Primary infection of goats with Eimeria ninakohlyakimovae does not provide protective immunity against high challenge infections

SUMMARYStrains of mice poorly (B10) or non-responsive (B10.BR) to a primary infection with Trichuris muris were protected against infection by vaccination with excretory/secretory (E/S) antigen in Complete Freund's Adjuvant (CFA). Protection in these mice was slow to be expressed compared to that in good responder strains. Vaccination boosted the IgG and IgG1 antibody responses to E/S antigen and altered the antigen recognition profiles, three high molecular weight antigens (80–85, 90–95, 105–110 kDa) being recognized by antibodies in sera from vaccinated but not control mice. B10. BR mice which had experienced a patent primary infection could not be protected against challenge infections by vaccination and this was correlated with depressed levels of IgG1, but not total IgG, to E'S antigen early post-challenge compared with vaccinated infected mice which had not seen an adult primary infection. There was also lack of recognition of the three high molecular weight antigens recognized by antibodies in sera from mice infected after vaccination. It is suggested that the rapid development of high levels of IgG1 antibodies, and the recognition of the three high molecular weight antigens, may reflect events that are important in protective immunity. Immunomodulation of host immunity by T. muris may therefore be achieved, at least in part, by the suppression of specific IgG1 levels, the production of an irrelevant IgG isotype and prevention of the recognition of critical antigens.

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Distinct Roles of CD28- and CD40 Ligand-Mediated Costimulation in the Development of Protective Immunity and Pathology during Chlamydia muridarum Urogenital Infection in Mice

Infection and Immunity ◽

10.1128/iai.00611-08 ◽

2009 ◽

Vol 77 (7) ◽

pp. 3080-3089 ◽

Cited By ~ 22

Author(s):

Lili Chen ◽

Wen Cheng ◽

Pooja Shivshankar ◽

Lei Lei ◽

Xiaoyun Zhang ◽

...

Keyword(s):

Primary Infection ◽

Protective Immunity ◽

Gene Knockout ◽

Secondary Infection ◽

Cd40 Ligand ◽

Wild Type ◽

Chlamydia Muridarum ◽

Urogenital Infection ◽

Costimulatory Signals ◽

Deficient Mice

ABSTRACT Infection with Chlamydia muridarum in the mouse urogenital tract can induce both protective immunity and inflammatory pathologies, which has been used as a model for understanding the immune and pathogenic mechanisms of C. trachomatis infection. We compared the roles of CD28- and CD40 ligand (CD40L)-mediated costimulation in C. muridarum infection. Mice with CD28 or CD80/CD86 gene knockout (KO) displayed an infection course similar to that of wild-type mice during both primary and secondary infection, suggesting that CD28-mediated costimulation is not required for protection against C. muridarum infection. However, mice deficient in CD40L or CD40 displayed a prolonged infection course after primary or secondary infection, suggesting that CD40-CD40L costimulation plays an essential role in the development of anti-C. muridarum immunity. Interestingly, the CD28- or CD80/CD86-deficient mice displayed significantly lower levels of inflammatory pathologies in the upper genital tracts after primary infection, although the attenuation in inflammation was no longer significant during secondary infection. However, the CD40L or CD40 KO mice developed inflammatory pathologies as severe as those in wild-type mice following either primary or secondary infection despite the obvious deficits in adaptive immunity in these KO mice. The resistance of CD28 or CD80/CD86 KO mice to chlamydial infection correlated with production of gamma interferon, while the development of inflammatory pathologies in CD40L or CD40 KO mice correlated with the production of other proinflammatory cytokines in mouse urogenital tracts during the early stages of the infection. These observations together suggest that C. muridarum-induced protective immunity and inflammatory pathologies can be mediated by distinct costimulatory signals.

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Assessment of the risk of SARS-CoV-2 reinfection in an intense re-exposure setting

10.1101/2020.08.24.20179457 ◽

2020 ◽

Cited By ~ 6

Author(s):

Laith J Abu-Raddad ◽

Hiam Chemaitelly ◽

Joel A Malek ◽

Ayeda A Ahmed ◽

Yasmin A Mohamoud ◽

...

Keyword(s):

Severe Acute Respiratory Syndrome ◽

Incidence Rate ◽

Genome Sequencing ◽

Viral Genome ◽

Primary Infection ◽

Protective Immunity ◽

Good Evidence ◽

Contact Tracing ◽

Random Testing ◽

Exposure Setting

Background: Reinfection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is debated. We assessed risk and incidence rate of documented SARS-CoV-2 reinfection in a large cohort of laboratory-confirmed cases in Qatar. Methods: All SARS-CoV-2 laboratory-confirmed cases with at least one PCR positive swab that is ≥45 days after a first-positive swab were individually investigated for evidence of reinfection, and classified as showing strong, good, some, or weak/no evidence for reinfection. Viral genome sequencing of the paired first-positive and reinfection viral specimens was conducted to confirm reinfection. Risk and incidence rate of reinfection were estimated. Results: Out of 133,266 laboratory-confirmed SARS-CoV-2 cases, 243 persons (0.18%) had at least one subsequent positive swab ≥45 days after the first-positive swab. Of these, 54 cases (22.2%) had strong or good evidence for reinfection. Median time between first and reinfection swab was 64.5 days (range: 45-129). Twenty-three of the 54 cases (42.6%) were diagnosed at a health facility suggesting presence of symptoms, while 31 (57.4%) were identified incidentally through random testing campaigns/surveys or contact tracing. Only one person was hospitalized at time of reinfection, but still with mild infection. No deaths were recorded. Viral genome sequencing confirmed four out of 12 cases with available genetic evidence. Risk of reinfection was estimated at 0.01% (95% CI: 0.01-0.02%) and incidence rate of reinfection was estimated at 0.36 (95% CI: 0.28-0.47) per 10,000 person-weeks. Conclusions: SARS-CoV-2 reinfection can occur but is a rare phenomenon suggestive of a strong protective immunity against reinfection that lasts for at least a few months post primary infection.

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Induction of protective immunity toBrugia pahangiin jirds by drug-abbreviated infection

Journal of Helminthology ◽

10.1017/s0022149x00012748 ◽

1992 ◽

Vol 66 (2) ◽

pp. 147-154 ◽

Cited By ~ 5

Author(s):

Y. Horii ◽

H. Nakanishi ◽

A. Mori ◽

M. Ueda ◽

K. Kurokawa ◽

...

Keyword(s):

Post Infection ◽

Primary Infection ◽

Protective Immunity ◽

Challenge Infection ◽

Significant Protection ◽

Patent Period ◽

Infection Period ◽

Degree Of Protection ◽

Infected Adult ◽

Homologous Challenge

ABSTRACTProtective immunity of homologous challenge infection was examined in jirds after drug-abbreviated infection withBrugia pahangi. Mebendazole (MBZ) treatment at the early prepatent (5–7 weeks of post infection) or the late prepatent (7–9 weeks of post infection) period was highly effective in causing almost complete eradication of the primary infection. After challenge infection, the worm burden was significantly reduced 19% (31·1 in average) and 77% (9·5) to that of the controls (38·8 and 41·7), respectively. The magnitude of eosinophil response paralleled the degree of protection. No or only a few microfilariae were seen after challenge infection in jirds treated during the prepatent periods. They were also resistant to intravenous challenge with the microfilariae ofB. pahangi. MBZ treatment at the patent period was, on the contrary, incomplete against primarily infected adult worms, and was not able to induce either significant protection (30·1 vs 33·1 in control) or eosinophil response to the challenge infection.

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Protective Immunity against Secondary Poxvirus Infection Is Dependent on Antibody but Not on CD4 or CD8 T-Cell Function

Journal of Virology ◽

10.1128/jvi.00115-06 ◽

2006 ◽

Vol 80 (13) ◽

pp. 6333-6338 ◽

Cited By ~ 79

Author(s):

Vijay Panchanathan ◽

Geeta Chaudhri ◽

Gunasegaran Karupiah

Keyword(s):

T Cells ◽

T Cell ◽

Cd8 T Cells ◽

Primary Infection ◽

Protective Immunity ◽

Cell Function ◽

Secondary Infection ◽

Cd8 T Cell ◽

Ectromelia Virus ◽

T Cell Function

ABSTRACT Renewed interest in smallpox and the need for safer vaccines have highlighted our lack of understanding of the requirements for protective immunity. Since smallpox has been eradicated, surrogate animal models of closely related orthopoxviruses, such as ectromelia virus, have been used to establish critical roles for CD8 T cells in the control of primary infection. To study the requirements for protection against secondary infection, we have used a prime-challenge regime, in which avirulent ectromelia virus was used to prime mice that were then challenged with virulent ectromelia virus. In contrast to primary infection, T cells are not required for recovery from secondary infection, since gene knockout mice deficient in CD8 T-cell function and wild-type mice acutely depleted of CD4, CD8, or both subsets were fully protected. Protection correlated with effective virus control and generation of neutralizing antibody. Notably, primed mice that lacked B cells, major histocompatibility complex class II, or CD40 succumbed to secondary infection. Thus, antibody is essential, but CD4 or CD8 T cells are not required for recovery from secondary poxvirus infection.

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A polyvalent DNA vaccine expressing an ESAT6–Ag85B fusion protein protects mice against a primary infection with Mycobacterium tuberculosis and boosts BCG-induced protective immunity

Vaccine ◽

10.1016/j.vaccine.2004.07.036 ◽

2004 ◽

Vol 23 (6) ◽

pp. 780-788 ◽

Cited By ~ 71

Author(s):

Steven C. Derrick ◽

Amy Li Yang ◽

Sheldon L. Morris

Keyword(s):

Mycobacterium Tuberculosis ◽

Fusion Protein ◽

Dna Vaccine ◽

Primary Infection ◽

Protective Immunity

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IL-17 mediates protective immunity against nasal infection with Bordetella pertussis by mobilizing neutrophils, especially Siglec-F+ neutrophils

Mucosal Immunology ◽

10.1038/s41385-021-00407-5 ◽

2021 ◽

Author(s):

Lisa Borkner ◽

Lucy M. Curham ◽

Mieszko M. Wilk ◽

Barry Moran ◽

Kingston H. G. Mills

Keyword(s):

T Cells ◽

Bordetella Pertussis ◽

Primary Infection ◽

Protective Immunity ◽

Bacterial Load ◽

Critical Role ◽

Neutrophil Extracellular Trap ◽

Acquired Immunity ◽

Nasal Tissue ◽

Extracellular Trap

AbstractUnderstanding the mechanism of protective immunity in the nasal mucosae is central to the design of more effective vaccines that prevent nasal infection and transmission of Bordetella pertussis. We found significant infiltration of IL-17-secreting CD4+ tissue-resident memory T (TRM) cells and Siglec-F+ neutrophils into the nasal tissue during primary infection with B. pertussis. Il17A−/− mice had significantly higher bacterial load in the nasal mucosae, associated with significantly reduced infiltration of Siglec-F+ neutrophils. Re-infected convalescent mice rapidly cleared B. pertussis from the nasal cavity and this was associated with local expansion of IL-17-producing CD4+ TRM cells. Depletion of CD4 T cells from the nasal tissue during primary infection or after re-challenge of convalescent mice significantly delayed clearance of bacteria from the nasal mucosae. Protection was lost in Il17A−/− mice and this was associated with significantly less infiltration of Siglec-F+ neutrophils and antimicrobial peptide (AMP) production. Finally, depletion of neutrophils reduced the clearance of B. pertussis following re-challenge of convalescent mice. Our findings demonstrate that IL-17 plays a critical role in natural and acquired immunity to B. pertussis in the nasal mucosae and this effect is mediated by mobilizing neutrophils, especially Siglec-F+ neutrophils, which have high neutrophil extracellular trap (NET) activity.

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Maintenance of neutralizing SARS-CoV-2 antibodies over five months in convalescent SARS-CoV-2 afflicted patients.

10.22541/au.160768745.52792441/v1 ◽

2020 ◽

Author(s):

Sissy Sonnleitner ◽

Martina Prelog ◽

Bainca Jansen ◽

Chantal Rodgarkia-Dara ◽

Sarah Gietl ◽

...

Keyword(s):

Neutralizing Antibodies ◽

Primary Infection ◽

Protective Immunity ◽

Neutralization Assay ◽

Immunofluorescence Assay ◽

Crucial Importance ◽

Wild Type ◽

Specific Antibodies ◽

Chemiluminescent Immunoassay ◽

Type Infection

Level and duration of protective immunity against SARS-CoV-2 after primary infection is of crucial importance for preventive approaches. In order to provide evidence for the longevity of specific antibodies, we investigated the generation and maintenance of neutralizing antibodies of convalescent SARS-CoV-2-afflicted patients over a five month period post primary infection using an immunofluorescence assay, a commercial chemiluminescent immunoassay and an in-house enzyme-linked plaque-reduction neutralization assay. We present the successful application of an improved version of the plaque-reduction neutralization assay, which can be analyzed optometrically, significantly simplifying the interpretation of the results. Based on the results of the plaque-reduction neutralization assay, neutralizing antibodies were maintained in 85.3% of convalescent individuals without significant decay over five months. Furthermore, a positive correlation between severity of infection and neutralizing titer was shown. In conclusion, SARS-CoV-2-afflicted individuals have been proven to be able to establish and maintain neutralizing antibodies over a five months’ period after primary infection which allows to hope for long-lasting presumably protective humoral immunity after wild-type infection or even after vaccination.

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Host predisposition to trichuriasis: the mouse — T. muris model

Parasitology ◽

10.1017/s0031182000062193 ◽

1989 ◽

Vol 98 (2) ◽

pp. 275-282 ◽

Cited By ~ 39

Author(s):

K. J. Else ◽

D. Wakelin ◽

T. I. A. Roach

Keyword(s):

Primary Infection ◽

Protective Immunity ◽

Poor Response ◽

Poor Responder ◽

Parasite Growth ◽

Parasite Development ◽

Poor Responders ◽

Serological Analysis ◽

Antibody Titres ◽

Resistance To Infection

SUMMARYPredisposition to trichuriasis in mice is reflected in the inability of certain strains, or certain individuals within strains, to express protective immunity. Poor responders fail to expel worms and harbour chronic patent infections. The mechanisms underlying this phenomenon were studied in poor responder mice challenged after abbreviated or prolonged primary infections. Mice exposed to a complete primary infection were fully susceptible when challenged after the removal of the primary infection by anthelmintic. Failure to expel either infection suggests (a) that non-responsiveness to a primary infection does not reflect an inability to expel worms of a certain size, i.e. is not a consequence of the speed of the immune response in relation to parasite growth and (b) that non-responsiveness is long-lasting. Challenge after abbreviation of primary infections at different stages of worm development showed that persistence of larvae beyond day 21 was critical in determining poor response to reinfection. By inference the same conclusion can be drawn about the inability of such mice to expel primary infections. Serological analysis suggested a relationship between low antibody titres, restricted antigen recognition profiles and resistance to infection. It is suggested that the later stages of parasite development are immunosuppressive; the implications for human trichuriasis are discussed.

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Immunological regulation of Angiostrongylus cantonensis infections in rats: modulation of population density and enhanced parasite growth following one or two superimposed infections

Journal of Helminthology ◽

10.1017/s0022149x0000941x ◽

1983 ◽

Vol 57 (2) ◽

pp. 155-165 ◽

Cited By ~ 3

Author(s):

W. K. Yong ◽

Colin Dobson

Keyword(s):

Population Density ◽

Adult Worm ◽

Primary Infection ◽

Protective Immunity ◽

Parasite Growth ◽

Angiostrongylus Cantonensis ◽

Single Infection ◽

Total Size ◽

Infective Larvae ◽

Immunological Regulation

ABSTRACTRats acquired a degree of protective immunity to reinfection with Angiostrongylus cantonensis after a single infection with 50 infective larvae. Infected rats resisted the establishment of most challenging larvae and protective immunity increased with subsequent reinfections. Part of the primary infection was lost after a superimposed second and also following a superimposed third infection, but the total size of the concurrent adult worm populations remained the same as that from a primary infection. Worms surviving from the primary infection showed enhanced growth after each reinfection but their fecundity was impaired.

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