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Kidney cell lines MA104 and BGM were infected with vaccinia and measles viruses respectively in the presence of 45Ca. Increased 45Ca level was detected in the virally infected cells as compared with control cells. An enhancement of 28 +/- 6% and 37 +/- 13% was shown in vaccinia and measles respectively following 5 h of infection. The effect of the calcium antagonist verapamil was studied in both vaccinia- and measles-infected cells. In one-step growth experiments, the mean inhibitory effect of 90 microM verapamil on viral yield after 13 h was 97 +/- 1% in the case of vaccinia. In the measles virus after 47 h a mean of 76 +/- 5% inhibition was detected. The suitability of verapamil as a potential antiviral agent is suggested and requires further investigation.

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Treatment of BGM (African Green Monkey kidney) cells with the calcium antagonist Verapamil resulted in a reduced yield of chlamydial infectious particles. The inhibitory effect was concentration-dependent, the maximal effect being achieved at 200 microM-Verapamil, which produced a 99.99% reduction of infectious particle yield. Electron microscopy showed that control Chlamydia trachomatis-infected BGM cells contained typical large inclusions in which most of the particles were elementary bodies, whereas Verapamil-treated infected cells contained small inclusions consisting predominantly of reticulate bodies. The findings indicate a possible therapeutic use of this calcium antagonist as an anti-chlamydial drug.

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Serum amyloid A concentrations were determined in serial serum samples of 41 patients with confirmed acute myocardial infarction (10 with acute ischaemia and two with myocarditis). A sharp increase in serum amyloid A concentration was observed early at onset of infarct; it peaked on the third day (up to 2200 fold of normal values) and declined towards normal during the following days, if no complications occurred. Different patterns were observed in patients with acute ischaemia or myocarditis. Although serum amyloid A is not a specific marker, it may, because of its high sensitivity and characteristic patterns of change, represent an additional useful biochemical variable in the diagnosis, follow up, and prognosis of acute ischaemic heart disease.

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The 'uremic toxin', guanidino propionic acid (GPA), which was detected in uremic serum in correlation with BUN level, modified the mitogenic response of normal lymphocytes to phytohemagglutinin (PHA). Mild modifications can be detected in the concentrations which are found in uremic patients. Other guanidino compounds which have been detected in uremic sera, such as guanidino succinic acid (GSA), guanidino butyric acid (GBA) and guanidino acetic acid (GAA), show similar inhibitory pathways. It is suggested that guanidino compounds contribute to the immunological disturbances in uremia. The complexity of their action on lymphocyte mitogenic response is probably the cause of the conflicting results which have been reported in the literature.

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Enzymatic activity for the degradation of serum amyloid A (SAA) and amyloid A (AA) was detected in erythrolysates of normal subjects and patients with familial mediterranean fever. A significant difference between the activity of normal subjects and patients was not found. Serum inhibited the SAA (but not the AA) haemolysate proteolytic activity. Interindividual variation in the susceptibility of SAA to degradation by RBC haemolysates was shown. The original digestible fraction of SAA became gradually resistant to proteolytic cleavage over a 9 month period while the susceptibility of AA to degradation remained unchanged in this time period. These findings suggest that enzymatic degradation of SAA depends on the source of SAA, as well as inhibitory activity in serum.

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Serum amyloid A (SAA) and acid phosphatase (AcP) levels were determined in serial serum samples of 35 patients in different stages of dissemination and correlated with activity of carcinoma of the prostate. Up to 500-fold increases in SAA level were detected during active periods of cancer with a decrease towards the normal range in remission, in comparison with a 10-fold increase of AcP. The correlation between these two parameters was highly significant (P less than 0.001), but while SAA shows 100% sensitivity during the active stage, AcP shows only 85% sensitivity. It is suggested that although SAA is not a specific marker for any particular illness, due to its characteristic pattern of change in malignant diseases and its high sensitivity, it represents a useful biochemical parameter for the assessment of the activity of the disease to monitor response to therapy during follow-up.

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Serum amyloid A (SAA) levels were determined in the serial serum samples of eight rubella, 10 measles and seven subacute sclerosing panencephalitis (SSPE) patients. An early rise in SAA levels was detected in the acute phase in rubella and measles, followed by a prompt decrease in the convalescent phase. In a number of measles and rubella patients from whom early serum samples were available, the rise of SAA levels could be demonstrated before specific viral antibodies could be detected by complement fixation (CF) (measles) and haemagglutination inhibition (HI) (rubella). In only one rubella and one measles patient was no rise of SAA level detected. In SSPE only a moderate increase in SAA levels was noted except in one patient during a temporary deterioration, at which time the SAA level was very high; it returned to close to normal shortly thereafter. The possibility that SAA levels might be of value in monitoring the severity of infections, the recovery process and effects of anti-viral agents is discussed.

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