**4. Antigenic structure**

known which cause a wide range of illnesses, from mild respiratory infections in young chil-

This family includes two genera designated based on genetic criteria (*Atadenovirus* and *Siadenovirus*) as well as three genera, in which adenoviruses are combined according to the type of host (*Aviadenovirus*, *Ichtadenovirus*, and *Mastadenovirus*) (https://talk.ictvonline.org/

Genus *Atadenovirus* presents the newly formed genus which combines adenoviruses with a high relative content of AT-pairs in genomic DNA. This genus includes also adenoviruses of

Genus *Siadenovirus* combines adenoviruses containing at the 5′ end which contains a gene of an enzyme sialidase that cuts off sialic acid residues from the surface glycoproteins of the host

Genus *Aviadenovirus* includes adenoviruses of turkeys, quail, chickens, and a number of other birds. The type species causes the death of embryos and respiratory disease in quails and chickens. Other members of this genus are pathogens of the egg drop syndrome, hemorrhagic

Genus *Ichtadenovirus* has the only characterized representative which infects white sturgeon—

Genus *Mastadenovirus* includes various viruses of mammals: viruses of cows, sheep, deer,

Adenoviruses are non-enveloped viruses, 80–90 nm in diameter. The icosahedral capsid of adenoviruses consists of hexones carrying group-specific and type-specific antigens and pentones containing mainly group-specific antigens at each apex. From each pentone there is a

Structural proteins of adenoviruses are designated by Roman numerals in descending order of molecular weight. The adenovirus capsid consists of seven structural proteins; three major capsid proteins hexon, fiber, and penton; and four minor proteins protein IIIa (pIIIa), VI, VIII, and protein IX [5]. Fibers provide binding to cellular receptors and participate in the discrimination of infected cells, causing inhibition of the synthesis of cellular macromolecules [6]. Soluble proteins of pentone cause a cytopathic effect similar to the action of infectious adenoviruses,

In humans, 57 adenoviruses are known, which are divided into 7 groups (A–G).

dren to life-threatening multi-organ disease in immunocompromised people.

**2. Adenoviruses' nomenclature**

snakes, possums, calves, chameleon, ducks, and lizard.

cells. These adenoviruses infect frogs and birds.

pigs, dogs along with all human adenoviruses.

fiber with a head at the end (**Figure 1**).

taxonomy).

2 Adenoviruses

enteritis, and hepatitis.

*Sturgeon ichtadenovirus A.*

**3. Structure**

Antigenic structure of *Mastadenovirus* is represented by three soluble antigens: the hexone A-antigen is common for all serotypes; pentone antigen (B-antigen) is a toxic antigen, it inhibits the action of interferon and increases the severity of associated respiratory infections; and fibril C-antigen is a type-specific which promotes the adsorption of adenoviruses on monkey or rat erythrocytes and causes their agglutination. Manifest forms of the disease cause epidemic serotypes (3, 4, 7, 14, 21) of subgroups B and E. Serotypes 1, 2, 5, and 6 subgroups C cause a latent current, contributing to the formation of chronic tonsillitis and adenoiditis. Clinical forms of adenovirus infection presented in **Table 1**.


of virus particles occurs in the nucleus, where crystal-like inclusions are formed. Several hundred viral particles are synthesized in each cell. The release of adenoviruses is accompanied by the destruction of the host cell. The cycle of reproduction of adenoviruses in the cell lasts

Introductory Chapter: Human Adenoviruses http://dx.doi.org/10.5772/intechopen.82554 5

Adenoviruses can multiply in different cells, including airway epithelial cells and lymphocytes. Virus-infected cells become targets for immunity effectors. However, adenoviruses impose such properties on cells that allow them to avoid destruction or at least reduce this possibility. Adenoviruses produce factors that block the synthesis and expression of HLA-I molecules on the cell surface and thereby inhibit the presentation of viral antigens attacked by CD8+T-lymphocytes. Cells infected with adenoviruses acquire increased resistance to interferons and TNF-a, a potent cytotoxic cytokine. In both cases, adenoviral proteins interfere with molecular mechanisms that determine antiviral effects. Among the products of early adenoviral genes are factors that delay the development of apoptosis. In general, this reflects a strategy aimed at improving the survival

From the pathogenetic point of view, adenoviruses damage the respiratory tract and belong to the "respiratory" viruses. However, adenoviruses also can cause lesions of the intestine and conjunctiva, as well as the central nervous system, bladder, and genitals. Adenoviruses multiply in the mucous membrane with a gradual, consistent involvement in the pathological process of the descending parts of the respiratory tract. Reproduction of adenoviruses also can occur in the intestinal tissue or lymph nodes which is accompanied by a multiple increase in lymph nodes. In addition to local changes, adenoviruses have a general toxic effect which appears as a fever and symptoms of general intoxication (weakness, lethargy, loss of appetite, headache, and nausea). The ability of adenoviruses to reproduce in the epithelial cells of the respiratory tract, conjunctiva, and intestine with the occurrence in some cases of hematogenous dissemination creates a wide range of clinical manifestations of this infection, including the appearance of generalized lymphadenopathy and widespread exanthema. In addition to adenoviruses in the genesis of acute pneumonia, the attachment of a secondary bacterial flora

is important, which is facilitated by the suppression of the immune system [23–24].

The term "adenoviruses" has an ecological coloration, reflecting the tendency to persistence in the lymphoid tissue, so that adenoviruses can be isolated from the tonsils, adenoids, appen-

After acute infections, many serotypes are not eliminated from the body for a long time. Most of the latent viruses belong to subgroups B2 and C. They can persist for years in the lymphoid tissue of the pharyngeal ring and, apparently, other localizations (e.g., in the mesenteric lymph

of infected cells and creating conditions for viral persistence [22].

14–24 h.

**7. Pathogenesis**

**8. Adenoviral latency**

dix, and lymph nodes of practically healthy people.

**Table 1.** Clinical forms of adenovirus infection.

The WHO have reported that data on the incidence and ramp prevalence of adenoviral infections are not exact, since in many cases, adenoviruses cause mild forms and therefore remain unregistered, according to general practitioners [16]. However, in recent years, adenoviruses caused widespread outbreaks in Asia [17–19] in which adenoviral infection was accompanied by the development of acute respiratory distress syndrome (ARDS) in Malaysia [18], China [16, 19], and South Korea [19].
