served as objects of research in the field of molecular biology. The intrigue around the pathogenetic function of adenoviruses aggravated after their tumorigenic properties, the ability to induce malignant tumors in animals (newborn hamsters), was recorded. In 1962, Trentin et al. described the first case of the induction of a malignant tumor in animals by the human pathogenic virus—adenovirus-12, which caused tumors in rodents [29]. The oncogenic potential of adenoviruses has served as a stimulus for their careful study, which has proved useful for studying the mechanisms of viral infection and molecular processes in eukaryotic cells. On the model of adenovirus infection, splicing, adenylation, and capturing of matrix RNA, sequence and expression regulation of viral genes, their integration with cellular chromosomes, etc. were first studied with human tumors. In a series of works [30, 31], it was shown that high-oncogenic type 12 adenoviruses and type 18 adenoviruses induce chromosomal aberrations in nonpermissive cells for them. The mutagenic effect at the chromosomal level has been demonstrated for human type 2 adenoviruses and type 5 in rat cells [32], as well as for bovine adenovirus type 3 in Chinese hamster cells [33]. In humans, despite intensive research, the association of malignant tumors with adenoviruses has not been identified.
