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Biomedical subjects

C A Daniels

Publications and source records attributed to C A Daniels.

33 records · Page 2Linked to original sources
PubMed1975

Shedding of infectious virus/antibody complexes from vesicular lesions of patients with recurrent herpes labialis.

The concentration of herpes-simplex virus (H.S.V.) in the lesions of adults with recurrent herpes labialis was determined. On the 1st day the vesicle appeared, the fluid within the lesion contained 10(5-3) plaque-forming units (P.F.U.) of H.S.V./mul. By swabbing the surface of the lesions with a sterile pledget, 10(6-2) P.F.U. of virus was isolated from the inflamed labial mucosa. The amount of virus obtained from the labial surface decreased on the 2nd and 3rd day to 10(5-0) and 10(3-0) P.F.U., respectively. In two patients on immunosuppressive drugs, high concentrations of virus (greater than 10(4-0) P.F.U.) were obtained per swab for more than 3 weeks. The presence of infectious virus-antibody (V.A.) complexes in herpetic lesions was demonstrated by examining fifty-two isolates from twenty-eight patients at various times during the course of their disease. 71% of the patients had V.A. complexes in their lesions on the 1st day of the vesicular eruption, and by the 3rd day all of the lesions examined contained complexes. It is concluded that patients with active lesions shed high concentrations of virus and that natural infection may be transmitted by an infectious V.A. complex.

Antibodies, Anti-Idiotypic↗
PubMed1975

Effect of staphylococcal protein A on complement-potentiated neutralization of herpes simplex virus and immune lysis of virus-infected cells.

Interaction of staphylococcal protein A (SPA) with human serum depressed the ability of such serum to neutralize herpes simpled virus (HSV)-antibody labialis. SPA-induced depression of serum-dependent virus neutralization appeared to be due to consumption of complement by SPA. In addition, SPA attached to antibody-treated, HSV-infected cells and inhibited complement mediated immune cytolysis. The amount of inhibition obtained depended upon the with the infected cells. The possible significance of SPA in the pathogenesis of viral disease complicated by secondary staphylococcal infection is discussed.

Animals↗
PubMed1975

The interaction of rheumatoid factor with hepatitis B surface antigen-antibody complexes.

A solid phase radioimmunoassay was developed in which the hepatitis B surface antigen was adsorbed to the surface of plastic beads. When the antigen-coated beads were incubated with human IgG antibody against hepatitis B surface antigen, immune complexes were formed on the solid phase surface. IgM rheumatoid factor was found to bind to the hepatitis B surface antigen-antibody complexes but not to the antigen or the IgG antibody alone. Since both hepatitis B surface antigen-antibody complexes and rheumatoid factor are commonly present in type B viral hepatitis, it is suggested that rheumatoid factor may play a role in the pathogenesis of this viral disease in man.

Antibodies, Viral↗
PubMed1975

Lymphoid cell necrosis, thymic atrophy, and growth retardation in newborn mice inoculated with murine cytomegalovirus.

During studies on the effect of murine cytomegalovirus on the developing retina, virus was inoculated into the eyes of newborn Swiss mice, and the animals were sacrificed at various times thereafter. Controls consisted of mice inoculated with ultraviolet-inactivated murine cytomegalovirus and uninjected mice. Marked lymphoid cell necrosis, thymic atrophy, pronounced growth retardation, bacteremia, and death occurred in the animals inoculated with live virus. this virus-induced injury resulted in a marked depletion of lymphocytes in the subcapsular and cortical areas of the thymus as well as in the spleen, lymph nodes, and Peyer's patches. Areas of necrosis with viral inclusions were present at the site of inoculation and in various other organs including the spleen and bone marrow. Since growth retardation has been associated with thymic atrophy due to other causes, the observed abnormal physical development in the present study was interpreted as a sequel to the thymic injury. An implication of this study is that some human infants with concomitant immune deficiency and viral infection may have a primary viral disease with resultant secondary lymphoid tissue alterations, rather than a thymic disorder with a subsequent viral infection.

Animals↗
PubMed1974

Experimental cytomegalovirus ophthalmitis.

Cytomegalovirus can produce a severe necrotizing chorioretinitis in patients on immunosuppressive therapy and infants born with congenital cytomegaloviral inclusion disease. To study the effect of cytomegalovirus on the eye, murine cytomegalovirus was injected into the eyes of nonimmunosuppressed Swiss CD-1 weanling mice. The eyes were then prepared for virus titer, as well as light and electron microscopy at variable periods after inoculation (1 to 28 days). From days 2 to 6, the hallmarks of cytomegalovirus infection, intranuclear and intracytoplasmic viral inclusions, were evident within cytomegalic cells. The major site of reaction was in the uveal tract, where necrosis and inflammation were prominent. Viral particles budding through the nuclear membranes into the perinuclear cisternae and vacuoles with viral particles could be seen in the cytoplasm of infected cells. In lesions older than 2 weeks, only a mild mixed inflammatory infiltrate and fibrosis were observed. Morphologic alterations unaccompanied by inflammation occurred in the outer sensory retina overlying infected retinal pigment epithelial cells. Multiple necrotic foci with inclusion-bearing cells in the liver indicated the systemic spread of virus from the eye. The titer of virus recovered from the eye peaked at day 4 and then declined to low levels, but infectious virus could still be isolated at day 28, even though viral particles were not seen morphologically at or after day 14. Many of the alterations seen in the model resemble those found in the human cytomegaloviral ophthalmitis.

Animals↗
PubMed1971

Interaction of rheumatoid factor with infectious herpes simplex virus-antibody complexes.

Rheumatoid factor, a human immunoglobulin of the IgM class, failed to attach to herpes simplex virus but did attach to infectious complexes composed of herpes simplex virus and antibody to herpes simplex virus. These newly formed complexes of infectious virus, antiviral antibody, and rheumatoid factor could be neutralized by complement or by antibody to human IgM. The ability of rheumatoid factor to enhance virus neutralization in the presence of complement represents a hitherto unrecognized biological role for rheumatoid factor.

Animals↗
PubMed1970

Neutralization of sensitized virus by purified components of complement.

Herpes simplex virus which had been sensitized with immunoglobulin M antibody was neutralized by serum deficient in the fifth and sixth components of complement (C) but not by serum deficient in the fourth component C (C4). The sequential addition of the functionally purified components of C showed that the activated first component of C (C1[unk]) failed to neutralize sensitized virus. However, in the presence of an optimal concentration of C1[unk], the addition of C4 resulted in neutralization. The amount of virus neutralized was dependent upon the concentration of immunoglobulin M used to sensitize the virus and the concentration of C1[unk] and C4. The addition of the second component of C (C2) to reaction mixtures containing an optimal concentration of C1[unk] and a limiting concentration of C4 resulted in increased neutralization and the amount of virus neutralized was dependent upon the concentration of C2. The addition of the third component of C (C3) to reaction mixtures containing an optimal concentration of C1[unk] and limiting concentrations of C4 and C2 also resulted in increased neutralization and the amount of virus neutralized was dependent upon the concentration of C3.

Animals↗
PubMed1969

Neutralization of sensitized virus by the fourth component of complement.

Herpes simplex virus which had been sensitized with IgM antibody was not neutralized by the addition of the purified activated first component of complement. In the presence of an optimum concentration of the first component of complement, however, the sensitized virus was neutralized by the addition of a high concentration of the purified fourth component of complement. Under these conditions, the addition of the purified second and third components of complement failed to enhance virus neutralization. With low concentrations of the fourth component of complement, the addition of the second and third components enhanced virus neutralization.

Animals↗