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PubMed2004

High avidity anti-beta 2-glycoprotein I antibodies in patients with antiphospholipid syndrome.

OBJECTIVE: To evaluate avidity of IgG anti-beta 2-glycoprotein I antibodies (anti-beta2-GPI) in patients with antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE) in relation to thrombosis, and to demonstrate a possible affinity maturation of IgG anti-beta 2-GPI during the disease course. METHODS: 64 sera from 32 patients (18 with primary or secondary APS, 14 with SLE without APS) and their respective IgG fractions or affinity purified anti-beta 2-GPI were studied by anticardiolipin (aCL) and anti-beta 2-GPI enzyme linked immunosorbent assay and by chaotropic assay. RESULTS: Six, 12, and 14 patients had high, low, and heterogeneous avidity IgG anti-beta 2-GPI, respectively. In 12 patients an increase in antibody avidity was observed over a period of between four and 12 years. More patients with APS were in the high avidity than in the low avidity anti-beta 2-GPI group, while the opposite was observed for SLE alone (both p<0.05). The most common clinical feature among patients with high avidity anti-beta 2-GPI was thrombosis, mainly venous thrombosis (p<0.05 and p<0.02, respectively, v the low avidity anti-beta 2-GPI group). CONCLUSIONS: Patients with APS with or without SLE may have anti-beta2-GPI of high, low, or heterogeneous avidity. High avidity anti-beta 2-GPI appear to be associated with thrombosis and APS, while in pure SLE low avidity anti-beta 2-GPI may prevail. Monitoring of avidity may help elucidate the role of anti-beta 2-GPI affinity maturation in the pathogenesis of APS.

Adult↗
PubMed2004

A new method for determination of varicella-zoster virus immunoglobulin G avidity in serum and cerebrospinal fluid.

BACKGROUND: Avidity determination of antigen-specific immunoglobulin G (IgG) antibodies is an established serological method to differentiate acute from past infections. In order to compare the avidity of varicella-zoster virus (VZV) IgG in pairs of serum and cerebrospinal fluid (CSF) samples, we developed a new technique of avidity testing, the results of which are not influenced by the concentration of specific IgG. METHODS: The modifications introduced for the new VZV IgG avidity method included the use of urea hydrogen peroxide as denaturing reagent, the adaptation of the assay parameters in order to increase the sensitivity for the detection of low-level VZV IgG in CSF, and the use of a new calculation method for avidity results. The calculation method is based on the observation that the relationship between the absorbance values of the enzyme immunoassays with and without denaturing washing step is linear. From this relationship, a virtual absorbance ratio can be calculated. To evaluate the new method, a panel of serum samples from patients with acute and past VZV infection was tested as well as pairs of serum and CSF. RESULTS: For the serum panel, avidity determination with the modified assay gave results comparable to standard avidity methods. Based on the coefficient of variation, the new calculation method was superior to established methods of avidity calculation. CONCLUSIONS: The new avidity method permits a meaningful comparison of VZV IgG avidity in serum and CSF and should be of general applicability for easy determination of avidity results, which are not affected by the concentration of specific IgG.

Acute Disease↗
PubMed1974

Isolation of antigen-binding cells from unprimed mice: demonstration of antibody-forming cell precursor activity and correlation between precursor and secreted antibody avidities.

Cells binding DNP groups conjugated to fluoresceinated mouse gamma globulin ((F)DNP-MGG) were isolated from spleens of unprimed mice using a fluorescence-activated cell sorter (FACS). The isolated cells were specifically enriched at least 100-fold for anti-DNP precursor activity in an adoptive transfer assay as compared to unfractionated spleen. The fraction depleted of binding cells, although depleted of anti-DNP precursor activity, responded as well as unfractionated spleen when assayed for anticarrier (keyhole limpet hemocyanin [KLH]) precursor activity. High avidity binding cells were stained using low concentrations of (F)DNP-MGG. Medium and low avidity binding cells were stained using high concentrations of (F)DNP-MGG in the presence of free hapten which selectively blocked staining of the high avidity binding cells. Cells were supplemented with an excess of carrier-primed (KLH), nylon-purified splenic T cells and transferred to irradiated recipients. DNP-KLH was given at transfer and 5 days later. The anti-DNP plaque-forming cell (DNP-PFC) response and the avidities of the DNP-PFC in the irradiated recipients were measured by hapten inhibition of direct PFC plaque formation 12 days after transfer. At this time, very few indirect PFC were found. There was a positive correlation between the avidity of the DNP-binding cells and the avidity of the anti-DNP antibody secreted by their progeny. High avidity DNP-binding cells gave rise to predominantly high avidity anti-DNP-PFC. Medium and low avidity binding cells gave rise to medium and low avidity DNP-PFC.

Animals↗
PubMed2007

Impact of spiramycin treatment and gestational age on maturation of Toxoplasma gondii immunoglobulin G avidity in pregnant women.

The objective of the present study was to investigate the maturation of immunoglobulin G (IgG) avidity after Toxoplasma gondii seroconversion during pregnancy and the factors that affect IgG avidity over time. The study used 309 serum samples from 117 women and a multiple linear mixed regression analysis to show the patterns of variation of IgG avidity throughout gestation. The IgG avidity ratios and the patterns of their evolution with time were quite diverse among the women and were statistically heterogeneous (P = 0.011); however, the trend was toward a statistically significant increase (P < 0.0001). On average, a 1.0167-fold increase was observed for each additional gestational week after the putative date of infection. At 12 weeks after putative infection (the expected IgG avidity maturation time), the mean avidity ratio was 16.6% (95% confidence interval, 15.4 to 17.9%). At all times, the avidity ratio remained significantly heterogeneous among the women (P < 0.05); for 95% of them, that ratio ranged from 7.8 to 35.3% at 12 weeks after putative infection. Maternal age at the putative time of infection did not influence the maturation of IgG avidity. However, on average, a 1.009-fold decrease (P = 0.03) in that avidity was observed for each additional week of gestational age before infection and a 1.03-fold increase (P = 0.0003) was observed for each additional week of delay to the onset of spiramycin treatment. The rate of increase in the avidity ratio was lower if infection occurred late in pregnancy and higher if the delay to treatment was long. This information cannot allow accurate determination of the delay since the time of infection. The present results provide support for interpretation of the assay and caution against overinterpretation.

Animals↗
PubMed2001

Avidity, potency, and cross-reactivity of monoclonal antibodies to pneumococcal capsular polysaccharide serotype 6B.

Many pneumococcal capsular polysaccharides (PSs) are similar in structure, and a pneumococcal antibody often binds to all of the PSs with a similar structure. Yet, these cross-reactive antibodies may bind to the structurally related pneumococcal capsular PSs with an avidity too low to be effective. If memory B cells producing such weakly cross-reactive antibodies are elicited with pneumococcal conjugate vaccines, the memory cells for low-avidity antibodies could compromise the subsequent immune responses to the cross-reactive PS (original antigenic sin). To investigate these issues, we produced 14 hybridomas secreting monoclonal antibodies (MAbs) to the capsular PS of Streptococcus pneumoniae serotype 6B by immunizing BALB/c mice with antigens containing 6B PS and studied their epitope, avidity, in vitro opsonizing capacity, in vivo protective capacity, and "antigen binding titer" by enzyme-linked immunosorbent assay (ELISA) of 6A and 6B capsular PSs. Six MAbs bound to the non-cross-reactive 6B-specific epitope, and seven MAbs bound to the cross-reactive epitope present in both 6A and 6B PSs One MAb (Hyp6BM6) revealed a novel epitope. This epitope was found on 6A PS in solution, but not on 6A PS adsorbed onto the plastic surface of the ELISA plates. The avidity of the MAb for 6A or 6B PS ranged from 7.8 x 10(6) M(-1) to 4.1 x 10(11) M(-1). No MAbs were weakly cross-reactive, since none of the cross-reactive MAbs showed any tendency toward having less avidity to 6A PS (the cross-reactive PS) than to 6B PS. Avidity influenced the results of several antibody assays. When all of the hybridomas were examined, avidity strongly correlated with the titer of a unit amount of MAb to bind antigen-coated ELISA plates (r = 0.91) or to opsonize pneumococci in vitro (r = -0.85). Because both assay results are avidity dependent, the ELISA and the opsonization assay results were strongly correlated (r = 0.91), regardless of avidity. Avidity also correlated with the potency of a MAb to passively protect mice against pneumococcal infections. When only the immunoglobulin G hybridomas were examined, little increase in opsonizing capacity and in vivo protective potency was observed above 10(9) M(-1). Taken together, an ELISA measuring antigen binding titer may be an adequate measure of the protective immunity induced with pneumococcal vaccines, and the absence of a partially cross-reactive MAb suggests that antigenic sin may not be significant in responses to vaccines against the S. pneumoniae 6B serotype.

Animals↗
PubMed1975

Antibody avidity for native DNA in lupus nephritis.

To study the participation of the antibody avidity in the pathogenesis of lupus nephritis, we measured the antibody avidity to native DNA by the method of Minden and Farr (14) in patients with SLE. The avidity to native DNA was almost less than 40%. The avidity and the histological activity of lupus nephritis were well correlated; the antibody avidity of the active-group sera was higher than that of the inactive-group sera and the group without nephritis. In the group with antibodies of relatively high avidity, the complexes were deposited mainly in the subendothelial side of GBM and in the mesangium. On the other hand, in the group with low-avidity antibodies, the complexes were localized in the subepithelial side of GBM. On investigating the quality of the complexes, we noted that the complexes composed of high-avidity antibodies prepared in vitro were larger than those of low avidity and the former were larger than 19S. If the native-DNA-anti-native DNA system is the mechanism basic to lupus nephritis, the differences in immune response of the host, namely the degree of antibody avidity may greatly affect complex formation and influence the histological activity and nephritogenicity of lupus nephritis.

Adult↗
PubMed2005

Developmental control of CD8 T cell-avidity maturation in autoimmune diabetes.

The progression of immune responses is generally associated with an increase in the overall avidity of antigen-specific T cell populations for peptide-MHC. This is thought to result from preferential expansion of high-avidity clonotypes at the expense of their low-avidity counterparts. Since T cell antigen-receptor genes do not mutate, it is puzzling that high-avidity clonotypes do not predominate from the outset. Here we provide a developmental basis for this phenomenon in the context of autoimmunity. We have carried out comprehensive studies of the diabetogenic CD8 T cell population that targets residues 206-214 of the beta cell antigen islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP(206-214)) and undergoes avidity maturation as disease progresses. We find that the succession of IGRP(206-214)-specific clonotypes with increasing avidities during the progression of islet inflammation to overt diabetes in nonobese diabetic mice is fueled by autoimmune inflammation but opposed by systemic tolerance. As expected, naive high-avidity IGRP(206-214)-specific T cells respond more efficiently to antigen and are significantly more diabetogenic than their intermediate- or low-avidity counterparts. However, central and peripheral tolerance selectively limit the contribution of these high-avidity T cells to the earliest stages of disease without abrogating their ability to progressively accumulate in inflamed islets and kill beta cells. These results illustrate the way in which incomplete deletion of autoreactive T cell populations of relatively high avidity can contribute to the development of pathogenic autoimmunity in the periphery.

Animals↗
PubMed1992

Antibody avidity in swine lymphocyte antigen-defined miniature pigs.

Antibody avidity to hen egg white lysozyme (HEWL) was measured by thiocyanate ion elution enzyme-linked immunosorbent assay (ELISA) in swine lymphocyte antigen (SLA) defined miniature pigs. Serum antibody avidity was evaluated on day 14 and 30 after primary (day 0) and secondary (day 14) immunizations in eight to ten week old miniature pigs previously typed for swine lymphocyte antigen genotype. The effect of SLA genotype, litter, and gender on anti-HEWL antibody avidity was determined by least squares. Antibody avidity varied amongst individuals. Antibody avidity maturation was observed as a mean rise in antibody avidity from primary response (0.89 +/- 0.64) to secondary response (1.23 +/- 0.54) (p < 0.0005). Overall, SLA genotype did not significantly influence antibody avidity or avidity maturation, but pigs of dd genotype had greater avidity maturation between primary and secondary responses than other genotypes. Litter effects significantly affected antibody avidity and maturation.

Analysis of Variance↗
PubMed1989

Comparison of concentration and avidity of specific antibodies to E. coli in breast milk and serum.

To investigate the relationship between mucosal and systemic immunity we analysed the specific anti-Escherichia coli antibody concentration and avidity of IgA in colostrum and IgG in paired blood samples from 47 mothers giving birth to premature neonates. The avidity of each sample, expressed as an avidity index, was determined using a novel enzyme immunoassay (EIA)-based procedure, while specific antibody determinations were performed by means of conventional sandwich EIA techniques. All subjects had detectable antibody to E. coli in serum and breast milk. The median avidity index for specific IgA antibody in breast milk (3.53 M NH4SCN, range 2.77-4.90) was significantly higher (P less than 0.0001) than that for specific IgG antibody in serum (median 2.03 M NH4SCN, range 1.15-3.65). Using Spearman correlation analysis, a weak but significant association was found between the avidity of colostral IgA antibody and the avidity of systemic IgG antibody to pooled E. coli polysaccharides (rs = 0.29, P = 0.02). There was also a weak correlation between the concentrations of specific serum IgG antibody and of specific colostral IgA antibody (rs = 0.36, P = 0.006). There was no correlation between the concentration of IgA anti-E. coli antibody in colostrum and the avidity of colostral IgA antibody (rs = 0.14, P less than 0.05). Similarly, there was no correlation between the concentration and the avidity of serum IgG anti-E. coli antibody (rs = 0.23, P less than 0.05). The findings of this study suggest independent regulation of concentration and avidity of specific IgA antibody in preterm breast milk. Similar results were seen for specific IgG antibody in serum. The correlations between systemic and mucosal antibody with respect to both concentration and avidity were significant, but are relatively weak and therefore suggest that there also may be independent factors which afford differential regulation of systemic and mucosal antibody responses.

Antibodies, Bacterial↗
PubMed2004

T cell avidity determines the level of CTL activation.

To investigate the influence of avidity on T cell activation in vitro and in vivo, we analyzed T cells from St40 and St42 mice, which express the same transgenic TCR specific for an E1a-derived epitope of adenovirus type 5 with different expression levels and therefore different avidities. Splenocytes from both strains showed comparable cytolytic activities and required identical peptide concentrations for efficient target cell lysis and up-regulation of activation markers. However, the kinetics of CD25 up-regulation were strikingly different: whereas the majority of the high-avidity St42 T cells up-regulated the IL-2Ralpha chain within a few hours, low-avidity St40 T cells expressed only 50% of the CD25 of high-avidity T cells after 2 days. In addition, low-avidity T cells proliferated poorly and displayed impaired secretion of IL-2 and IFN-gamma. Similar results were seen with high-avidity St42 T cells stimulated with a partial agonistic peptide. Upon adoptive transfer and subsequent immunization with adenovirus, both high- and low-avidity T cells expanded, but St40 T cells were undetectable 10 days after immunization. Our model system now allows analysis of whether T cells with identical specificities but different avidities influence each other during activation and homeostatic proliferation.

Adenoviridae↗
PubMed2003

Measurement of EBV-IgG anti-VCA avidity aids the early and reliable diagnosis of primary EBV infection.

Current serological methods for the diagnosis of Epstein-Barr virus (EBV) infection still differentiate poorly between primary infection and reactivation. This is particularly true when IgG and IgM antibodies are present simultaneously and only a single serum sample is provided for analysis. The demonstration of the IgG avidity state has the potential to distinguish recent from past or reactivated infection. An analysis of the kinetics of avidity maturation of anti-VCA antibodies in primary EBV infection was undertaken with longitudinally collected sets of sera from 28 well-characterised EBV cases and in sera from 35 cases with previous EBV infection and recent primary infection due to HIV, CMV, or hepatitis A. Antibodies directed against the viral capsid antigen (VCA) and Epstein-Barr nuclear antigen (EBNA-1) were sought, using a commercial enzyme immunoassay (EIA). In parallel with standard IgG anti-VCA detection, serum was incubated with 8 M urea to disrupt low-avidity complexes to allow calculation of the percentage avidity. In cases with primary EBV infection, the mean avidity rose from 54% at 6 weeks to 82% by 28 weeks after the onset of symptoms, but remained lower than that of the control sera (96%). The addition of the avidity measurement improved the sensitivity of IgG and IgM anti-VCA testing in diagnosis of primary EBV infection from 93% to 100%. The specificity of IgM anti-VCA testing alone was poor, with 14 of 35 cases (49%) demonstrating false-positive results, but it improved to 97% by the demonstration of high-avidity IgG anti-VCA. The combination of negative IgG anti-EBNA and low-avidity IgG anti-VCA had a sensitivity and specificity of 100%. The routine addition of IgG anti-VCA avidity estimation to diagnostic EBV serology is recommended.

Adolescent↗
PubMed1994

Maturation of antibody avidity after primary human cytomegalovirus infection is delayed in immunosuppressed solid organ transplant patients.

An IgG antibody avidity assay which uses urea to modify a commercial enzyme-linked immunosorbent assay (ELISA) has been investigated for its ability to distinguish primary human cytomegalovirus (CMV) from recurrent or long-term infection. Twenty-four immunosuppressed solid organ transplant patients were studied. The avidity indices for IgG to CMV were low for 12 out of 13 patients with primary infection (mean 18%), high for all 11 patients with long-term infection (mean 85%), and the 1 patient with primary infection showing an intermediate avidity index (51%) was found to have acquired passively large amounts of CMV immunoglobulin, presumably of high avidity, during therapy. From the results, low and high avidity indices were defined as lying between 0-34% and 60-100%, respectively, and it was thus clear that the avidity assay can discriminate between primary and recurrent or long-term CMV infection. The avidity indices of eight of the immunosuppressed organ transplant patients with primary infection were followed in serial serum samples over time and IgG antibody to CMV was found to take at least a year to mature to high avidity in contrast to the 2-6 months expected for normal subjects. This finding provides evidence that immunosuppression has subtle, hitherto unsuspected, effects on humoral immunity to CMV in addition to the well-known depression of cell-mediated responses. It is concluded that this reliable avidity assay will be of importance in the diagnosis of CMV infection and in elucidating the pathogenesis of CMV-induced disease in organ transplant recipients.

Adult↗
PubMed2006

Delayed maturation of immunoglobulin G avidity: implication for the diagnosis of toxoplasmosis in pregnant women.

The low avidity of immunoglobulin G has been reported to be a useful marker of recent infection with Toxoplasma. Several investigators, however, have published discrepant result on the maturation of avidity over time. The aim of this study was to analyse persistent low avidity of immunoglobulin G in immunocompetent individuals and in pregnant women and how it could interfere in the flowchart of antenatal diagnosis of toxoplasmosis in the latter group. An international literature search was conducted together with a retrospective study of a hospital database. Eleven publications that met the inclusion criteria reported delayed maturation of avidity at a frequency ranging from 0 to 66.6% of the patients. Examination of those publications demonstrated an important heterogeneity in the type of assay used, the calculation of avidity, the cutoff above which avidity was considered to be elevated, and the delay since infection after which indices are expected to be high. In the hospital database, persistent low avidity was found even after a median follow-up period of 6 years. Different factors could interfere with maturation of avidity, such as variations between individuals, the assay system used, and, possibly, the treatment administered. The results of this study clearly demonstrate that, in a pregnant woman, an acute infection cannot be reliably diagnosed solely on the basis of low avidity of immunoglobulin G. Further investigations and standardization of assays are urgently needed. Estimation of the time of infection remains difficult, especially in cases in which the samples are drawn late in pregnancy; the final estimate must be based on several tests repeated at intervals of weeks.

Animals↗
PubMed1992

Antibody avidity in Yorkshire pigs of high and low immune response groups.

Avidity indices of antibody to hen egg-white lysozyme (HEWL) were measured by chaotropic ion (SCN-) elution enzyme-linked immunosorbent assay (ELISA) in pigs grouped as high, control or low for various immune and innate resistance-related traits. The avidity index was the molar concentration of SCN- required to reduce by 50% the ELISA optical density value for a given serum. The index was independent of the amount of antibody. Eight- to ten-week-old Yorkshire pigs were immunized with HEWL and serum antibody measured by ELISA as one of five traits used to assign them to high, low or control response groups. Serum antibody avidity for HEWL was evaluated on Day 14 and Day 30 after primary (Day 0) and secondary (Day 14) immunization. The effects of response group, gender, litter, serum IgG concentration and anti-HEWL antibody on avidity were determined using a linear model. Antibody avidity indices varied amongst individuals. Mean avidity indices for sera collected on Days 14 and 30 were 0.61 +/- 0.43 and 1.22 +/- 0.56, with maximum indices of 2.64 and 2.86 respectively. Avidity of secondary response antibody was significantly higher (P less than or equal to 0.05). Pigs of the high response group had significantly higher secondary antibody avidity than those of the control (P less than or equal to 0.08) and low groups (P less than or equal to 0.01). Avidity index was positively correlated with antibody to HEWL on Days 14 and 30 but not to preimmunization serum IgG concentration or to other measured traits.

Animals↗
PubMed2005

Avidity of anti-beta-2-glycoprotein I antibodies.

The terms affinity and avidity are often used indiscriminately, despite clearly differing. Since affinity refers to monovalent binding of antibodies to a monovalent epitope, the majority of data on the binding of anti-beta2-glycoprotein I antibodies (anti-beta2-GPI) characterized their avidity rather than affinity. Anti-beta2-GPI were generally believed to be of low avidity, but heterogeneous avidity of patients' IgG anti-beta2-GPI has been demonstrated. High avidity anti-beta2-GPI monoclonals were reported to possess higher pathogenicity than low avidity anti-beta2-GPI. Polyclonal high avidity anti-beta2-GPI were found to be more common in patients with antiphospholipid syndrome (APS) and associated with thrombosis. Some conformational changes of beta2-GPI are required for the binding of polyclonal anti-beta2-GPI to the antigen: neither high density of the antigen nor high avidity of the anti-beta2-GPI alone is sufficient for the recognition. Avidity of anti-beta2-GPI should be considered in any attempt of inter-laboratory standardisation and/or evaluation of anti-beta2-GPI enzyme-linked immunosorbent assay (ELISA).

Animals↗
PubMedDate not supplied

Comparison of two commercially available avidity tests for toxoplasma-specific IgG antibodies.

BACKGROUND: IgG anti-Toxoplasma avidity tests have proven useful to discriminate between recent and distant infection in management of pregnant women with anti-Toxoplasma-IgM antibodies. This study was performed to compare two commercially available IgG anti-Toxoplasma avidity test kits. METHODS: Sixty-four samples positive for IgM and IgG anti-Toxoplasma antibodies were analyzed with two IgG anti-Toxoplasma avidity tests: VIDAS Toxo IgG avidity kit (BioMérieux, Marcy-l'Etoile, France) and Toxoplasma gondii IgG avidity EIA kit (Labsystems, Helsinki, Finland). Samples were obtained from both pregnant women and subjects in different clinical settings. RESULTS: Of 64 sera positive in both VIDAS Toxo IgG and VIDAS Toxo IgM tests, 19 (29.7%) had high avidity antibodies in VIDAS and 17 (26.6%), high avidity antibodies in Labsystems kit. A total of 48 (75.0%) of 64 sera showed concordant results between VIDAS and Labsystems Toxo IgG avidity tests; one (1.2%) serum sample showed discordant results and in 15 (23.4%) sera, results were high or low in one test and borderline in the other. Overall correlation coefficient for results obtained in both tests was 0.80 (0.60 in sera of pregnant women and 0.88 in sera of other patients, respectively). CONCLUSIONS: Correlation between results obtained in BioMérieux and Labsystems Toxo IgG avidity kits in sera from pregnant women as well other individuals was high. BioMérieux assay possesses the advantage of automatization but requires the VIDAS machine; in contrast, Labsystems assay is less costly but requires time-intensive manual performance and calculation of test results.

Animals↗
PubMed2004

IL-15/IL-15Ralpha-mediated avidity maturation of memory CD8+ T cells.

T cell avidity is critical to viral clearance, but mechanisms of CD8(+) T cell avidity maturation are poorly understood. Here, we find that IL-15 mediates two mechanisms of avidity maturation. (i) By selection at the population level, IL-15 promotes greater survival of high- compared with low-avidity cytotoxic T lymphocytes (CTLs). High-avidity CTLs express higher levels of IL-15Ralpha and persist longer by homeostatic proliferation. (ii) At the individual cell level, IL-15 induces higher levels of surface coreceptor CD8alphabeta, increasing functional avidity. IL-15 during priming selects or induces higher-avidity CTLs. Conversely, high-avidity CTLs are diminished in IL-15Ralpha knockout mice. These results provide an explanation of CD8+ T cell avidity maturation and may contribute to the design of novel vaccines.

Animals↗
PubMed2004

Avidity of antibodies to cytomegalovirus in HIV-seropositive patients with and without CMV retinitis.

Antibodies of high avidity may protect the fetus from CMV infection, but the association of avidity with other CMV infections is unknown. To determine if anti-CMV antibody avidity is altered in HIV-seropositive patients, either untreated or treated with HAART, and to determine if alterations in avidity are associated with CMV retinitis, we obtained sera from 164 CMV-seropositive adults: 68 were HIV-seronegative healthy adults and 96 were HIV seropositive. Of the HIV-positive, 57 had no current or prior evidence of CMV retinitis (29 were being treated with HAART, and 28 were receiving no therapy when sampled), and 39 had either active CMV retinitis or were immunorestored by HAART with quiescent CMV retinitis. IgG antibody avidity was determined for each serum run in duplicate using an EIA assay and 5M urea as a dissociating agent. After correction for the significantly higher levels of IgG antibodies to CMV in the HIV-seropositive sera as compared to the normal healthy individuals, both HIV-infected and HIV-uninfected individuals had nearly identical average avidity indices (avidity index = 76). There was also no significant difference in average avidity index between HAART-treated and untreated patients, or between patients with active and immunorestored, quiescent CMV retinitis). These results indicate antibody avidity is unaltered in HIV disease and does not play an important role in the pathogenesis of AIDS-related CMV disease.

AIDS-Related Opportunistic Infections↗