Cytomegalovirus injected intramuscularly or intraperitoneally into mice on the 8th day of pregnancy resulted in a significant retardation in foetal growth and a reduced number of offspring surviving until near-term. Pathological changes consisted of inflammatory cell infiltration in the liver, heart, salivary glands and adrenal cortex of affected animals. Necrotic changes were also present in the adrenal cortex in most severely affected animals following intraperitoneal injection of virus. Intraperitoneal infection led to a frank peritonitis and marked splenic necrosis with a degeneration and inflammation of visceral fatty tissue and lymphadenitis. In contrast, intramuscular injection of virus did not produce a peritonitis but the spleen was greatly enlarged with reaction centres and increased numbers of lymphocytes being identified at histology. As a consequence of cytomegalovirus infection in pregnant mice foetal growth impairment and intrauterine death was seen. This was related to the severity of pathological changes in the mothers. In those animals dying or appearing sick at near-term, most foetuses were dead and resorbing. Since murine cytomegalovirus was not identified by inclusion body formation in foetal or placental tissues in this study and virus has not been isolated from these tissues previously, it was concluded that the mechanism for the impaired foetal growth was of an indirect nature and attributable primarily to a severe generalised maternal illness.
White clover mosaic virus was isolated from glasshouse‐grown sweet pea plants with conspicuous flower ‘break’ symptoms. Plant growth was severely affected. The virus was transmissible by sap inoculation to sweet pea and other leguminous species. It was found naturally in Trifolium repens growing nearby. No natural vector is known.
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