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Biomedical subjects

D A Fuccillo

Publications and source records attributed to D A Fuccillo.

At least 55 records · Page 3Linked to original sources
PubMed1975

Distribution of serotypes of hepatitis B surface antigen in an institution for the mentally retarded.

The serotypes of hepatitis B surface antigen present in patients at the Lynchburg Training School and Hospital were determined by counterelectrophoresis. Hepatitis B surface antigen was detected by counterelectrophoresis in 72 of 82 samples that were positive by complement fixation or passive hemagglutination techniques. Of the isolates that were serotyped, 51 (71 percent) were ad, and 21 (29 percent) were ay; thus the ad:ay ratio was about 2.4:1. The incidence of the ay serotype was significantly higher in females and in patients with Down's syndrome. The ay serotype was not randomly distributed in the institution but was clustered in two of seven female wards and four of 11 male wards, all of which contained younger patients who had been institutionalized at an early age.

Age Factors↗
PubMed1975

Cervical cytomegalovirus excretion in pregnant and nonpregnant women: suppression in early gestation.

Comparison of 659 pregnant and 202 nonpregnant women with similar demographic characteristics showed overall rates of cervical cytomegalovirus excretion that were identical (9.5% vs. 9.4%) and were surprisingly high, especially since 89% of the pregnant group possessed antibody to cytomegalovirus when admitted to the study. Prevalence of cytomegalovirus among gravidas was significantly lower during the first (1.6%) than during the third (11.3%) trimester. Thus, early pregnancy appeared to exert a suppressive effect on viral excretion that waned with advancing gestation. A similar but less significant occurrence was observed in the two groups with respect to viuria. Increasing age also appeared to suppress the virologic expression of cervical and urinary tract infection, whereas multiparity seemingly produced such an effect only in the cervix. Among both cervical and urinary excreters, a few shed virus thoughout pregnancy, and others shed virus intermittently; however, viral shedding most commonly began in late gestation and frequently continued into the postpartum period. Primary infection was not documented, and antibody status remained unchanged with the advent of viral excretion in most cases. Thus, reactivation of endogenous virus seems the most likely explanation for viral shedding in our population. Similar rates of isolation of Neisseria gonorrhoeae in excreters and nonexcreters further argue against the other major possibility, venereal reinfection.

Amniotic Fluid↗
PubMed1975

Cellular immune responses to Herpes simplex virus type 1 in recurrent herpes labialis: in vitro blastogenesis and cytotoxicity to infected cell line.

Cellular immunity to herpes simplex virus type 1 (HSV-1) in 12 volunteers with recurrent herpes labialis was evaluated by means of two microassays. In the blastogenesis assay, lymphocytes were incubated with tissue culture cells persistently infected with HSV-1. Uninfected cells were used as controls, and a blastogenic index was calculated. The mean blastogenic index (plus or minus SD) for subjects with recurrent herpes labialis was 26.9 (plus or minus 8.3); the mean blastogenic index (plus or minus SD) in control donors with antibody to HSV-1 was 13.4 (plus or minus 7.2). The difference between these values was statistically significant (t equals 4.154; P smaller than 0.001). In the cytotoxicity assay, cells of the same persistently infected line were used as target cells, and release of 51-Cr from these cells or from control cells served as the index of lymphocyte reactivity. Specific immune release attributable to HSV-1 averages 3.7% (plus or minus 1.8%) in subjects with recurrent herpes labialis, compared with 23.1% (plus or minus 9.8%) in controls (t equals 6.135; P smaller than 0.001). These data suggest a dissociation between mechanisms of cellular immunity, with enhanced lymphocyte blastogenesis but decreased cytotoxicity. Recurrent herpes labialis may thus result from subtle cellular immune deficiency involving at least one of the efferent mechanisms.

Adenoma↗
PubMed1975

Comparative serial virologic and serologic studies of symptomatic and subclinical congenitally and natally acquired cytomegalovirus infections.

Infants with congenitally (38) and natally (17) acquired cytomegalovirus infection were prospectively studied by means of virologic and multiple serologic assays. These infections were characterized by chronic viral excretion (measured in years). The quantity of virus excreted in the urine during early infancy was significantly greater in infants who acquired infection in utero, particularly amon those born with overt disease; thereafter, all three groups (congenital symptomatic, congenital asymptomatic, and natal) excreted similar amounts of virus. The patterns of antibody responses, particularly the fluorescent antibody response to the early antigen and the complement-fixing antibody response, further indicated that congenitally infected infants (especially symptomatic ones) bear a greater antigenic burden than do natally infected infants. From a diagnostic standpoint, the test for fluorescent antibody to the late antigen was the most sensitive assay, whereas the test for complement-fixing antibody proved to be the least useful, The indirect hemagglutination assay, although performed only in infants with natal infection, was only slightly less sensitive than the fluorescent antibody procedure; by the former technique, diagnostic rises were detected in all but one infant after the onset of viruria.

Antibodies↗
PubMed1975

Depressed specific cell-mediated immunity to Herpes simplex virus type 1 in patients with recurrent herpes labialis.

Cell-mediated immunity to herpes simplex virus type 1 (HSV-1) was assessed by a lymphocytotoxicity 51-Cr-release microassay procedure, using the MA-160 human prostatic adenoma cell line chronically infected with HSV-1 and its parent cell line as control. The specific immune release mean plus or minus standard deviation for nine asymptomatic patients with recurrent HSV-1 infections was 13.7 plus or minus 8.1%, compared to 28.9 plus or minus 8.4% in seven normal seropositive controls (P is less than 0.01). In four additional patients studied serially, the cell-mediated immunity was significantly increased during the recrudescence of herpetic infection, with a mean specific immune release value of 51.7 plus or minus 27.8%, compared to 8.7 plus or minus 1.5% during the convalescent period 2 to 10 weeks later (P is less than 0.05). These findings suggest that patients with recurrent HSV-1 infections have vigorous cellular immune responses during the acute phase but a specific impairment of cell-mediated immunity during the quiescent period, which may in part account for their susceptibility to recurrent herpetic infections.

Adenoma↗
PubMed1974

Utilization of a further miniaturized serological microtechnique.

A new 0.01-ml serological microtechnique system produced accurate and reproducible complement-fixation and indirect hemagglutination tests. This equipment involves the use of smaller amounts of antigens and sera, and thus increases the value of the method when employed with expensive reagents or limited qualities of sera.

Antibodies, Viral↗
PubMed1974

Impaired cellular immunity to rubella virus in congenital rubella.

Specific cell-mediated immunity (CMI) responses to rubella virus were studied in 12 children with documented congenital rubella syndrome employing a (51)Cr lymphocytotoxicity microassay. Hemagglutination inhibition antibody was detected in 11 of the 12 children, with titers ranging from 1:4 to 1:128. CMI to rubella virus was demonstrated in only 3 of the 11 antibody-positive children. The 12th child was negative for both hemagglutination inhibition and CMI. Of the three children with a positive CMI response, two had histories of reinfection with rubella virus. These data suggest that congenital rubella infection produces an impaired CMI response which subsequently may be altered by reinfection with rubella virus. The lack of CMI in the presence of antibody and concurrent excretion of live virus in the child with documented congenital rubella infection suggest a factor to be explored in the pathogenesis of this disease.

Adolescent↗
PubMed1973

Viral teratology.

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Animal Diseases↗