The virus attaches to host cells via the coxsackie‑adenovirus receptor (CAR) and subsequently enters through receptor‑mediated endocytosis. Once inside, the viral genome is transported to the nucleus where early genes are expressed, initiating the replication machinery. Later stages of the life cycle produce new virions that are assembled in the nucleus and egress by budding through the nuclear membrane followed by release from the cell by lysis. Adenovira particles are released into the airway lumen and can subsequently be spread by respiratory droplets, direct contact or fomites.
Clinical disease caused by adenovira is typically self‑limited, presenting as upper respiratory tract infection characterized by sore throat, fever and cough. In immunocompromised hosts, the virus can cause more severe illnesses, including viral pneumonia, hepatitis and disseminated disease. Infections of the conjunctiva (adenoviral keratoconjunctivitis) may lead to corneal involvement and temporary visual impairment.
Diagnosis is performed by detecting viral antigen or nucleic acid in respiratory, ocular or stool specimens. Polymerase chain reaction and rapid antigen tests are common tools, while viral culture remains an adjunctive method. Because no specific antivirals are approved for adenovira, management primarily focuses on supportive care. Clinical trials investigating monoclonal antibodies and antiviral agents such as cidofovir have shown limited effectiveness, and most cases resolve without intervention.
The epidemiology of adenovira mirrors that of other human adenoviruses: it is common, especially in children and military recruits, with seasonal peaks in temperate climates and a higher incidence during school terms. Vaccination against adenoviral serotypes exists for specific strains, but no vaccine targets adenovira specifically. Continued surveillance and virologic research are required to clarify its pathogenic potential and to develop targeted therapies.