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Biomedical subjects

D W Reynolds

Publications and source records attributed to D W Reynolds.

At least 55 records · Page 3Linked to original sources
PubMed1978

Use of isolated nuclei in the indirect fluorescent-antibody test for human cytomegalovirus infection: comparison with microneutralization, anticomplement, and conventional indirect fluorescent-antibody assays.

Use of an antigen consisting of purified isolated nuclei from a mixture of human cytomegalovirus-infected and uninfected fibroblasts in a 2:1 ratio is a simple and reliable method for eliminating nonspecific fluorescence associated with the presence of Fc-immunoglobulin G receptors in the cytoplasm of infected cells. The specificity obtained with this antigen on 100 normal human sera was 99, 100, and 98% when compared with microneutralization, anticomplement immunofluorescence, and conventional indirect fluorescent-antibody assays, respectively. Also, 95% of the antibody titers obtained with the nuclear antigen had a perfect correlation with or were within a fourfold-dilution difference of the antibody levels obtained by anticomplement immunofluorescence and the conventional indirect fluorescent-antibody test.

Antibodies, Viral↗
PubMed1978

Alteration of the growth of cytomegalovirus and herpes simplex virus type 1 by epidermal growth factor, a contaminant of crude human chorionic gonadotropin preparations.

Pretreatment (12-48 h) of human fibroblasts with crude, human chorionic gonadotropin (HCG) was found to suppress cytomegalovirus infection and enhance productive herpes simplex type 1 (HSV) infection in vitro. Maximal effect on virus replication occurred at the time of maximal infectivity of control cultures (48 h and 6 days after viral innoculation for HSV and cytomegalovirus, respectively). The alteration in viral growth was not due to the HCG itself, but rather to epidermal growth factor, a contaminant of crude HCG. The effect of epidermal growth factor on viral infectivity was shown to be a cell-mediated event requiring protein synthesis.

Chorionic Gonadotropin↗
PubMed1977

Congenital cytomegalovirus infection.

The overall prevalence of congenital cytomegalovirus infection among the offspring of a highly immune young female population was 2.4 per cent (23 of 939). To ascertain whether the presence of anticytomegalovirus antibodies protects the developing fetus, we examined the offspring of 239 prospectively studied women. Despite substantial levels of preconceptional antibodies, intrauterine cytomegalovirus infection occured in seven of 208 (3.4 per cent) seroimmune women. Three neonates with congenital infection were born to 31 initially seronegative women. All the congenitally infected infants had subclinical involvement. Maternal humoral immunity may not protect the fetus against congenital cytomegalovirus infection. Neutralization kinetics and restriction enzyme analysis with endonucleases (EcoR-1 and HinD 111) demonstrated antigenic and genetic homology between viral strains isolated from two siblings consecutively infected in utero, indicating that repeat maternal infection with the same virus is transmissible to sequential products of conception.

Adolescent↗
PubMed1977

Specific impairment of cell-mediated immunity in mothers of infants with congenital infection due to cytomegalovirus.

Specific lymphocyte-mediated cytotoxicity to cytomegalovirus (CMV) in eight infants (six to 27 months old) with congenital CMV infection and in the mothers of six of these infants was evaluated with use of a 51chromium (51Cr)-release microassay. The control population consisted of 25 normal newborns, children, and adults. The titers of indirect hemagglutinating (IHA) antibody to CMV in the infected infants ranged from 1:16 to 1:1,024. All of these infants had detectable specific immune release of 51Cr that ranged from 3.3% to 48.9% (mean +/-SE, 21.0%+/-5.6%). The mothers of these infants demonstrated significantly elevated titers of IHA antibody to CMV (geometric mean titer, 1:410) as compared with a mean titer of 1:22 in controls (t = 5.71; P less than 0.001) but showed significantly depressed specific immune release (9.2% +/- 3.2%) compared with that of normal seropositive controls (24.8% +/- 2.8%; t = 3.31; P less than 0.001). In addition, two adult nulliparous women with persistent CMV viruria were also found to have depressed specific immune release to CMV (10.8% and 16.2%). These data suggest that a specific impairment in cell-mediated immunity to CMV occurs in mothers of infants with congenital CMV infection and in some persons who persistently excrete CMV.

Adult↗
PubMed1977

Immune complexes in congenital and natal cytomegalovirus infections of man.

The occurrence of circulating immune complexes was investigated in 31 patients with cytomegalovirus infection (29 infected in utero and 2 with natal infection) and 34 uninfected controls. Anti-complementary activity above 1:20 occurred in 34% (29/86) of the sera tested from the infected group in contrast to 7.5% (3/40) in the controls (P < 0.005). When assayed by means of a lymphoblastoid cell line (Raji cell test), the reactivity in these groups was 45 (39/86) and 2.7% (1/36), respectively (P < 0.001). Correlation of results between these two complement-dependent assays occurred in 75% of samples collected from the infected group. Frequency of reactivity was higher in severe intrauterine infection and during the 1st yr of life paralleling the patterns of viral excretion and humoral immune responses. Physicochemical characterization demonstrated that reactive substances in sera were acid-dissociable and, in one sample tested, contained 7S IgG antibodies with cytomegalovirus (CMV) specificity. Circulating immune complexes were heavier (18-22S) in sick, as opposed to subclinically CMV-infected patients, in whom intermediate size complexes (12-16S) were found. In three of four symptomatic patients whose demise was due to severe congenital infection, granular deposits of immunoglobulins and C3 were detected in a pattern typical of immune complexes along the glomerular basal membrane of the glomeruli. Whether or not circulation and deposition of heavier immune complexes contributed to the adverse clinical outcome is unresolved. Because of the high incidence of both congenital and natal CMV infections, definition of the pathogenetic potentials of both heavy and intermediate size immune complexes is required to design more effective therapeutic measures.

Antibodies, Viral↗
PubMed1977

Auditory and visual defects resulting from symptomatic and subclinical congenital cytomegaloviral and toxoplasma infections.

Sensorineural hearing loss was present in ten of 59 (17%) patients with congenital cytomegalovirus (CMV) infection (three of eight born with symptomatic and seven of 51 born with subclinical infection). The defect was bilateral in eight, moderate to profound in eight, and of progressive nature in two. Hearing loss did not occur in 21 patients with natal CMV infection nor in seven of 12 patients with congenital toxoplasmosis. Histopathologic and immunofluorescent studies of the inner ear in two of three neonates who died with severe infection revealed that viral antigens were widely distributed in cochlear structures. Eye pathology was associated only with congenital Toxoplasma (nine of 12) and CMV (seven of 43) infections. Visual impairments were more prominent and severe in those born with symptomatic infections, exclusively so with CMV. However, ocular defects, in particular chorioretinitis, developed after birth in five of eight patients born with asymptomatic congenital toxoplasmosis. These data firmly establish clinically inapparent congenital CMV infection as a major public health problem and confirm the fact that congenital toxoplasmosis may be associated with late-appearing, debilitating chorioretinitis.

Audiometry↗
PubMed1976

Protracted pneumonitis in young infants associated with perinatally acquired cytomegaloviral infection.

Two infants developed a protracted pneumonitis with lower respiratory obstruction beginning at one month of age. Lung biopsy in one suggested a viral etiology which prompted an extensive investigation of each infant for specific etiology. Virologic, serologic, immunologic, and electronmicroscopic studies indicated that cytomegalovirus was a major causative factor. The infections were apparently acquired at birth from infected maternal genital tracts and have persisted for prolonged periods of time. Evidence for gross immunologic defect as a precipitating cause was lacking. These infants serve to emphasize the possible pathologic potential of CMV when acquired in early life even in the absence of iatrogenic immunosuppression.

B-Lymphocytes↗
PubMed1976

Perinatal infection: diagnosis, treatment, and prevention.

The majority of clinically recognizable acute infections in the neonate are bacterial. Such infections may be acquired from the mother prior to or at birth or from environmental sources. Because of the limited ability of neonates--especially those born prematurely--to express symptoms, even minor deviations from normal behavior should suggest bacterial disease. Chronic congenital and perinatal infections, unlike acute bacterial disease, are generally asymptomatic in mother and neonate and may remain latent or subclinically active in host tissue for prolonged periods, possibly causing insidious injury to the central nervous and perceptual systems. When overt, these infections almost invariably cause mental or perceptual handicaps or both. In view of the significant mortality and morbidity associated with either acute or chronic infections, diagnosis and treatment should be aggressive.

Acute Disease↗
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↗