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At least 19 recordsLinked to original sources
PubMed1979

Antibody to early antigens of varicella-zoster virus during varicella and zoster.

IgG antibody to the early antigens of varicella-zoster virus (VZV) was studied during both varicella and zoster by the indirect immunoperoxidase antibody technique. In parallel, complement-fixing, immune-adherence hemagglutinating, IgG, and IgM antibodies to VZV were studied. In both varicella and zoster infections, antibody to the early antigens of VZV appeared three to five days after onset of infection, reached a peak during the second week, and progressively decreased in titer until it disappeared, usually within two months. This antibody usually appeared slightly later than IgG or IgM antibody and grossly correlated with IgM antibody in varicella. In zoster infections, IgM antibody to VZV was not found by the immune-adherence hemagglutination assay at a titer of greater than or equal to 1:4, whereas antibody to the early antigens showed a curve similar to that found in varicella. It is suggested that antibody to the early antigens of VZV be considered as a marker of acute VZV infection, which is associated with a specific and significant IgM antibody response in varicella but not in zoster.

Adolescent↗
PubMed1975

Varicella-Zoster Immunoglobulins during Varicella, Latency, and Zoster.

Antibodies to membrane antigens of cells infected by varicella-zoster virus were detected by immunofluorescence. Rises in varicella-zoster IgA, IgG, and tigM were detected after both varicella and zoster. Prompt antibody responses were observed in patients with generalized zoster as well as in those with localized zoster. A delayed response was found, moreover, in one patient who did not develop disseminated disease. Antibody to varicella-zoster virus was detected in the sera of all three patients tested prior to and in all but one of 63 patients tested soon after onset of zoster. The level of varicella-zoster IgA and IgG rose in two of three immune patients after household exposure to infection with varicella-zoster virus. Varicella-zoster IgG was detected in the cord blood of infants whose mothers were immune to varicella.

Adolescent↗
PubMed1979

Cellular and humoral immune responses to varicella-zoster virus in immunocompromised patients during and after varicella-zoster infections.

Humoral and cell-mediated immune responses to varicella-zoster (V-Z) virus were assessed in patients during and after V-Z infections. Ongoing V-Z infections was associated with minimal cellular immunity but not necessarily with poor humoral immunity. Recovery from V-Z infection was associated with a vigorous cellular immune response. Cell-mediated immunity to V-Z virus was demonstrable for years after varicella, but responses were lower in immunocompromised patients than in normal individuals.

Adolescent↗
PubMed1979

Studies on the polypeptides of varicella-zoster (V-Z) virus. 1. Detection of varicella-zoster virus polypeptides in infected cells.

Virus-induced polypeptides in cells infected with varicella-zoster virus (VZV) were analyzed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and autoradiography. When human embryonic lung (HEL) cells infected with the Oka strain of VZV were labelled with 35S-methionine or 14C-glucosamine from 40 hr to 46 hr after infection, at least 18 VZV-induced polypeptides and 10 glycoproteins could be identified in the infected cells. The molecular weights of the polypeptides and glycoproteins ranged from about 145,000 to 23,000, and from about 105,000 to 48,000, respectively. Lysates of VZV-infected cells were treated with specific antisera prepared in green monkeys or guinea-pigs, and analysed by SDS-PAGE and fluorography. In all, 33 polypeptides (with molecular weight of about 145,000 to 22,000) and 13 glycoproteins (molecular weight, about 105,000 to 38,000) were found in the immunoprecipitates. None of these polypeptides and glycoproteins were detected when infected cells cultured in the presence of phosphonoacetic acid (PAA) were treated in the same way.

Cell Line↗
PubMed1979

Varicella-zoster virus immunizes patas monkeys against simian varicella-like disease.

To define further the antigenic relationship between human varicella-zoster virus and herpesviruses which produce varicella-like disease in certain simian species, patas monkeys were inoculated with varicella-zoster virus and then challenged with Delta herpesvirus, which uniformly produces severe, clinically apparent disease in susceptible animals. Protection against Delta herpesvirus was conferred both by hyperimmunization with varicella-zoster virus and by a single immunization with a cell-free preparation of varicella-zoster virus. Although the immunological relationship between the human and simian varicella viruses is not completely reciprocal, these studies confirmed that antigens which induce immunity are shared by the human and simian viruses. No clinical symptoms were seen in monkeys inoculated with varicella-zoster virus, but the rapid and marked antibody responses to the virus suggested that subclinical infection had occurred. In contrast, a chimpanzee inoculated with one of the same varicella-zoster virus preparations produced only low levels of antibody.

Animals↗
PubMed1979

Nervous system complications of herpes zoster: immunofluorescent demonstration of varicella-zoster antigen in CSF cells.

In nine out of 11 patients with herpes zoster and neurological symptoms varicella-zoster antigen was demonstrated in CSF cells by indirect immunofluorescent staining. Cerebrospinal fluid cytology was in most cases highly suggestive of viral infection. This study demonstrates the value of both immunofluorescent staining on CSF cells and CSF cytology, as corroboration of an otherwise exclusively serologically based virological diagnosis.

Adolescent↗
PubMed1975

Infection of guinea-pig embryo cells with varicella-zoster virus.

Varicella-zoster (VZ) virus has been shown to replicate in guinea-pig embryo (GPE) cells. When cell-free virus inocula were used, no infectious virus was liberated from these cells, either by freezing-thawing or ultrasonic disruption. However, cell-free virus was separated from GPE cells inoculated with infected human embryonic lung (HEL) cells.

Animals↗
PubMed1978

Effect of transfer factor and zoster immunoglobulin in patients with varicella-zoster infection and malignancy.

Immunotherapy was given to 13 patients suffering from lymphoproliferative diseases complicated by varicella-zoster (VZ) infection. Five patients received transfer factor (TF) only, 6 received TF and zoster immunoglobulin (ZIG), and 2 received ZIG only. ZIG did not seem to alter the course of the infection. Cessation of vesicle formation and initiation of crust formation took place within 1 day after the first injection of TF in 5 patients with a localized zoster. In 4 patients suffering from an early dissemination of VZ infection, cessation of vesicle formation took place within 1 day (1 patient), 2 days (1 patient), 3 days (1 patient) or 4 days (1 patient) after the first injection of TF. An increase in serum interferon was observed in 4 of 9 patients who received TF, while no increase in serum interferon was observed in the control groups. Administration of a high-titer ZIG preparation did not seem to depress the humoral antibody response when combined with TF therapy. Therapy with TF in combination with ZIG seemed to have a beneficial effect in patients with malignancy when administered early in the acute VZ infection.

Adolescent↗
PubMed1979

Appearance of immunoglobulin G Fc receptor in cultured human cells infected with varicella-zoster virus.

After infection with varicella-zoster virus, HeLa and human embryo lung cells developed a receptor for the Fc portion of human and rabbit immunoglobulin G. The receptor was detected by both hemadsorption and immunofluorescence, using antibody-coated erythrocytes and heat-aggregated immunoglobulin G. However, sheep erythrocytes sensitized with F(ab')2 of anti-sheep erythrocyte antibody did not adsorb to the receptor. When cell-free varicella-zoster virus was inoculated into the HeLa cell monolayer, the Fc receptor appeared at first 6 h after infection; varicella-zoster virus antigen in the cytoplasm and detectable cytopathic effects appeared later.

Animals↗
PubMed1977

[Prognosis of prenatal varicella-zoster-infections in relation to their onset during pregnancy (author's transl)].

7 children were observed, whose mothers had Varicella-Zoster-Virus-infection. 3 of these children developed postnatal Herpes Zoster without Varicella in their history; 1 child had Varicella in the neonatal period. There are indications that primary infection with Varicella-Zoster-Virus during the first four months of pregnancy may cause deformities in the child; the same during the last five days of pregnancy increases the risk of varicella with a complicated course in the newborn. Independent of the time of infection during pregnancy the prognosis of a secondary Varicella-Zoster-Virus-infection in the mother seems always to be good for the child. Aspects of the child's immunological maturation, still incomplete at birth, are discussed and can help to understand the different prognoses during pregnancy. The importance of serological diagnosis has been emphasized.

Chickenpox↗
PubMed1977

A longitudinal study of varicella-zoster virus infections in renal transplant recipients.

A serum bank maintained for renal transplant recipients allowed for a longitudinal study of antibody responses before and after herpes zoster. Renal transplant recipients without herpes zoster served as controls. Antibody responses to varicella-zoster virus, herpes simplex virus type 1, and cytomegalovirus were measured. The serological responses following herpes zoster were prompt and sustained (in the majority of cases), transient, or not present at all. Zoster without an eruption occurred (apparent only on retrospective chart review) and furnished an explanation for unexplained unilateral pain syndromes in these patients. Asymptomatic rises in titer of antibody to varicella-zoster virus not explained by rises in antibody to herpes simplex virus occurred in both groups. This latter finding points to an unstable relation between virus and host and supports and hypothesis of Hope-Simpson that subclinical release of virus with resulting antigenic stimulation may maintain immunity to varicella-zoster virus. Patients with herpes zoster and controls did not differ in several humoral immune parameters that might have explained the occurrence of herpes zoster. There was no evidence that herpes zoster precipitated renal graft rejection.

Antibodies, Viral↗
PubMed1975

Neutralizing antibody responses to varicella-zoster virus.

Neutralization of varicella-zoster (V-Z) virus by human sera and immune rhesus monkey sera was enhanced by fresh guinea pig complement. There was no marked difference in the degree to which complement enhanced neutralization by sera from current V-Z virus infections and sera from long-past varicella infections. Immunoglobulin G neutralizing antibody in sera from varicella cases was enhanced by complement to a slightly higher degree than was immunoglobulin M (IgM) antibody, and immunoglobulin G neutralizing antibody in immune monkey sera was enhanced to a much greater degree than was IgM antibody. There was a rapid decline in the complement requirement of IgM neutralizing antibodies over the course of immunization of the rhesus monkeys. V-Z neutralizing antibody titers in the presence of complement were higher than complement-fixing titers of the same sera in all groups of individuals studied. IgM neutralizing antibody for V-Z virus was demonstrable in all cases of varicella but in only 1 of 22 zoster cases, and V-Z IgM neutralizing antibody was not detectable in primary herpes simplex virus infections in which heterotypic antibody titer rises occurred to V-Z virus. Complement-fixing antibody for V-Z virus was absent in 19S serum fractions which contained IgM neutralizing antibody for the virus.

Animals↗
PubMed1978

Quantitation of antibodies to varicella-zoster virus by immune adherence hemagglutination.

Immune adherence hemagglutination was compared with the complement fixation test as a means of measuring antibodies to varicella-zoster virus. Analysis of acute- and convalescent-phase sera from patients infected with varicella-zoster or with herpes simplex virus showed the immune adherence hemagglutination test to be more sensitive than the complement fixation test, and greater cross-reactivity between the two viruses appeared to be associated with the increased sensitivity. The two assay methods were used to measure antibodies to varicella-zoster virus in 265 sera obtained from patients of different ages as well as sera from 26 patients with leukemia. There were 35 cases where antibodies were detected by immune adherence hemagglutination but not by complement fixation, whereas in five cases the converse was found. Our findings support the contention that immune adherence hemagglutination is the method of choice for detecting antibodies to varicella-zoster virus.

Acute Disease↗
PubMedDate not supplied

The ocular manifestations of herpes zoster, varicella, infectious mononucleosis, and cytomegalovirus disease.

Herpes zoster, caused by varicella-zoster (V-Z) virus which also causes varicella (chickenpox), is usually a benign self-limited disease. However, when the ophthalmic division of the trigeminal nerve is affected, the ocular disease (ophthalmic zoster), although also usually mild and self-limited, may have severe complications (corneal scarring, glaucoma, iris atrophy, posterior synechiae, scleritis, motor disturbances, optic neuritis, retinitis, anterior segment necrosis, and phthisis bulbi and servere postherpetic neuralgia). Varicella affects the eye rarely (except for the typical lid lesions), but associated conjunctival and corneal lesions, iridocyclitis, glaucoma, chorioretinitis, and optic nerve lesions have been described. Infectious mononucleosis may involve the eye either by direct involvement or from a remote focus such as the central nervous system. Ocular manifestations of cytomegalovirus disease is usually limited to the choroid and retina unless involvement of the developing embryo occurs prior to the development of the eye.

Adolescent↗
PubMed1978

Antibody assays for varicella-zoster virus: comparison of enzyme immunoassay with neutralization, immune adherence hemagglutination, and complement fixation.

An enzyme immunossay (EIA) was adapted for detection of antibody to varicella-zoster virus, and its sensitivity and specificity were compared with those of neutralization, immune adherence hemagglutination (IAHA), and complement fixation tests. Test sera showed little nonspecific reactivity in the EIA system, and valid results could usually be obtained at serum dilutions as low as 1:8. Demonstration of the presence or absence of varicella-zoster viral antibody by EIA showed 94% correlation with results obtained in neutralization tests, but EIA titers were 2- to 16-fold higher than neutralizing antibody titers. Results by IAHA showed 87% correlation with those obtained by neutralization. No false positive IAHA results were seen, but a number of false negative IAHA results were seen at the 1:8 serum dilution, particularly in older individuals. With increasing age (>40 years), and presumably increased time from varicella infection, neutralizing antibody levels generally declined to 1:8 or 1:16, EIA levels fell to 1:128 or 1:256, and IAHA and complement fixation antibody titers were usually <1:8 or 1:8. EIA and IAHA were as reliable as the neutralization and complement fixation tests for serodiagnosis of varicella and zoster infections. All tests demonstrated heterotypic varicella-zoster antibody titer rises in selected patients with initial herpes simplex virus infections, but fewer heterotypic responses were seen by EIA than by the other methods. EIA offers a rapid, sensitive, and specific method for varicella-zoster antibody assay that is applicable to use in a clinical setting.

Adolescent↗
PubMed1976

Improved yields of cell-free varicella-zoster virus.

Systematic studies on the replication of varicella-zoster virus in infected human fetal diploid lung cells have defined more optimal conditions for infection and harvesting of cultures and have led to the production of cell-free virus preparations with infectivity titers of greater than or equal to 10(6) plaque-forming units per ml. The highest yields of cell-free virus were obtained by (i) sonic treatment of the cellular phase of cultures inoculated with trypsin-dispersed infected cells at ratios of 1 infected cell to 6 to 10 uninfected cells in the monolayer and (ii) harvesting cells after 24 to 36 h of incubation at 36 degrees C. At this time the cultures showed minimal viral cytopathic effect. Spread of infectivity occurred much more rapidly in cultures inoculated with whole infected cells than in those infected with cell-free virus. Complement-fixing antigens with improved titers of greater than or equal to 1:128 were prepared from varicella-zoster virus-infected cell cultures in the same manner as cell-free virus, but harvested after 3 to 4 days of incubation when the cultures showed an advanced cytopathic effect.

Antigens, Viral↗