Adenovirus infections of man generally occur in childhood, and the outcome varies in severity from asymptomatic to explosive outbreaks of upper or lower respiratory tract manifestations. Less commonly, adenoviruses cause gastrointestinal, ophthalmic, urinary, and neurological diseases. The vast majority of adenovirus-caused diseases are self-limiting. However, immunocompromised patients, above all organ transplant recipients, individuals infected with human immunodeficiency virus (HIV) developing AIDS, and those receiving radiation and chemotherapy against tumors, represent special populations that are prone to experience grave, frequently fatal consequences of adenovirus infection. In numerous cases, the organ to be transplanted itself proves to be the source of invasive adenoviruses. Sporadic fatal infections may occasionally occur in healthy, immunocompetent individuals. In such cases, the presence of certain predisposing immu-nogenetic factors cannot be excluded. Cellular immune responses are also important for the recovery from acute adenovirus infection. Peripheral blood mononuclear cells have been found to exhibit proliferative responses to
HAdV-2 antigen. This function is mediated by CD4+ T cells, which seem to recognize conserved antigens among different human adenovirus serotypes.
The incubation period from infection to clinical symptoms is estimated to be 1—7 days and may be dose dependent. Clinical symptoms during the initial viremia are dominated by fever and general malaise. Recovery from infection is associated with the development of serotype-specific neutralizing antibodies that protect against disease or reinfection with the same serotype of the virus but do not cross-react with other serotypes.
Pathology by adenoviruses is partially the consequence of viral replication and cell lysis. Correspondingly, in various tissues and organs, such as bronchial epithelium, liver, kidney, and spleen, disseminated necrotic foci can be observed upon necropsy or histopathological examination. Characteristic intranuclear inclusion bodies and so-called smudge cells contain large amounts of adenovi-rus capsid proteins. Besides the lesions caused by virus replication, direct toxic effects of high doses of structural proteins, as well as the host's inflammatory respond, may contribute to the aggravation of pathology. Experimental infection of animals with various adenovirus types seldom results in a pathology similar to that experienced with the same virus under natural circumstances. One of the few exceptions is turkey hemorrhagic enteritis, the pathogen-esis of which has been studied in detail and is due to TAdV-3, which causes intestinal hemorrhages and immunosuppression. By in situ DNA hybridization and PCR, the presence of virus-specific DNA as evidence for virus replication has been demonstrated in the immuno-globulin M-bearing B lymphocytes and macrophage-like cells, but not in CD4+ or CD8+ T lymphocytes. Interestingly, fewer virions were present in the intestines, which are the principal site of pathology, than in the neighboring lymphoid organs including spleen and cecal tonsils. This finding strongly suggests that the intestinal lesions induced by TAdV-3 are mediated by the immune system. Systemic or intestinal hemorrhagic disease of ruminants seems to be related to virus replication in endothelial cells.
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