This group of DNA viruses were so called because they were isolated from the adenoids (and tonsils) in 1953. They induce latent infections in lymphoid tissues of man, especially tonsils and adenoids, pharyngitis, conjunctivitis and serve as helpers for the replication of other viruses, adeno-associated viruses (AAVs).The infection is subclinical or mild in normal individuals but it may be severe and fatal in immunocompromized subjects. Severe and fatal hepatitis with severe respiratory infection may develop in these individuals. Intranuclear viral antigen n has been detected in cases of hepatitis. They are presently classified in 41 serologic types.

They were isolated in Coxsackie, New York, in 1948 during studies poliomyelitis. They rarely produce hepatitis. They commonly induce epidemic myalgia, myocarditis, pericarditis, aseptic meningitis pleurodynia, herpangina. Hepatitis is frequently associated with myocarditis and consists of necroinflammatory changes involving lobules and porta tracts, to be distinguished from congestive changes due to heart failure. They are divided in tow groups according to lesions produced in the suckling mouse. Group A (23 types) produces diffuse myocytis with inflammation and necrosis of voluntary muscles; group B (6 types) produces brain degeneration, pancreatitis, panniculitis and focal myocytis of skeletal muscles and myocardium. The virus is similar to poliovirus. Isolation of the viral agent in each infection is necessary for diagnosis.

Is another group of viruses isolated during studies for poliomyelitis. It is an enterovirus and produces enteritis, acute respiratory infection, rash, fever, encephalitis , aseptic meningitis, paralysis. The liver is rarely involved but it may be severely affected in severe infections contracted in the neonatal period.

It was isolated in 1962.It produces a syndrome similar to measles bu much milder. In 1941 an ophthalmologist in Australia discovered that I the infection contracted in the first trimester of pregnancy may produce congenital defects. Circa 20% of children born from infected mothers (during the first trimester of pregnancy) are affected by the rubella syndrome which consists of cataracts, deafness, cardiac malformations, mental retardation, microcephaly. The liver may be involved with variable degree of acute hepatitis, biliary obstruction and destruction. The virus can be recovered from the liver.

A cuban physician, Carlos Finlay associated this infection with mosquitoes and Dr. Walter Reed of the U.S. army confirmed the theory by exposing volunteers to the mosquitoes during the Spanish-american war of 1901 and demonstrated the viral ultrafiltrability of the agent causing this disease. The mode of controlling the infection was found. Until that time, the devastating effects of this infection in the Caribbean region had bee responsible, for many deaths and for the France's failure of digging the Panama canal. The virus is a RNA particle that replicates in the cytoplasm of infected cells. In the forests (sylvan cycle), the monkeys are the reservoir of the virus. In urban areas (urban cycle) man are infected through the aedes aegypti mosquito. The disease may be asymptomatic, mild and severe fatal. It affects liver together with heart, kidneys and spleen causing jaundice hemorrhages and marked albuminuria.Mortality is 50% in severe cases. Diagnosis is made by virus isolation and serology. There is an effective vaccine, 17D which confers a long-standing immunity (35 years). It is safe for adults but should not be used in children under 6 months because it may cause encephalitis.

This group comprises Lassa fever (Nigeria 1969), Tacaribe, Machupo (Bolivia 1962), Junin (Argentina 1950), Tamiami, viruses. They are transmitted through excrements of rodents and produce illnesses of variable severity with a fatality rate of over 20%.The liver is involved together with conjunctiva, pharynx, lymph nodes, skin. There is marked hepatocyte damage in the liver consisting in eosinophilic necrosis of individual cells but jaundice is rare.

It is carried by the african green monkey which is used for biomedical experiments. The first infection occurred in 1967 among laboratory personnel in Marburg, Germany and in Yugoslavia with 7 deaths. It is 100% fatal for the monkeys. Fever, rash, diarrhea, hemorrhages are the clinical manifestations in man. The liver suffers a necroinflammatory picture suggestive of a viral disease. No other infections have been reported lately.

This virus produces an illness and liver lesions similar to Marburg virus: hemorrhagic fever, highly fatal. It exploded in East Africa: 70 cases with 33 deaths in Nzara, Sudan; 76 cases with 41 deaths in Maridi hospital; 237 cases in Zaire with 211 deaths. The virus, like Marburg virus is an RNA particle that has been named Ebola after a small river in Zaire and belongs to the family of Filoviridae consisting of filamentous and branched forms. It replicates in the cytoplasm of infected cells. Maximum security viral laboratories are needed for the isolation of these deadly viruses. No treatment exists.

This infection which affected sheep in the subsaharan region was introduced to Egypt in 1977 where it caused an epidemic among humans with , at least 400 cases with considerable high mortality. No other cases occurred after that outbreak but the virus may reappear. The virus is a single strand RNA particle which replicates in the cytoplasm of infected cells. Clinically it produces hemorrhages encephalitis and macular degeneration of the eyes. The liver shows focal or diffuse hepatic necrosis. The pathological damage is more concentrated and more severe in the sheep. An effective vaccine is available for man and animals.

It is an infection caused by a virus affecting man, animals and ticks in the Middle East up to southern Russia. The virus is similar to Rift Valley virus, single stranded, RNA particle. Clinical manifestations are similar to the other hemorrhagic viroses described above: Extensive perioral and perinasal bleeding followed by thrombocytopenia, leukopenia and liver involvement. There is high mortality (20-70%) especially when the infection is acquired from fluids of human patients.

Oxford Textbook of Clinical Hepatology, Mc Intire at al., Editors, pp 630-646.
Pathology of the Liver,R.N.M.MacSween et al., Editors, pp 224-233.
Microbiology, Davis et al., Editors, 2nd ed., pp 1007-1409
Histopathology of the Liver, G.Klatskin & H.O.Conn, pp 317-321