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PubMed1995

Avidity of antibody responses to Actinobacillus actinomycetemcomitans in periodontitis.

We designed a study to examine the serum IgG antibody avidity characteristics in: (i) normal subjects (N); (ii) Actinobacillus actinomycetemcomitans-infected adult periodontitis (AP Aa+); (iii) A. actinomycetemcomitans-infected localized juvenile periodontitis (LJP Aa+); and (iv) AP subjects (AP) with various antibody patterns and disease presentation. Although there were significant elevations in antibody levels for AP Aa+ and LJP Aa+ patients compared with AP and normal patients (P < 0.0001), there were no significant differences in the avidity indices (AI). Correlations of antibody levels to avidity revealed that functional activity of the antibody as measured by avidity was independent of antibody levels. Increasing antibody levels correlated with an increase in the number of infected sites, yet there was a trend for A1 to decrease with increased infection. Avidity indices for all patient groups did not appear to show a strong biologic relationship to plaque; however, in AP Aa+ and LJP Aa+ patients there was a generally positive relationship between avidity and bleeding on probing or pocket depth. In AP Aa+ and LJP Aa+ patients, and in AP patients there was a positive relationship of avidity through a threshold of approximately 8 active disease sites. This study hypothesized that antibody avidity to A. actinomycetemcomitans could help to explain the relationship between the active host response and chronic infection with this pathogen. The results provide evidence that both antibody levels and avidity may contribute to the variation in host resistance to infection and disease associated with A. actinomycetemcomitans.

Actinobacillus Infections↗
PubMed1996

IgG avidity in the serodiagnosis of acute Toxoplasma gondii infection: a multicenter study.

OBJECTIVE: To evaluate the validity of the IgG avidity test in the serodiagnosis of acute T. gondii infection; to verify the maturation of IgG avidity during the course of infection; to observe whether the kinetics of IgG maturation could be affected by antibiotic treatment. METHODS: Serial serum samples, collected in three Italian hospitals (Perugia, Treviso and Bologna), from untreated and antibiotic-treated patients with primary toxoplasmic infection, were assayed for IgG avidity, and IgM and IgA positivity. Single serum samples from patients at different stages of infection were assayed for IgG avidity and the results were correlated to the likely stage of infection. RESULTS: The IgG avidity value increased from 3.5% in the first month to 38.7% 1 year from the onset of infection. Antibiotic-treated patients showed significantly different values of IgG avidity at 2 and 4 months after the onset of infection. In single serum samples the IgG avidity values correlated with the likely stage of infection. CONCLUSIONS: The IgG avidity test was confirmed as a useful tool in the serodiagnosis of acute T. gondii infection and could be predictive of the stage of infection. Antibiotic treatment may affect the kinetics of the maturation of IgG avidity.

Journal Article↗
PubMed2001

Multicenter evaluation of a rapid and convenient method for determination of cytomegalovirus immunoglobulin G avidity.

An easy, rapid, and reproducible test to distinguish residual cytomegalovirus (CMV) immunoglobulin M (IgM) antibodies from antibodies produced in primary infection could be useful, especially for pregnant women. The CMV avidity of IgG antibodies with the VIDAS automated enzyme-linked fluorescent assay and 6 M urea was evaluated in a multicenter study to differentiate between primary CMV infections and past infections or reactivations. A total of 416 serum specimens were tested: 159 specimens were from follow-up of primary infections, and 257 were from past infections. All of the specimens from primary infections collected within 4 months (17 weeks) after the onset of the infection had an avidity index lower than 0.8. An avidity index higher than 0.8 excludes a recent primary infection of less than 4 months. However, an avidity index higher than 0.8 cannot confirm all past infections, since 48 specimens (18%) from past infections had an avidity index lower than 0.8 (between 0.5 and 0.8). The exclusion capacity could be improved (96.9%) by using a cutoff of 0.7, but this index would decrease the specificity of the technique, since the avidity index was found to be between 0.7 and 0.8 in two patients with recent primary infection. All specimens from primary infections obtained more than 4 months after the onset of infection had an avidity index more than 0.2. In this study, an avidity index less than 0.2 confirms the presence of a recent primary infection of less than 4 months. The VIDAS CMV IgG avidity test is a rapid, reproducible test with very good performance.

Antibodies, Viral↗
PubMed1999

Avidity as a determinant of the protective efficacy of human antibodies to pneumococcal capsular polysaccharides.

Antibodies reactive with capsular polysaccharides are considered the principal mediators of immunity against invasive diseases caused by Streptococcus pneumoniae. In this study, we tested the hypothesis that anti-pneumococcal capsular polysaccharide (PPS) antibody avidity can influence protective efficacy. We measured the avidities of individual adult postvaccination immunoglobulin G2 (IgG2) antibodies to PPS serotypes 6B and 23F and examined the relationship between avidity and opsonophagocytic and mouse-protective activities. The avidities of PPS 6B- and PPS 23F-specific IgG2 antibodies ranged from 6 to 31 nM-1 and from 3 to 20 nM-1, respectively. We observed an inverse correlation between the magnitude of avidity and the amount of antibody required to protect mice against lethal bacteremia caused by serotype 6B pneumococci. Similarly, higher-avidity antibodies were more effective than lower-avidity antibodies in vitro in mediating complement-dependent opsonophagocytosis of both 6B and 23F pneumococci. These data suggest that in adults, PPS antibodies are sufficiently polymorphic to possess biologically significant variations in avidity. We conclude that avidity functions as an important determinant of anticapsular antibody protective efficacy against pneumococci.

Adult↗
PubMed2003

Anti-dsDNA antibody avidity determination by a simple reliable ELISA method for SLE diagnosis and monitoring.

High avidity anti-dsDNA antibodies are more specific for SLE diagnosis, and more closely associated with renal involvement than intermediate or low-affinity anti-dsDNA antibodies. ELISA methods are largely used to detect anti-dsDNA, but their high sensitivity is inversely related to specificity because they also detect low avidity antibodies. We developed an ELISA assay based on the law of mass action and the competitive binding of dsDNA in solution and coated to microwells with anti-dsDNA antibodies. A simplified Scatchard plot analysis system was used to measure anti-dsDNA antibody avidity which was expressed as apparent affinity constant (Kaa), and quantified in liters per unit (I/U). We prospectively studied 101 consecutive SLE patients, who were followed for 3 years; three serum samples were sequentially collected from each patient during follow-up for determination of IgG anti-dsDNA antibody concentration, and anti-dsDNA avidity. SLE disease activity was estimated using the European Consensus Lupus Activity Measure (ECLAM) index. Sera from 100 healthy subjects and 133 patients with other connective tissue diseases or infectious diseases were also assayed as controls. The mean Kaa in SLE patients was 65.2 +/- 47.3 l/U, with no variations over time. Anti-dsDNA-positive SLE patients had higher Kaa values (79.1 +/- 46.8) than anti-dsDNA negative patients (27.2 +/- 20.1; P < 0.001). No correlation emerged between anti-dsDNA avidity and the ECLAM activity index score. Avidity was significantly higher in patients with renal involvement vs patients without this complication (78.2 +/- 50 vs 59.9 +/- 45.6 l/U; P = 0.0013). This simple ELISA method could be very useful in the diagnostic phase to differentiate high avidity anti-dsDNA autoantibodies that are characteristically found in SLE patients from low avidity antibodies that can also be found in other inflammatory diseases. Moreover, our data confirm the predictive value of high avidity anti-dsDNA antibodies for the development of lupus nephritis.

Adult↗
PubMed2003

High avidity antigen-specific CTL identified by CD8-independent tetramer staining.

Tetrameric MHC/peptide complexes are important tools for enumerating, phenotyping, and rapidly cloning Ag-specific T cells. It remains however unclear whether they can reliably distinguish between high and low avidity T cell clones. In this report, tetramers with mutated CD8 binding site selectively stain higher avidity human and murine CTL capable of recognizing physiological levels of Ag. Furthermore, we demonstrate that CD8 binding significantly enhances the avidity as well as the stability of interactions between CTL and cognate tetramers. The use of CD8-null tetramers to identify high avidity CTL provides a tool to compare vaccination strategies for their ability to enhance the frequency of high avidity CTL. Using this technique, we show that DNA priming and vaccinia boosting of HHD A2 transgenic mice fail to selectively expand large numbers of high avidity NY-ESO-1(157-165)-specific CTL, possibly due to the large amounts of antigenic peptide delivered by the vaccinia virus. Furthermore, development of a protocol for rapid identification of high avidity human and murine T cells using tetramers with impaired CD8 binding provides an opportunity not only to monitor expansion of high avidity T cell responses ex vivo, but also to sort high avidity CTL clones for adoptive T cell transfer therapy.

Animals↗
PubMed2002

[Evaluation of the usefulness examination of IgG avidity for serodiagnosis of toxoplasmosis].

An assay measuring the avidity of T. gondii-specific IgG is a useful serological indicator of toxoplasmosis which in many cases allows on the basis of single serum sample testing to confirm or exclude acute infection. IgG antibodies against T. gondii produced in the recent primary infection are of low-avidity while IgG antibodies in the chronic toxoplasmosis are of high-avidity. In the present study 80 sera: 47 sera of patients with suspected acute toxoplasmosis, 23 sera of pregnant women and 10 sera of healthy blood donors, were evaluated for the presence of IgM, IgA and IgG antibodies and for the avidity of IgG. Among the 80 tested sera IgM antibodies were present in 34 (42.5%) cases of which 22 (64.7%) showed low-avidity of IgG and the presence of IgA antibodies confirming acute toxoplasmosis. In the rest of these 34 sera three of them showed low avidity index and nine other high avidity in spite of the presence of IgM antibodies. In these 12 sera IgA antibodies were not present. In 46 (57.5%) examined sera IgM or IgA antibodies were not detectable and the present the IgG antibodies showed high-avidity what is characteristic of chronic infection. An assay for evaluation of avidity of IgG antibodies specific for T. gondii is valuable in complementing existing tests and in many cases it has decisive value for interpretation of results.

Adolescent↗
PubMed1978

Age-dependent variations of antibody avidity.

Age-dependent variations of antibody avidity were studied in the C3HeB/FeJ mouse. Spleen cells from donors of different ages (10--720 days) were transferred and stimulated with TNP-HRBC in lethally irradiated syngenic recipients. The anti-TNP antibody response of the donor cells was estimated from the number of direct PFC per recipient spleen by the Jerne technique with TNP-SRBC. Avidity of the antibodies secreted by PFC was evaluated from the amount of added TNP-BSA that inhibited 50% of the anti-TNP PFC. Under these experimental conditions allowing the exclusion of any influence of the donor milieu during the immune response, age-dependent variations of the antibody response and avidity could be attributed to changes in the donor spleen cell population. Avidity was found to increase with the response and to vary parabolically with age. After appropriate correction of the number of PFC to make it independent from age, avidity values were fitted by a multiple curvilinear regression in which the independent variables playing a significant role were the corrected number of PFC in its linear term and the age in its linear and quadratic terms. From comparison of the standard coefficients of this regression, the observed variations of avidity could be attributed in part (82%) to the response and in part (18%) to the age. For any value of response, avidity increased 15-fold from day 10 to reach a maximum at day 110 and then declined 5-fold at the age of 720 days. Heterogeneity of avidity also changed parabolically with age as high avidity classes were present in adulthood and absent at 10 and 720 days.

Aging↗
PubMed1993

Signal transduction pathways involved in T cell receptor-induced regulation of CD2 avidity for CD58.

Through physiologic interactions with its ligands CD58 (lymphocyte function-associated Ag-3, LFA-3) and CD59, the T cell glycoprotein CD2 plays a role in T cell signaling and promotes lymphocyte adhesion. We have recently demonstrated that the interaction of CD2 with CD58 is dynamic: TCR stimulation or treatment with the phorbol ester PMA rapidly up-regulates CD2 ligand avidity, and this regulation requires the carboxyl-terminal asparagine residue of the CD2 cytoplasmic domain. Here we have analyzed the regulation of CD2 avidity for CD58, as assessed by the binding of CD2+ cells to purified CD58 and by the formation of rosettes between CD2+ cells and SRBC. In murine T cell hybridomas transfected with human CD2, we show that, unlike CD2-mediated IL-2 production, cell surface expression of the TCR-CD3 structure is not required for up-regulation of CD2 ligand avidity. TCR-initiated up-regulation of CD2 avidity requires the activity of both protein tyrosine kinases and protein kinase C. Agents which elevate intracellular levels of cAMP also up-regulate CD2 ligand avidity and act either distal to or independently of protein kinase C and protein tyrosine kinases. Cell lines expressing single amino acid substitutions of the carboxyl-terminal asparagine of CD2 are incapable of avidity regulation by TCR signaling, PMA treatment, or elevation of intracellular cAMP levels, demonstrating that each of these stimuli utilizes a common structural element for regulating CD2 avidity. The response to both cAMP and phorbol ester treatment distinguishes the regulation of CD2 avidity from that of a second major adhesion pathway, LFA-1 (CD11a/CD18)/ICAM-1 (CD54) and from that of the TCR coreceptor CD8. These observations identify the signaling events involved in the regulation of CD2 avidity and help to define the signal transduction processes that participate in "inside-out" signaling.

Animals↗
PubMed1998

The use of semi-automated EBV IgG avidity determination for the diagnosis of infectious mononucleosis.

The diagnosis of acute Epstein-Barr virus (EBV) infection is based frequently on the combination of positive viral capsid antigen (VCA) IgM antibodies and negative EB viral nuclear antigen 1 (EBNA-1) IgG antibodies. However, both VCA IgM and EBNA-1 IgG can provide false positive and false negative results. Therefore, situations in which the EBV serology remains unclear are not uncommon. Determination of EBV IgG avidity can clarify the EBV status in these patients. So far, mainly immunofluorescence assays have been used for this purpose. These tests are laborious, their evaluation is subjective, and automation is difficult. Therefore, two commercially available microtiter plate enzyme immunoassays (EIA) were compared for their usefulness for semi-automated EBV IgG avidity determination. One assay is based on a mixture of EBV antigens, the other assay uses a synthetic peptide of the VCA-complex. Patient sera of confirmed acute and past EBV infections were tested for avidity by both assays. The results with the antigen mixture assay proved to be highly sensitive (100%) and specific (100%). Avidity index calculations on the basis of one-point-quantification titers gave better results than calculations using OD values. Determination of EBV IgG avidity by the peptide assay was complicated by the fact that it was less sensitive than the antigen mixture assay for IgG detection in acute EBV infections. On the other hand, about 30% of the samples had to be retested with the peptide assay in a higher dilution because the IgG units in initial testing fell outside the range covered by the standard curve. Using OD values of the peptide EIA, the sensitivity was 99% but the specificity of detection of acute EBV infections was only 86%. Thus, while the peptide EBV avidity assay is unsuitable as a confirmatory assay, avidity testing with the antigen mixture assay is a useful tool to resolve equivocal EBV serologies. Avidity assays on the basis of EIA can be automated which should lead to wider use of this methodology.

Antibodies, Viral↗
PubMed2004

Delayed maturation of IgG avidity in congenital toxoplasmosis.

The aim of this comparative study was to investigate the clinical usefulness of the measurement of Toxoplasma gondii IgG avidity in the postnatal diagnosis of congenital toxoplasmosis. IgG avidity values in serum samples from infants with congenital infection were compared with those in samples from uninfected infants, all born to mothers with toxoplasmosis acquired during gestation. This analysis revealed that IgG avidity values soon after birth reflected maternal values in the large majority of the samples. Low or borderline IgG avidity values were systematically found in the cohort of congenitally infected subjects. After birth, IgG avidity values slowly increased over time for up to 2 years in congenitally infected subjects. On the contrary, IgG avidity values in the uninfected infants remained stable over time. The presence of low IgG avidity in a newborn can be considered a marker of maternal seroconversion in the second or third trimester of gestation and, as a consequence, an indicator of risk for congenital toxoplasmosis. An IgG avidity assay can be easily carried out with antibodies eluted from dried blood spots (Guthrie cards), providing an opportunity to retrospectively evaluate the risk of congenital infection in special clinical circumstances, for example when suspicion of congenital infection arises during late infancy.

Aging↗
PubMed1995

Effects of aging on antibody avidity to Mycoplasma pulmonis.

Antibody avidity of serum and lung lavage responses was examined in rats to determine aging effects on functional differences in antibody to Mycoplasma pulmonis. Three age groups of animals (weanling, adult and senescent) were immunized with either of two doses of formalinized M. pulmonis as the antigen, or a placebo control. Total immunoglobulin levels and specific antibody responses were examined in serum and lung lavage fluids and subsequently avidity measurements of the same samples were made for the specific antibody to M. pulmonis. The concentration of NH4SCN that dissociated 50% of the antibody was used to determine the avidity index of the serum and lung lavage samples. Total serum IgG and IgA were decreased in the weanling animals when compared to the other two age groups of animals. In contrast, serum IgA levels were substantially increased in senescent animals. Significant increases in serum IgA levels were noted following immunization that was not observed for IgG levels. Substantial increases in both serum antibody and lung lavage antibody were observed in response to immunization with either dose of antigen, but only the lung lavage samples showed both IgG and IgA isotypes differences that were attributable to age. Serum IgG avidity indices gradually increased over time following immunization with higher indices being observed in the weanling animals immunized with the higher M. pulmonis dose. Serum IgA avidity indices also increased over time with no significant differences noted among the age groups. Lung lavage IgG avidity demonstrated slightly higher indices in the weanling animals, while lung lavage IgA avidity showed higher avidity indices in the senescent animals at the higher antigen dose. These data suggest that senescent animals are capable of producing an apparently functional antibody response and that differences noted in increased disease susceptibility in older animals may be attributed to mechanisms other than a dysfunctional humoral immune response at mucosal surfaces.

Age Factors↗
PubMed2005

Absence of avidity maturation of autoantibodies to the protein tyrosine phosphatase-like IA-2 molecule and glutamic acid decarboxylase (GAD65) during progression to type 1 diabetes.

Immunoglobulin G avidity assays are used to distinguish between the acute and chronic phase of several infectious diseases, and there is evidence of autoantibody affinity maturation also in autoimmune diseases. To assess whether the analysis of the avidity of autoantibodies against the protein tyrosine phosphatase-like IA-2 molecule and glutamic acid decarboxylase (GAD65) could improve the accuracy of risk assessment of progression to clinical type 1 diabetes, we established methods for the determination of the autoantibody avidity based on our previously developed time-resolved fluorometric IA-2 and GAD65 autoantibody (IA-2A and GADA) assays. The avidity indices of sequential plasma samples from six IA-2A-positive and seven GADA-positive prediabetic children were analysed applying elution with urea and diethylamine (DEA). For comparison, corresponding avidity indices of control children, who have remained non-diabetic for at least 3 years after seroconversion to IA-2A and GADA positivity, were analysed. For most of the children, only a slight fluctuation in the avidity index values was observed over time, although the titres for IA-2A and GADA varied substantially in some cases. The avidity indices of the prediabetic children remained within the same range as those of the control group throughout the follow-up. Our results indicate that the analysis of the avidity index levels of IA-2A and GADA does not improve the accuracy of the prediction of type 1 diabetes based on autoantibody detection.

Aged↗
PubMed1988

Avidity of IgA antibody to Escherichia coli polysaccharide and diphtheria toxin in breast milk from Swedish and Pakistani mothers.

The avidity of breast milk IgA antibody was studied with the aid of thiocyanate elution of antibody from solid-phase bound E.coli polysaccharides and diphtheria toxoid. The relative avidity index for each sample was determined by the molarity of thiocyanate required to elute 50% of the bound IgA antibody under conditions of antigen excess. Milk samples collected from Pakistani mothers during early lactation (2-4 weeks after delivery; n = 12) had a significantly lower median relative avidity index of IgA antibody to E.coli antigens than did early lactation samples from Swedish mothers (n = 11; avidity indices 1.78 M and 2.65 M; P less than 0.02). Samples collected from Pakistani mothers in mid-lactation showed a significant rise in the relative avidity index to a median of 2.50 M (P less than 0.01), with a subsequent fall in late lactation (28-36 weeks after delivery) to 1.75 M (P less than 0.01). Milk samples from Pakistani mothers in mid-lactation (n = 12) also had a lower median relative avidity index of IgA antibody to diphtheria toxoid than did samples from Swedish mothers (n = 14; avidity indices 2.35 M and 4.30 M; P less than 0.002). The lower avidity of breast milk IgA in Pakistani mothers in comparison with Swedish mothers may arise from differences in antigen exposure or nutritional status or could possibly be genetically determined.

Antibody Affinity↗
PubMed1997

Increased titre and avidity of IgG antibodies to Porphyromonas gingivalis whole cells and a cell surface protein in subjects with adult periodontitis.

The titre and avidity of IgG antibodies to Porphyromonas gingivalis whole cells and a 47 kDa cell surface protein were determined in serum samples taken from 20 subjects with adult periodontitis and 20 controls, matched for age, gender, ethnic origin and oral hygiene status. Antibody titres were measured by ELISA and antibody avidity was determined by a chaotrope-dissociation ELISA. Avidity was defined as the molarity of chaotrope required to reduce absorbance by 50% (ID50). The mean IgG antibody log titre to whole cells (8.29 vs. 6.92; p < 0.01) and to the 47 kDa antigen (7.61 vs. 6.77; p < 0.05) were higher in cases than in controls. Mean IgG antibody avidity to whole cells (4.59 vs. 2.47; p < 0.001) and to the surface protein (2.54 vs. 1.67; p < 0.001) were also higher in cases than in controls. In cases, IgG antibody titre was highly correlated with avidity for both whole cells (r = 0.878; p = < 0.001) and the 47 kDa protein (r = 0.683; p < 0.001). There was a weaker positive correlation between the titre and the avidity of antibody to whole cells (r = 0.591; p < 0.01) in the control population but antibody titre and avidity for the 47 kDa sonicate antigen were not correlated in the controls (r = 0.104). We conclude that many patients with adult periodontitis have effective humoral immunity to P. gingivalis. However, in up to half the patients with adult periodontitis, antibody titres and avidities were low and similar to control values, indicating either susceptibility due to poor host response or that disease is not associated with this particular pathogen.

Adult↗
PubMed1992

Immunoglobulin G antibody avidity in patients with respiratory syncytial virus infection.

The titer and avidity of respiratory syncytial virus-specific antibodies were measured in 196 serum specimens from 93 children with an acute, laboratory-confirmed respiratory syncytial virus infection. An enzyme immunoassay method based on the ability of urea to dissociate the bound antibodies with low avidity from the antigen was used. Three patterns of immune responses were observed. Children less than 6 months of age usually had low titers of antibodies with high avidity in their acute-phase serum samples. These antibodies were concluded to be of maternal origin, since their reaction pattern was similar to that of healthy adults. During the next few weeks, a slight increase in titers with a concurrent decrease in antibody avidity was observed. All children 6 to 24 months of age had low-avidity antibodies in their acute-phase serum samples, which matured to high avidity during the follow-up. On the contrary, about half of the children greater than 24 months of age had high-avidity antibodies already in the acute-phase serum samples. We conclude that the former children were experiencing primary infections with respiratory syncytial virus and the latter were experiencing reinfections. All adults with remote immunity had antibodies with high avidity.

Adult↗
PubMed2004

Evaluation of the immunoglobulin G avidity test for diagnosis of toxoplasmic lymphadenopathy.

Toxoplasmic lymphadenopathy (TL) is the most common clinical manifestation of acute acquired toxoplasma infection in normal individuals. The diagnosis is established by serologic methods and lymph node biopsy. Recently, tests for avidity of toxoplasma immunoglobulin G (IgG) antibodies have been introduced to help discriminate between recently acquired and distant infection with the parasite. We studied an avidity test to define the usefulness of this method and to determine the evolution of the IgG avidity in TL. Seventy-three consecutive patients diagnosed as having TL were studied. IgG avidity test titers were noted to be time dependent from the clinical onset of lymphadenopathy. Low IgG avidity test results were observed in patients who had developed lymphadenopathy from <1 month to 17 months prior to the sampling of sera, emphasizing that low IgG avidity test results are not reliable for diagnosis of recently acquired infection. In contrast, high IgG avidity test results were observed only in patients who had developed lymphadenopathy at least 4 months earlier. Thus, a high IgG avidity test result in an individual who has recent onset of lymphadenopathy (e.g., within 2 to 3 months of sera sampling) suggests a cause other than toxoplasmosis. In such cases, further workup is warranted in order to determine the cause of the lymphadenopathy.

Adolescent↗
PubMed2004

Diagnostic relevance of immunoglobulin G avidity for hepatitis A virus.

Diagnosis of acute hepatitis A virus (HAV) infection is based on the detection of HAV immunoglobulin M (IgM). However, IgM could be detected due to nonspecific polyclonal activation of the immune system. An avidity test for anti-HAV IgG was developed to distinguish acute infection, where low-avidity antibodies are detected, from immune reactivation. The assay was tested on 104 samples, including 11 sera from patients with past infection, 15 sera from patients with acute infection and 4 collected after recovery, 10 sera from vaccinated subjects, 4 sera from patients with suspected immune reactivation, and 60 unselected HAV-IgM positive sera, collected over 1 year in a routine laboratory. The avidity index (AI) was expressed as percentage. The results were provided as the mean +/- one standard deviation. Patients with a history of prior infection had AIs of >70% (mean, 86% +/- 10), whereas the mean AI was 36% +/- 16 during acute HAV infection (P < 0.001). Within the first month after the onset of hepatitis, avidity was either noncalculable due to a very low IgG titer or <50%. In patients with immune reactivation, avidity was >70% (88% +/- 10%), a finding consistent with a prior infection. Among the 60 unselected sera, 35 (58%) had a noncalculable or <50% avidity, and most of them had a detectable HAV RNA, confirming HAV infection. In contrast, 16 (27%) had an avidity of >70%, and none was reverse transcription-PCR positive, suggesting immune reactivation. These 16 patients were significantly older than the others (50 +/- 16 years versus 26 +/- 14 years). The new anti-HAV IgG avidity assay we developed could improve HAV infection diagnosis, particularly in elderly patients.

Antibody Affinity↗