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PubMed2006

Tuberculin skin test conversion and reactivity rates among adults with and without human immunodeficiency virus in urban settings in Ethiopia.

To investigate whether low CD4+ T-cell counts in healthy and human immunodeficiency virus (HIV)-infected Ethiopians influence tuberculosis (TB) immunological memory, tuberculin skin test (TST) conversion and reactivity rates were investigated among adults with and without HIV infection in urban settings in Ethiopia. Reaction to the TST was analyzed with purified protein derivative by the Mantoux technique. A total of 1,286 individuals with TST results of > or = 5-mm (n = 851) and < or = 4-mm (n = 435) induration diameters were included. Individuals with < or = 4-mm induration sizes were followed up for 21.4 +/- 9.5 months (mean +/- standard deviation) to observe skin test conversion. The overall TST reactivity (> or = 5-mm induration diameter) was 66.2% (n = 851). Reactivity was significantly lower among HIV-positive persons (40.5%) than among HIV-negative persons (68.7%) (P < 0.001). Of the above persons, 32 incident TB patients were checked for their TST status 13.05 +/- 11.1 months before diagnosis and reactivity was found among 22 (68.7%) of them. Of the TST-negative persons with 0- to 4-mm indurations who were followed up for 3 years, the conversion rate to positivity was 17.9/100 person-years of observation (PYO) (14.4/100 PYO and 18.3/100 PYO in HIV-positive and -negative persons, respectively). Despite lower absolute CD4+ T-cell numbers in Ethiopians, higher TST conversion and reactivity rates show the presence of a higher rate of latent TB infection and/or transmission. The lower TST positivity rate before a diagnosis of TB disease showed the lower sensitivity of the test. This indicates the need for other sensitive and specific diagnostic and screening methods to detect TB infection, particularly among HIV-positive persons, so that they can be given prophylactic isoniazid therapy.

AIDS-Related Opportunistic Infections↗
PubMed1975

Immunological sequelae of Trichinella spiralis infection in mice: effect on the antibody responses to sheep erythrocytes and Japanse B encephalitis virus.

Immunosuppression of the antibody response to Japanese B encephalitis (JBE) virus and sheep erythrocytes (SRBC) was observed in mice infected with Trichinella spiralis. This suppression was paralleled by the presence of fewer antibody-forming cells to SRBC in the spleens of parasitized mice. Both primary and secondary complement-fixing antibody responses to JBE virus were suppressed, but the development of immunological memory was not affected. Parasitized mice demonstrated a normal blastogenic response to phytohemagglutinin and normal serum clearance rate of injected (125)I-labeled immunoglobulin G(2b), although the size of the extravascular fluid compartment was significantly increased. The data presented here and in previous reports suggest that sequential antigenic competition is a possible explanation for the humoral immunosuppression to heterologous antigens caused by T. spiralis infection.

Animals↗
PubMed1980

Host defenses in murine malaria: immunological characteristics of a protracted state of immunity to Plasmodium yoelii.

Random-bred ICR mice recovered from infection with avirulent Plasmodium yoelii were challenged at various later times with virulent P. yoelii or with another species of Plasmodium, P. berghei, to characterize the immunological nature of the long-term state of immunity generated in response to the avirulent infection. It was found that recovered mice resisted lethal challenge with virulent P. yoelii through at least 416 days after primary infection. However, the quality of this immunity changed as the time after avirulent infection increased. Mice challenged early after recovery were able to prevent the development of patent parasitemia. Later, these immune animals lost this capacity and after challenge infections progressed to patency at the same rate as did nonimmune controls. However, after the establishment of parasitemia, those animals which had encountered the homologous parasite a long time before controlled, and then eliminated, blood infection and survived. The "early" state of immunity was expressed by animals which may have harbored small numbers of viable avirulent parasites and possessed a protective humoral factor which could passively transfer anti-P. yoelii activity to naive recipients. In contrast, animals with "late" immunity showed evidence of neither persisting avirulent parasites nor serum anti-P. yoelii activity. The results support the proposition that immunity to this parasite exists as two distinct but interrelated states of immunological reactivity: an early "active" immunity and a later state which has characteristics suggestive of a state of immunological memory wherewith the animals were capable of anamnestically responding to P. yoelii challenge. Little evidence of heterologous immunity to P. berghei was observed for animals recovered from P. yoelii.

Animals↗
PubMed1981

Immunization of chimpanzees with hepatitis B virus-derived polypeptides.

Previous studies established that the purified polypeptides derived from the 22-nm particles associated with hepatitis B surface antigen (HBsAg) produce both humoral and cellular immunity against HBsAg in guinea pigs. Therefore, the two major polypeptides with molecular weights of 22,000 and 25,000 (P22 and P25, respectively) were isolated, adsorbed to an alum adjuvant, and used to immunize four nonimmune chimpanzees. A vigorous anti-HBs response was observed in all four animals after one inoculation of an alum-adsorbed polypeptide vaccine containing 40 micrograms of protein. After one to two booster inoculations, anti-HBs switched from being predominantly immunoglobulin M to the immunoglobin G class, indicating the establishment of immunological memory. Challenge of the vaccinated chimpanzees with 30,000 chimpanzee infectious doses of hepatitis B virus provided evidence for the efficacy of this vaccine. None of the four animals developed serological markers associated with an active hepatitis B infection, and no biochemical or histopathological changes of hepatitis were observed. A nonvaccinated control chimpanzee that was inoculated with the same hepatitis B virus material developed hepatitis B infection, confirming infectivity of the challenge inoculum.

Alanine Transaminase↗
PubMed1988

Immunogenicity of liposomes and iscoms containing the major outer membrane protein of Neisseria gonorrhoeae: influence of protein content and liposomal bilayer composition.

The influences of Neisseria gonorrhoeae protein IB content and bilayer composition of liposomes and protein content of iscoms on immunogenicity were investigated. Changes in the protein content of liposomes did not influence the immunoglobulin G response, whereas the response was lowered when the amount of protein in iscoms was increased. Bilayer composition only influenced the primary immunoglobulin G response; immunological memory was not affected.

Animals↗
PubMed1989

Interactions between endogenous gamma interferon and tumor necrosis factor in host resistance against primary and secondary Listeria monocytogenes infections.

Intravenous injection of rat anti-mouse gamma interferon (IFN-gamma) monoclonal antibody as well as rabbit anti-mouse tumor necrosis factor (TNF) antibody into mice which had received a sublethal infection with Listeria monocytogenes cells resulted in acceleration of listeriosis. Endogenous IFN-gamma seemed to be produced early in infection, because suppression of antilisterial resistance was significant when a single injection of anti-IFN-gamma monoclonal antibody was given on day 0 or day 1 of infection. Production of TNF but not of IFN-gamma in the bloodstream early in infection was inhibited by administration of anti-IFN-gamma monoclonal antibody. The suppressive effect of anti-IFN-gamma and anti-TNF antibodies on antilisterial resistance was not augmented by simultaneous administration of these antibodies. On the other hand, in the secondary infection, simultaneous administration of anti-IFN-gamma and anti-TNF antibodies, but not of either of these antibodies alone, into L. monocytogenes-immune mice resulted in high mortality and explosive multiplication of bacterial cells in the spleens and livers. These results suggest that endogenously produced IFN-gamma and TNF are both essential to the host defense against L. monocytogenes infection and that these cytokines might act by different modes between the primary infection and the secondary infection.

Animals↗
PubMed1991

Protective ribosomal preparation from Shigella sonnei as a parenteral candidate vaccine.

A parenteral Shigella ribosomal vaccine (SRV) was investigated in animals for safety, antibody-inducing capacity, and protective activity. Ribosomal preparations from a Shigella sonnei phase I avirulent strain were obtained and shown to possess chemical, sedimentation, and other properties typical of bacterial ribosomes. No endotoxin contamination was revealed by a ketodeoxyoctonate assay, although the presence of some kind of O antigen was evidenced by serological findings and the high activity of SRV in inducing the O-antibody response and immunological memory in animals. SRV was nontoxic in mice, guinea pigs, and monkeys and induced no local reactions when injected subcutaneously in reasonable doses. Significant protection against a local Shigella infection (Sereny test) was seen in guinea pigs injected with SRV (efficiency index, about 60%) and the specificity of the protection was evident from cross-challenge experiments. The protective efficiency of SRV was especially high in rhesus monkeys challenged orally with virulent Shigella cells (89%, as calculated from the summarized data of several experiments in 71 animals). Protection in monkeys was long lasting and could be demonstrated several months after injection of SRV. An inexpensive technique can be used for the production of SRV on a large scale. The high immunogenicity of SRV is discussed in terms of the amplifying effect of the ribosome, which serves as a delivery system for polysaccharide O antigen. Further study of SRV as a candidate vaccine for humans seems justified by the data obtained.

Animals↗
PubMed1999

Transformed Toxoplasma gondii tachyzoites expressing the circumsporozoite protein of Plasmodium knowlesi elicit a specific immune response in rhesus monkeys.

Toxoplasma gondii tachyzoites were transformed with the coding sequence of the circumsporozoite (CS) protein of the primate malaria parasite Plasmodium knowlesi. A single inoculation of live transformed tachyzoites elicited an antibody response directed against the immunodominant repeat epitope (EQPAAGAGG)2 of the P. knowlesi CS protein in rhesus monkeys. Notably, these animals failed to show a positive serum conversion against T. gondii. Antibodies against Toxoplasma antigens were detected only after a second inoculation with a higher number of transformed tachyzoites. This boost induced an increased antibody response against the P. knowlesi CS protein associated with immunoglobulin class switching, thus demonstrating the establishment of immunological memory. These results indicate that the Toxoplasma-derived CS protein is efficiently recognized by the monkey immune system and represents an immunodominant antigen in transformed parasites.

Amino Acid Sequence↗
PubMed1999

A longitudinal study of human antibody responses to Plasmodium falciparum rhoptry-associated protein 1 in a region of seasonal and unstable malaria transmission.

Rhoptry-associated protein 1 (RAP1) of Plasmodium falciparum is a nonpolymorphic merozoite antigen that is considered a potential candidate for a malaria vaccine against asexual blood stages. In this longitudinal study, recombinant RAP1 (rRAP1) proteins with antigenicity similar to that of P. falciparum-derived RAP1 were used to analyze antibody responses to RAP1 over a period of 4 years (1991 to 1995) of 53 individuals naturally exposed to P. falciparum malaria. In any 1 year during the study, between 23 and 39% of individuals who had malaria developed immunoglobulin G (IgG) antibodies detectable with at least one rRAP1 protein. However, the anti-RAP1 antibody responses were detected only during or shortly after clinical malarial infections. RAP1 antibody levels declined rapidly (within 1 to 2 months) following drug treatment of the infections. No anti-RAP1 antibodies were usually detected a few months after the end of malaria transmission, during the dry season, or by the start of the next malaria season. Thus, RAP1 IgG responses were very short-lived. The short duration of RAP1 antibody response may explain the apparent lack of response in a surprisingly high proportion of individuals after clinical malarial infections. For some individuals who experienced more than one malarial infection, a higher anti-RAP1 antibody response to subsequent infections than to earlier infections was observed. This suggested secondary responses to RAP1 and thus the development of immunological memory for RAP1.

Adult↗
PubMed1999

Limited local and systemic antibody responses to Neisseria gonorrhoeae during uncomplicated genital infections.

Repeated infections with Neisseria gonorrhoeae are common among patients attending sexually transmitted disease clinics. We examined whether previous infections or site of infection altered the local and systemic antigonococcal antibody levels in males and females. Antibodies against N. gonorrhoeae MS11 and the patients' homologous infecting isolates were measured by enzyme-linked immunosorbent assay. In general, the local and systemic immune responses to gonococci were extremely modest. There was a slight increase in serum immunoglobulin G (IgG) against the MS11 strain and the homologous isolates in infected males. Levels of serum IgA1 antibodies against MS11 were slightly higher in infected than in uninfected females. A history of previous infections with N. gonorrhoeae did not alter the antibody levels in patients with a current infection, suggesting that immunological memory is not induced by uncomplicated gonococcal infections. Antibody responses to infected subjects' homologous isolates were observed in cervical mucus; IgA1 levels increased while IgG levels decreased. The decline in mucosal IgG against the homologous isolates was less common in subjects having both rectal and cervical infections; otherwise, no effect of rectal involvement was observed. The absence of substantially higher antibody levels to gonococci where there is infection at a site known to contain organized lymphoid tissue suggests that the low levels of responses to uncomplicated infections may not be due simply to an absence of inductive sites in the genital tract. We propose that in addition to its potential ability to avoid the effects of an immune response, N. gonorrhoeae does not elicit strong humoral immune responses during uncomplicated genital infections.

Antibodies, Bacterial↗
PubMed2000

Immunity to murine Chlamydia trachomatis genital tract reinfection involves B cells and CD4(+) T cells but not CD8(+) T cells.

CD4(+) T-helper type 1 (Th1) responses are essential for the resolution of a primary Chlamydia trachomatis genital tract infection; however, elements of the immune response that function in resistance to reinfection are poorly understood. Defining the mechanisms of immune resistance to reinfection is important because the elements of protective adaptive immunity are distinguished by immunological memory and high-affinity antigen recognition, both of which are crucial to the development of efficacious vaccines. Using in vivo antibody depletion of CD4(+) and CD8(+) T cells prior to secondary intravaginal challenge, we identified lymphocyte populations that functioned in resistance to secondary chlamydial infection of the genital tract. Depletion of either CD4(+) or CD8(+) T cells in immune wild-type C57BL/6 mice had a limited effect on resistance to reinfection. However, depletion of CD4(+) T cells, but not CD8(+) T cells, in immune B-cell-deficient mice profoundly altered the course of secondary infection. CD4-depleted B-cell-deficient mice were unable to resolve a secondary infection, shed high levels of infectious chlamydiae, and did not resolve the infection until 3 to 4 weeks following the discontinuation of anti-CD4 treatment. These findings substantiated a predominant role for CD4(+) T cells in host resistance to chlamydial reinfection of the female genital tract and demonstrated that CD8(+) T cells are unnecessary for adaptive immune resistance. More importantly, however, this study establishes a previously unrecognized but very significant role for B cells in resistance to chlamydial reinfection and suggests that B cells and CD4(+) T cells may function synergistically in providing immunity in this model of chlamydial infection. Whether CD4(+) T cells and B cells function independently or dependently is unknown, but definition of those mechanisms is fundamental to understanding optimum protective immunity and to the development of highly efficacious immunotherapies against chlamydial urogenital infections.

Animals↗
PubMed2000

Genital antibody responses in mice after intranasal infection with an attenuated candidate vector strain of Bordetella pertussis.

Intranasal administration of live attenuated Bordetella pertussis, from which the pertussis toxin gene has been deleted, has previously been shown to give rise to high levels of serum immunoglobulin G (IgG) antibodies against both the protective antigen filamentous hemagglutinin (FHA) and heterologous antigens genetically fused to FHA. Here, we extend these results by demonstrating that anti-FHA IgA and IgG antibodies are also produced in the genital tract of mice, both in the vagina and in the uterus, after a single intranasal administration of B. pertussis. By comparing the immune responses induced after infection with wild-type virulent B. pertussis with that induced by infection with an attenuated pertussis toxin-deficient strain, we conclude that pertussis toxin produced by the virulent bacteria does not modify antibody production to FHA in the genital tract of B. pertussis-infected mice. The intranasal infection with either the attenuated or the virulent B. pertussis strain also led to the development of immunologic memory that could be efficiently boosted with purified FHA administered either intranasally or intravaginally to give rise to a significant increase in the levels of specific IgA and IgG produced locally in the genital tract, as well as of specific antibodies in the serum. These observations suggest that attenuated B. pertussis could be a promising vector for intranasal administration to induce antibody responses against antigens from sexually transmitted pathogens fused to FHA.

Adhesins, Bacterial↗
PubMed2001

Serological basis for use of meningococcal serogroup C conjugate vaccines in the United Kingdom: reevaluation of correlates of protection.

The antibody data supporting the use of meningococcal serogroup C conjugate (MCC) vaccines in the United Kingdom were generated by serum bactericidal assay (SBA) using rabbit complement (rSBA). This may give higher titers than those obtained with human complement (hSBA), for which the "gold standard" correlate of protection for meningococcal C disease is a titer of > or =4. Comparison of rSBA and hSBA titers in sera from unvaccinated adults with an rSBA titer of > or =8 showed that for 93% (27 of 29) the titer was > or =4 by hSBA, confirming natural protection. Furthermore, sera from MCC vaccinees showed that an rSBA titer of <8 or > or =128 discriminated susceptibility and protection well (85% with rSBA titers of <8 had hSBA titers of <4, and 99% with rSBA titers of > or =128 had hSBA titers of > or =4). However, discrimination was poor in the rSBA titer range 8 to 64, with only 60% having hSBA titers of > or =4. In such cases we propose that protection can be assumed if there is a fourfold rise in titer between pre- and postvaccination sera or if there is a characteristic booster response to a polysaccharide challenge dose with, if available, evidence of antibody avidity maturation or an hSBA titer of result > or =4. Applying these criteria to toddlers, 10 to 40% of whom had titers in the range 8 to 64 after a single dose of MCC vaccine, showed that 94% had a fourfold rise in titer, including 98% of those in the titer range 8 to 64. In addition, of those with titers of <128 post-MCC vaccination, 90% had titers of > or =128 after a 10-microg polysaccharide booster dose, compared with only 7% of unprimed age-matched toddlers given a full 50-microg dose. Furthermore, the increase in geometric mean avidity index pre- and postbooster was independent of post-primary MCC titer. These results indicated that the majority of toddlers with an rSBA titer between 8 and 64, and some of those with an hSBA result of <4, have mounted a protective immune response with the induction of immunological memory.

Adolescent↗
PubMed2002

Tolerance to self gangliosides is the major factor restricting the antibody response to lipopolysaccharide core oligosaccharides in Campylobacter jejuni strains associated with Guillain-Barré syndrome.

Guillain-Barré syndrome following Campylobacter jejuni infection is frequently associated with anti-ganglioside autoantibodies mediated by molecular mimicry with ganglioside-like oligosaccharides on bacterial lipopolysaccharide (LPS). The regulation of antibody responses to these T-cell-independent antigens is poorly understood, and only a minority of Campylobacter-infected individuals develop anti-ganglioside antibodies. This study investigates the response to gangliosides and LPS in strains of mice by using a range of immunization strategies. In normal mice following intraperitoneal immunization, antibody responses to gangliosides and LPS are low level but can be enhanced by the antigen format or coadministration of protein to recruit T-cell help. Class switching from the predominant immunoglobulin M (IgM) response to IgG3 occurs at low levels, suggesting B1-cell involvement. Systemic immunization results in poor responses. In GalNAc transferase knockout mice that lack all complex gangliosides and instead express high levels of GM3 and GD3, generation of anti-ganglioside antibodies upon immunization with either complex gangliosides or ganglioside-mimicking LPS is greatly enhanced and exhibits class switching to T-cell-dependent IgG isotypes and immunological memory, indicating that tolerance to self gangliosides is a major regulatory factor. Responses to GD3 are suppressed in knockout mice compared with wild-type mice, in which responses to GD3 are induced specifically by GD3 and as a result of polyclonal B-cell activation by LPS. The anti-ganglioside response generated in response to LPS is also dependent on the epitope density of the ganglioside mimicked and can be further manipulated by providing secondary signals via lipid A and CD40 ligation.

Animals↗
PubMed2006

Splenic gammadelta T cells regulated by CD4+ T cells are required to control chronic Plasmodium chabaudi malaria in the B-cell-deficient mouse.

Little is known about the function and regulation of splenic gammadelta T cells during chronic Plasmodium chabaudi malaria. The splenic gammadelta T-cell population continues to expand, reaching levels equal to 4 times the number of splenocytes in an uninfected mouse. Splenic gammadelta T cells from J(H)-/- mice with chronic malaria expressed Vgamma1+ or Vdelta4+ in the same ratio as uninfected controls with Vgamma1 cells dominating, but the Vgamma2 ratio declined about twofold. Gammadelta T cells from G8 mice specific for the TL antigen increased only 2-fold in number, compared with 10-fold in BALB/c controls, but G8 gammadelta T cells failed to express the B220 activation marker. Elimination of the parasite by drug treatment caused a slow depletion in the number of splenic gammadelta, CD4+, and CD8+ T cells. Following challenge, drug-cured J(H)-/- mice exhibited nearly identical parasitemia time courses as naïve controls. Depletion of either CD4+ T cells or gammadelta T cells from chronically infected J(H)-/- mice by monoclonal antibody treatment resulted in an immediate and significant (P < 0.05) exacerbation of parasitemia coupled with a marked decrease in splenic gammadelta T-cell numbers. The number of CD4+ T cells, in contrast, did not decrease in mice after anti-T-cell receptor gammadelta treatment. The results indicate that cell-mediated immunity against blood-stage malarial parasites during chronic malaria (i) requires the continued presence of blood-stage parasites to remain functional, (ii) is dependent upon both gammadelta T cells and CD4+ T cells, and (iii) lacks immunological memory.

Animals↗
PubMed1969

Secondary and tertiary responses of the induced bactericidin from the West Indian spiny lobster, Panulirus argus.

West Indian spiny lobsters, Panulirus argus, synthesized a hemolymph bactericidin after being injected with killed suspensions of gram-negative bacillus EMB-1 isolated from the normal gut of this lobster. To study differences between the primary response and secondary response, animals were given a primary antigen injection of EMB-1 followed by a second injection of the same antigen 22 to 51 days later. As a rule, secondary bactericidal responses were enhanced over the primary in a manner reminiscent of specific anamnesis in mammalian immunoglobulin synthesis. Immunological memory was also suggested when tertiary responses were compared to secondary and by the persistence of residual titers for many days or weeks without additional antigenic stimulation.

Animals↗
PubMed2000

Characterization of chemokine receptor utilization of viruses in the latent reservoir for human immunodeficiency virus type 1.

Latently infected resting CD4(+) T cells provide a long-term reservoir for human immunodeficiency virus type 1 (HIV-1) and are likely to represent the major barrier to virus eradication in patients on combination antiretroviral therapy. The mechanisms by which viruses enter the latent reservoir and the nature of the chemokine receptors involved have not been determined. To evaluate the phenotype of the virus in this compartment with respect to chemokine receptor utilization, full-length HIV-1 env genes were cloned from latently infected cells and assayed functionally. We demonstrate that the majority of the viruses in the latent reservoir utilize CCR5 during entry, although utilization of several other receptors, including CXCR4, was observed. No alternative coreceptors were shown to be involved in a systematic fashion. Although R5 viruses are present in the latent reservoir, CCR5 was not expressed at high levels on resting CD4(+) T cells. To understand the mechanism by which R5 viruses enter latent reservoir, the ability of an R5 virus, HIV-1 Ba-L, to infect highly purified resting CD4(+) T lymphocytes from uninfected donors was evaluated. Entry of Ba-L could be observed when virus was applied at a multiplicity approaching 1. However, infection was limited to a subset of cells expressing low levels of CCR5 and markers of immunologic memory. Naive cells could not be infected by an R5 virus even when challenged with a large inoculum. Direct cell fractionation studies showed that latent virus is present predominantly in resting memory cells but also at lower levels in resting naive cells. Taken together, these findings provide support for the hypothesis that the direct infection of naive T cells is not the major mechanism by which the latent infection of resting T cells is established.

CD4-Positive T-Lymphocytes↗
PubMed2003

Codelivery of CCR7 ligands as molecular adjuvants enhances the protective immune response against herpes simplex virus type 1.

Humoral and cellular immunity, associated with long-term protective immunological memory, defines the efficacy of a given vaccine formulation. However, few vaccines achieve this target without the aid of a suitable adjuvant. Molecular adjuvants in vaccination against infectious agents offer a noninvasive means of enhancing the immune response against target antigens. To examine the potency of two beta-chemokines as immunomodulators, plasmid DNA encoding beta-chemokines CCL19 and CCL21 (CCR7L) was codelivered intranasally with plasmid DNA or recombinant vaccinia virus encoding herpes simplex virus (HSV) gB (HSV-gB) in a prime-and-boost vaccination strategy. This vaccination regimen increased serum and vaginal immunoglobulin G (IgG) and IgA, respectively, as well as the numbers of HSV-gB(498-505) peptide-specific gamma interferon-producing CD8(+) T cells. Distinctively, a high number of cytotoxic T lymphocytes was achieved when pCCR7L was applied at both prime and boost as opposed to omission of pCCR7L. A rapid-recall response was induced in the genital tract upon challenge with the HSV McKrae strain, affording a high level of protection and survival of vaccinated mice. Our results demonstrate that high innate immune kinetics and distribution of adaptive response induced in the nasal mucosa appears to be key factors in generating protective memory responses against HSV. Thus CCR7L expressed ectopically may serve as a molecular adjuvant to boost the immune response to a codelivered antigen in mucosal surfaces.

Animals↗