Maternal immunoglobulins and parainfluenza 3 virus inhibitors in the nasal and lachrymal secretions and serum of newborn lambs.

Concentrations of IgG, IgM and IgA were measured in the serum, nasal secretions and lachrymal secretions of suckled newborn lambs. The major immunoglobulin constituent of precolostral serum was IgM. Maternal immunoglobulins, of which IgG was predominant, reached peak values on day 1 of life and then declined over the next 3 weeks. Half lives were calculated as: IgG, 13-7 days; IgM, 4-1 days; and IgA 1-8 days. No immunoglobulin was detectable in nasal or lachrymal secretions prior to sucking but IgG was present in all samples of these secretions obtained approximately 24 hr after first sucking. IgG was present in nasal washings from suckled lambs, reared either naturally or on immunoglobulin-free milk substitute and levels declined as the lambs grew older. IgM and IgA did not appear consistently in the secretions until lambs were 2-3 weeks old. It was concluded, therefore, that colostral IgG reaches the nasal and lachrymal secretions of the newborn lamb. However, because the ewes in this experiment had only low serum titres, no maternal antibody to parainfluenza 3 virus (PI3) was detected in the nasal secretions of the lambs, although non-specific inhibitors were present. It is suggested, however, that low levels of maternal antibody in the secretions may play a valuable role in preventing respiratory virus infections of young ruminants before active local production of IgA and IgM begins at 2 to 3 weeks of age.     

Antibody responses in arthritic and uncomplicatedYersinia enterocolitica infections

Concentrations of antiyersinia antibody isotypes IgG1, IgG2, IgG3, IgG4, IgA and IgM were measured in 33 patients with yersiniosis using a solid-phase radioimmunoassay. Sixteen patients had a complicating reactive arthritis. Throughout the observation period IgG1 and IgM antibodies both constituted approximately one-third of the total antibodies, while IgA accounted for 10%, IgG3 accounted for 1%, and IgG4 antibodies could not be detected. IgG1, IgM, and IgA antibodies (and the total titer) had reached their peak at the beginning of the observation period (ca. day 20 after the onset of symptoms). The levels then gradually decreased; the total titers averaged 40 times the background at the beginning of the observation period and 4 times the background on day 350. IgM antibodies could be detected as late as a year after the infection. The concentration of IgG2 antibodies varied greatly from patient to patient. In most patients it increased until a plateau was reached approximately 2 months after the onset of symptoms. A decline was observed later. Five arthritic but no nonarthritic patients had a pronounced IgG2 response (more than half of the IgG antibodies were IgG2 in one or several samples).     

Chronological evolution of IgM, IgA, IgG and neutralisation antibodies after infection with SARS-associated coronavirus

Abstract Serum levels of IgG, IgM and IgA against severe acute respiratory distress syndrome (SARS)-associated coronavirus (SARS-CoV) were detected serially with the use of immunofluorescent antibody assays in 30 patients with SARS. Seroconversion for IgG (mean 10 days) occurred simultaneously, or 1 day earlier, than that for IgM and IgA (mean 11 days for both). IgG could be detected as early as 4 days after the onset of illness. The earliest time at which these three antibodies reached peak levels was similar (mean 15 days). A high IgG level (1:800) could persist for > 3 months. The kinetics of neutralisation antibodies obtained with 100x the tissue culture infective dose (TCID50) of the SARS-CoV TW1 strain in five patients with SARS nearly paralleled those for IgG. There were no significant differences in the kinetics of the IgG, IgM and IgA responses between patients with or without underlying medical disease, steroid or intravenous immunoglobulin therapy, or mechanical ventilation.     

Isotype distribution and specificity of the antibody response to primary Moloney murine sarcoma virus infection in BALB/c mice

The development and isotype distribution of Moloney murine leukemia virus (M-MuLV)-specific serum antibodies following primary inoculation with Moloney murine sarcoma/leukemia virus (M-MuSV/M-MuLV) in adult BALB/c mice have been investigated using an enzyme-linked immunosorbent assay (ELISA). The primary antibody responses to M-MuSV/M-MuLV consisted of the IgM, IgG2a, IgG2b, and IgG3 isotypes; no M-MuLV-specific serum IgG1 or IgA antibodies were detected. The detectable antibody response was biphasic, with an early peak of virus-specific titers seen between 10 and 15 days after inoculation and a second peak seen in regressor sera. Pooled regressor sera contained IgM, IgG2a, and IgG2b antibodies which bound to M-MuLV-expressing lymphoma cells. Immunoelectron microscopy with regressor sera showed IgG bound both to infected cell surfaces and to mature viral particles, while IgM bound only to infected cell surfaces. These findings were supported by immunoprecipitation analyses which demonstrated binding of the M-MuLV-specific antibodies to both virion-associated and cell-associated antigens encoded by the gag and env genes.     

Immune response of the ileum to invasive Escherichia coli diarrheal disease in rabbits.

We have previously characterized a rabbit model of invasive Escherichia coli diarrhea. The purpose of this study was to measure the in vitro synthesis of immunoglobulin and anti-invasive E. coli antibody by ileal tissue and levels of anti-invasive E. coli antibody in sera and ileal contents at intervals after diarrhea. Immunoglobulin synthesis by the ileum peaked at 7 to 9 days, but returned to normal by 11 to 13 days post-diarrhea.l Secretory immunoglobulin A (IgA) was synthesized in greater quantity than was IgG or IgM. Anti-invasive E. coli antibody synthesis peaked at 11 to 13 days, decreased to less than half of maximum by 21 to 24 days, but was increased again at 30 to 33 days post-diarrhea. Secretory IgA anti-invasive E. coli antibody was synthesized in greater quantity than was IgG or IgM antibody. Specific antibody of the IgG and IgM classes, but not of the IgA class, appeared in sera by 4 to 6 days and peaked at 7 to 15 days post-diarrhea. Secretory IgA anti-invasive E. coli antibody was detected in ileal contents by 7 to 13 days, but maximum levels were not reached until 50 to 55 days post-diarrhea. IgG and IgM anti-invasive E. coli antibodies were not detected in ileal contents. The synthesis and secretion of secretory IgA antibody were major components of the immune response of the ileum after infection with an invasive bacterium.     

Cell-free and cell-bound antibody in nasal secretions from infants with respiratory syncytial virus infection.

Twenty-two infants under 9 months of age hospitalized with bronchiolitis or pneumonia due to respiratory syncytial virus (RSV) were serially sampled to determine the pattern of secretory antibody response. Using double labeling techniques, we found several types of immunoglobulin in secretions: cell-free antibody to RSV of the immunoglobulin A (IgA), immunoglobulin G (IgG), and immunoglobulin M (IgM) classes; and immunoglobulins of all three classes bound to RSV-infected cells shed from the nasal epithelium (presumably cell-bound antibody to RSV). IgA attached to RSV-infected epithelial cells was almost always detected in the first available nasal sample (day 1 or 2 of hospitalization). In contrast, cell-free anti-RSV IgA first appeared an average of 3.5 days later at a time when virus antigen was disappearing from the secretion. IgG and IgM attached to RSV-infected cells appeared more irregularly. The titer of cell-free anti-RSV IgM was often higher than that of IgA early in the illness and declined as the infection resolved. Cell-free anti-RSV IgG was usually present earlier than IgA and rose during convalescence.     

Antibody response detected by immunoblot in respiratory tract washings of chickens after infection with Mycoplasma gallisepticum.

Two experiments were conducted to test the sensitivity of Western blotting for detection of M. gallisepticum antibodies in respiratory washings and sera of infected chickens by mouse monoclonal antibodies to chicken IgG, IgM and IgA. In the first experiment, birds infected at 10 days of age were examined 2 weeks later. In the respiratory washings, IgA antibodies reacted with eight polypeptides of M. gallisepticum, while IgM and IgG reacted with three. In the serum IgA antibodies were not detected but IgM antibodies reacted with eight polypeptides and IgG with 16. In the second experiment birds were infected at 3 weeks of age and a subgroup was examined every week for 3 weeks post-infection. In the respiratory washings IgA was the principle immunoglobulin detected in the first week and it reacted to six major polypeptides of M. gallisepticum (p72, p64-67, p60, p56, p45, p40). In serum IgM was predominant in the first week and reacted to nine polypeptides. From the second week IgG antibodies were the most important as they reacted to 13 polypeptides in respiratory washings and to 11 polypeptides in the serum, while they reacted to nine polypeptides in respiratory washings and to 13 in the serum in the third week.     

Early detection of antibody to human immunodeficiency virus type 1 by using an antigen conjugate immunoassay correlates with the presence of immunoglobulin M antibody.

Sequential plasma samples obtained from 16 individuals who seroconverted were tested for the presence of antibody to human immunodeficiency virus type 1 (HIV-1) by an antigen conjugate enzyme immunoassay (EIA) and a conventional antibody conjugate assay. In 11 of these individuals, the antigen conjugate assay detected antibody to HIV-1 2 to 11 days (mean, 5.5 days) earlier than the antibody conjugate assay. In 11 individuals, HIV-1 p24 antigen was detected a median of 6.5 days (range, 3 to 14 days) prior to positivity by the antigen conjugate EIA. Using class-specific probes, we determined the profiles of immunoglobulin M (IgM), IgG, and IgA antibodies for each individual and correlated these profiles with the EIA signals from both assays. In general, the appearance of IgM exhibited a peak at about 1 week postseroconversion, which was followed by gradually declining levels. Absorbance levels for IgG antibody, however, rose steadily and reached a plateau after 3 to 5 weeks. The levels of IgA were generally low and variable. In contrast to the progressive increase in EIA absorbance observed by the antibody conjugate assay, the antigen conjugate assay displayed a rapid early rise in absorbance which generally coincided with the transient expression of IgM antibody. The subsequent gradual increase coincided with rising levels of IgG. Because the configuration of the antigen conjugate EIA allows for an increased sensitivity for IgM compared with that for other classes of immunoglobulins, these results suggest that earlier detection of antibody to HIV-1 is due to the detection of IgM antibody during the early phase of seroconversion.     

Proportions of Ig Classes and Subclasses in Rubella Antibodies

The proportions of six immunoglobulin isotypcs (IgA. IgM. IgGl. lgG2, IgG3. and IgCi4) in rubella antibody responses were quantified in 40 scrum samples (20 patients). The first sample from each patient was taken during the first days of the illness, and the second sample 10±1 days later. A tenfold average increase in antibody concentration was observed between the first and the second sample. IgM was the predominant isotype in the first sample (average, 73% of all antibodies), followed by IgGl (19%). IgA and IgG3 antibodies were detected in only a few of the first samples, and IgG2 or IgG4 in none. In the second samples IgGl was the predominant antibody isotype (average, 59%). Next came IgM (23%), followed by IgA (8%) and IgG3 (3%). No IgG2 or IgG4 antibodies were detected. Although the proportion of IgM antibodies was lower in the second than in the first samples, their concentration increased in all patients (the average factor was 7). The kinetics of the IgA response was irregular. In some patients there was a strong (up to 90-fold) increase in IgA antibodies, hut in two patients a small drop was delected. The kappa- to lamhda-ehain ratio of rubella antibodies appears to be close to the expected 2:1. It decreased in some patients during the Ml days and increased in others.     

Presence of viral antigens and antibody in the trachea of chickens infected with avian infectious bronchitis virus

Following infection of chickens with infectious bronchitis virus (strain M41) viral antigens were detected by immunofluorescence in the basal layer of the tracheal mucosal epithelium for 44 days. The enzyme-linked immunosorbent assay (ELISA) first detected virus-specific antibody in tracheal washes 7 days after infection and at 10 days these antibodies reached a level that was maintained for at least 44 days, although there was considerable variation between chickens. In contrast a neutralisation test did not detect antibody until day 20 ; titres were in the range 2.2 to 3.2 log2 reaching a maximum at day 27. ELISA detected anti-viral IgA in tracheal washes only on day 7, whereas IgG was detected in all samples containing anti-viral antibody. Serum anti-viral antibodies were detected by ELISA at 7 days and reached peak titres at 10 days, which were maintained. In contrast, serum neutralising antibodies were first detected at 10 days and increased to peak titres on day 24. The implications of the differences between the results of ELISA and neutralisation tests are discussed.     

Immunoglobulin isotypes of anti-HBc and anti-HBe and hepatitis B virus (HBV) DNA elimination in acute hepatitis B

Antibodies to hepatitis B core antigen (anti-HBc) and e antigen (anti-HBe) were assayed in 46 sera from ten patients with acute hepatitis B utilizing immunoglobulin class- and subclass-specific enzyme immunoassays (EIAs). The sera were sampled 1 to 512 days after onset of hepatic symptoms. Four patients cleared HBsAg rapidly, within 24 days, and six patients cleared HBsAg slowly, within 27-74 days after the onset of symptoms. In three of the patients with rapid clearance of HBsAg, hepatitis B virus (HBV) DNA was not detected in sera tested during the first week after onset. The fourth patient was not tested until 12 days after onset and was then found to be negative for HBV DNA. In four of the patients with slow clearance of HBsAg, HBV DNA was present during the first week of illness. In the other two patients, HBV DNA was not detected in the first serum, 11 and 17 days after the onset of illness. Anti-HBc IgM and IgA1 were detected in all patients, with maximum titers shortly after onset. Anti-HBc IgG1 was present in all sera tested. Anti-HBc IgG2 was not detected in any of the sera. Anti-HBc IgG3 and IgG4 were detected in all patient sera, with IgG3 paralleling IgG1, and IgG4 mainly in sera long after onset. Anti-HBe IgG1, IgG3, and IgG4 were detected in three, two, and two patients, respectively. Anti-HBe IgG2, IgM, IgA1, or IgA2 was not found in any patient. The time required for maximum titer of anti-HBc IgG1 was shorter in the patients with rapid clearance of HBsAg.(ABSTRACT TRUNCATED AT 250 WORDS)     

Murine Intestinal Humoral Responses in Chronic Schistosoma mansoni Infections

Specific and non-specific production of immunoglobulins (Ig) by the intestinal mucosa was examined in mice infected with the human blood fluke Schistosoma mansoni. Ileal and colonic mucosal tissue samples were cultured for 2 days, the medium replaced and the culture continued for a further 2 days. Ig concentrations and specific antibodies to soluble schistosome egg antigens in culture supernatants were estimated by isotype-specific ELISA. Cultured mucosae from control mice produced little IgG, but significant amounts of IgA and IgM on prolonged culture. IgG concentrations were increased in infected animals, mainly in the initial culture period, indicative of systemic, rather than local origins. By contrast, significantly increased local production of IgA and IgM occurred after the start of egg deposition in the intestinal mucosae. Although specific anti-egg antibodies of the IgG and IgM class were detected, none of the local IgA response was specific for schistosome eggs. We conclude that specific intestinal immune responses to schistosome eggs reflect systemic responses, whereas locally increased IgA production is largely non-specific. This pattern of response is likely to be related to the prior systemic exposure to schistosome eggs, which results in polyclonal local B-cell activation, but fails to trigger an antigen-specific IgA mucosal response.     

Development and persistence of West Nile virus-specific immunoglobulin M (IgM), IgA, and IgG in viremic blood donors

West Nile Virus (WNV) antibody development and persistence were investigated in blood donors who made WNV RNA-positive (viremic) donations in 2003. Plasma samples from the index donations and follow-up serum or plasma samples were tested for WNV immunoglobulin M (IgM), IgA, and IgG by using enzyme-linked immunosorbent assays. Antibody development was investigated with 154 samples collected from 84 donors 1 to 21 days after their RNA-positive, antibody-negative, index donation. WNV IgM and IgA were first detected on day 3, and all samples collected after day 9 were WNV IgM and IgA positive; WNV IgG was first detected on day 4, and all samples collected after day 16 were positive. Antibody persistence in this donor group (index donations antibody negative) was evaluated by using 128 samples collected from 89 donors on days 22 to 440 of follow-up; 88% of samples were WNV IgM positive, 86% were WNV IgA positive, and 100% were WNV IgG positive. In linear regression analysis, trendlines for WNV IgM and IgA reached the value discriminating positive from negative results at 218 days and 232 days of follow-up, respectively. Similar WNV IgM and IgA persistence trends characterized 27 donors whose index samples were positive for WNV IgM and IgA, as well as 14 donors whose index samples were positive for WNV IgG but negative for WNV IgM. These findings show that WNV IgG emerges after WNV IgM and IgA and that both WNV IgM and IgA typically persist for at least 6 months after infection. Thus, unlike some other flavivirus infections, WNV infection is not characterized by a relatively rapid disappearance of virus-specific IgA.     

Immunoglobulin concentrations in children receiving treatment for acute lymphoblastic leukaemia

As part of a wider survey of infections and defence mechanisms, concentrations of serum immunoglobulins IgG, IgA, and IgM were measured regularly by single radial immunodiffusion in a group of children receiving treatment for acute lymphoblastic leukaemia while in their first remission. IgM concentrations were often markedly raised at diagnosis, and IgG and IgA concentrations both began falling within one month of diagnosis. Four months after diagnosis all three had fallen significantly, but this tendency stopped after six months. Only IgG partially recovered, and non returned to pretreatment concentrations even in children followed for two years. The results suggest that vincristine and prednisone are the major factors that initiated the fall in IgG and IgA. Lowered IgM concentrations may have been due to cranial irradiation or continuous maintenance treatment, or both.     

Induction of Salivary Antibody Responses in Rats after Immunization in Peyer''s Patches

We examined salivary, milk, and serum antibody levels after immunization in the Peyer's patches (Pp) of rats with horse spleen ferritin. Priming of the Pp one day after parturition led to the appearance of IgG, but not IgA or IgM, anti-ferritin antibodies in saliva 9 days later. IgG and IgM antibodies were detected both in milk and in serum, whereas IgA antibodies could only be demonstrated in milk. During a second lactation period the salivary antibodies had vanished but IgG antibodies could still be detected in milk and serum. During a third lactation period, when the rats were immunized in the Pp a second time, not only IgG but also IgA anti-ferritin antibodies appeared in the saliva. Salivary IgG antibody levels and milk IgG, IgM, and IgA antibody levels were higher than those observed after primary immunization in the Pp. The IgG antibody activity in the saliva was positively correlated to the serum IgG antibody activity. It is concluded that salivary IgA antibody responses can be induced by immunization in the Pp. The results of this study suggests that IgA antibodies detected in saliva are produced locally by cells that have migrated from the intestinal lymphoid tissue to the salivary glands.     

A method for the rapid purification of serum IgM for the diagnosis of recent viral infections of chickens

The rapid purification of chicken IgM from serum was achieved by affinity chromatography. IgM immunoadsorbent gels were prepared using monoclonal antibodies specific to chicken IgM. Five different eluting agents were compared for the dissociation of the adsorbed IgM; the most convenient for routine purposes was 2 M NaCl, Tris-HCl, EDTA (NTE), as this enabled direct assay of eluents by ELISA without requiring the intermediate step of dialysis, which the other eluting agents did. Eluents prepared from sera obtained from infectious bronchitis virus (IBV) and infectious laryngotracheitis (ILTV)-infected chickens, together with samples of the same serum fractionated by gel chromatography, were tested by ELISA for virus-specific antibodies and to confirm the identity of the antibody class. In the case of both IBV and ILTV, similar results were obtained using immunoaffinity and gel chromatography. IBV-specific IgM, as determined by both methods in the ELISA, reached its highest concentration at the 8th day after inoculation and was virtually absent by the 24th day, whilst the highest concentration of ILT-specific IgM was detected at 6 days and no or little IgM was present at 16 days after inoculation. Purification of serum IgM by affinity chromatography followed by ELISA was considered suitable for routine serological diagnosis of IB and ILT, since the time required to complete the assay (3 hours) was considerably less than that for gel chromatography and many samples could be assayed simultaneously.     

Human immunoglobulin class and IgG subclass regulation: Dual action of interleukin-4

Epstein-Barr virus (EBV) was used as a polyclonal human B cell mitogen to investigate the regulation of immunoglobulin class and IgG subclass responses by interleukin-4 (IL-4). Activation of tonsillar B cells with EBV resulted in an early peak of polyclonal immunoglobulin secretion between days 13 and 14 consisting of IgM, IgA, and IgG1, IgG2, IgG3 and IgG4, but not IgE. Addition of IL-4 to EBV-activated B cells at concentrations of 100 U/ml or greater induced the production of IgE and enhanced IgG4 secretion, but had no effect, or more often inhibited the other isotypes. In contrast, low concentrations of IL-4 (1-5 U/ml) significantly increased the production of IgM, IgA, IgG1, IgG2and IgG3, but had no effect on IgG4 or IgE. The increase in immunoglobulin secretion obtained with low concentrations of IL-4 was found to occur only with high-density (resting) B cells, suggesting that IL-4 was not functioning simply as a late-acting differentiation factor. Low concentrations of IL-4 significantly increased IgG1, IgG2, IgG3, and IgA production by surface (s)IgM⁺ (sIgG^?/sIgA^?) B cells which is consistent with heavy chain switching. In some experiments, however, IL-4 enhanced IgM secretion by sIgM⁺ B cells, and IgA, IgG1, IgG2, IgG3 by sIgM B cells, suggesting that it may have an additional B cell differentiation factor activity which was not isotype specific. The different effect of IL-4 at high and low concentrations were similar to those observed in B cell activation experiments, and may be due to the existence of high- and low-affinity IL-4 receptors.     

Lung injury induced by short-term intermittent trimellitic anhydride (TMA) inhalation

We have developed a rat model of lung injury with interstitial pneumonitis, lung hemorrhage, and a systemic and pulmonary immune response to trimellitic anhydride (TMA)-haptenized proteins induced by TMA inhalation for 10 days. The present studies explored the induction of lung injury induced by short-term intermittent TMA inhalation, a model more likely to simulate short-term industrial exposures during inadvertent spills of TMA. Sprague-Dawley rats inhaled TMA powder (500 micrograms/m3) on days 1, 5, and 10, and were necropsied on day 30, 18 hours after a 6-hour TMA-inhalation challenge on day 29. Rats were bled every second day and at necropsy. Serum IgG, IgA, and IgM antibody to trimellityl rat serum albumin was measured by ELISA. There was a rise in IgM and IgA antibody to trimellityl rat serum albumin starting at day 5 that peaked at day 20 with a decline in IgM by day 30. IgG antibody rose at day 7, peaked at day 20, and plateaued. The IgG antibody level was 10 times higher than the IgA or IgM level. In a second experiment, 18 rats were administered TMA-inhalation exposure on days 1, 5, and 10, and a TMA challenge on day 22. The number of hemorrhagic foci, lung weights, and lung-displacement volumes at necropsy on day 23 were highly correlated with IgG, IgA, and IgM serum-antibody levels. In a final experiment, rats developed a mean of 112 hemorrhagic foci per lung on day 30 after receiving only two TMA-inhalation exposures on days 1 and 5 with a rechallenge on day 29. (ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of immunoglobulin M (IgM), IgA, and IgG Norwalk virus-specific antibodies by indirect enzyme-linked immunosorbent assay with baculovirus-expressed Norwalk virus capsid antigen in adult volunteers challenged with Norwalk virus.

Pre- and postexposure sera collected from 17 adult volunteers challenged with Norwalk virus as described previously (D. Y. Graham, X. Jiang, T. Tanaka, A. Opekun, P. Madore, and M. K. Estes, J. Infect. Dis. 170:34-43, 1994) were examined for Norwalk virus-specific immunoglobulin M (IgM), IgA, and IgG by indirect enzyme-linked immunosorbent assays with recombinant Norwalk virus antigen bound to the solid phase. Sixteen of the 17 volunteers had evidence of past infection, all presenting with preexisting IgG antibody of high avidity; only one volunteer had no evidence of previous infection. Virus infection was detected in 14 of the 16 volunteers with evidence of past infection, and 9 of the infected volunteers had symptomatic illness. A significant rise in both virus-specific IgA and IgG titers was detected after challenge in all of the volunteers who became ill. Five of the asymptomatic volunteers who were infected had rising titers of virus-specific IgG, but only two of the five had a concomitant rise in their virus-specific IgA antibody titers. Antibody rises were detectable in eight of nine ill volunteers 8 to 11 days after challenge but in the asymptomatic volunteers only after more than 15 days had elapsed. Virus-specific IgM was detected after challenge in all 14 infected volunteers. Between symptomatic and asymptomatic volunteers there were no significant differences in titers of virus-specific IgG and IgA in serum before challenge; however, there were significantly higher titers in symptomatic volunteers between 8 and > 90 days after challenge for virus-specific IgG and 8 and 24 days after challenge for virus-specific IgA.     

用重组汉坦病毒NP、GP检测急性期HFRS患者血清中特异性IgG、IgM、IgA抗体

目的 探讨肾综合征出血热(HFRS)患者急性期IgA、IgG、IgM抗体的变化规律。方法 使用套式RT-PCR检测此次病毒感染情况。用杆状病毒表达的汉坦病毒重组核蛋白(rNP)和糖蛋白(rGP)为抗原，使用ELISA方法检测了14例急性期肾综合征出血热患者的6l份系列血清中的IgA、IgG、IgM抗体。结果 14例肾综合征出血热患者中，ll例患者的血清用RT-PCR检出家鼠型汉坦病毒核酸。几乎所有肾综合征出血热患者早期即有IgA、IgM、IgG抗体的迅速升高，抗rNP抗体滴度明显高于rGP。3种抗rNP抗体中早期IgG上升趋势最为显著，IgM与IgA次之，IgM与IgA上升趋势相近，但IgA的滴度明显高于IgM。抗rGP抗体中XgA变化最显著，IgG次之。IgM发病2周内总的变化趋势不明显，但是发病l周内滴度上升趋势明显，而发病第2周内则呈下降趋势。其中l例RT-PCR阳性的患者，早期IgM未测出，IgA的滴度却较高。l例重度患者，抗糖蛋白IgG、IgM和IgA抗体滴度均低于其他患者，且整个急性期一直维持较低水平。结论 肾综合征出血热急性期IgA、IgG、lgM变化具有明显的规律，抗糖蛋白和核蛋白抗体病患规律不同，检测IgM的同时检测IgA，可以提高诊断的准确性。