Widespread immunization against pertussis was implemented with whole cell wP vaccines in the s and s in many industrialized countries. This article reviews data on the duration of immunity acquired by infection with B. Before the implementation of immunization programs, pertussis was widely recognized as a severe disease among children. Adults in the prevaccine era rarely presented with typical forms of pertussis. Symptomatic reinfections with B. A prospective cohort study in the Netherlands documented B.
This study provided well-documented evidence that the duration of infection-acquired immunity in children may be as short as 3. A study in Senegal of children documented 2 episodes of confirmed symptomatic pertussis in unvaccinated children 0. The current estimates of the duration of infection-acquired immunity range from 7—10 years 12,16 to 20 years.
Estimates of the duration of immunity acquired after wP vaccination range from 4 to 12 years Table 2. Estimates of duration of immunity after vaccination have been most frequently based on 2 studies. Jenkinson, 17 a private physician in the United Kingdom, studied a semirural community consisting of 11, people for a period of 10 years and identified cases of pertussis.
Vaccine efficacy was calculated for each age group by excluding the unvaccinated cases and subtracting the attack rate number of cases divided by the number at risk from 1. Although children from each age group would have been born in different years, each age group was treated as its own cohort. A recent study based on Australian notification data investigated the effect of age at administration of last vaccine dose on the average age of childhood pertussis cases. Australia introduced a fifth dose of wP vaccine at 4—5 years of age in late In the peak rate of disease was among 8- to 9-year-olds, whereas in the peak rate of disease was in to year-olds.
This study thus provides evidence that immunity acquired by wP vaccination wanes 6—9 years after the last dose. Although vaccine efficacy studies have demonstrated that there is no loss of protective immunity after wP vaccination during the first 2 years after vaccination, 22 asymptomatic infections have been reported to occur within the first year after vaccination with wP vaccine.
In the s, aP vaccine efficacy trials were conducted in various countries. In the United States, the first aP vaccine was licensed for use in Although aP vaccines were only recently introduced, some published reports on the duration of immunity are available. Results suggest that the duration of protective immunity after vaccination with aP vaccines is not substantially different from that after vaccination with wP vaccines Table 3.
Whereas in children 18 months-4 years old, the pertussis incidence rate was higher in those vaccinated with aP vaccine than in those vaccinated with wP vaccine [incidence rate ratio IRR , 1. This may suggest a longer duration of protective immunity acquired by wP vaccination than by aP vaccination. In contrast, 2 studies monitoring the long term effectiveness of pertussis vaccines did not find a difference between the duration of immunity after aP 2-component JNIH-6 and wP vaccine monovalent Wellcome.
There are many limitations in our understanding of the duration of immunity after both natural infection and vaccination. No clear serologic marker exists for protective immunity against pertussis. Studies have not been able to control for levels of circulating B.
This may be important because asymptomatic infections will boost the level of immunity and can thus lead to an overestimation of the duration of protection against symptomatic disease. Pertussis vaccine efficacy studies have demonstrated a decrease in the transmission of B. Another limitation of follow-up of vaccine efficacy trials lies in the difficulty of separating vaccine efficacy from waning immunity. Nonetheless the potential overall impact on the population remains considerable.
Despite the limitations in measuring persistence of immunity to pertussis disease after natural infection or vaccination, some common themes have emerged.
Protective immunity after infection was probably never lifelong and wanes after 7—20 years. Duration of immunity after either wP or aP immunization does not appear to substantially differ and likely lasts 4—12 years in children. Clear differences between immunity after vaccination and disease are difficult to distinguish based on available published data. The interplay between waning immunity and boosting of pertussis immunity by B. Further research into the rate of waning of vaccine-acquired immunity will help determine the optimal age and frequency of booster immunizations and their role in pertussis control.
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TABLE 2. TABLE 3. The return of pertussis. Pediatr Infect Dis J. Cited Here Centers for Disease Control and Prevention. Pertussis : United States, — Black S. Epidemiology of pertussis. Sustained efficacy during the first 6 years of life of 3-component acellular pertussis vaccines administered in infancy: the Italian experience. Effect of the preschool pertussis booster on national notifications of disease in Australia.
Bordetella pertussis surveillance in England and Wales: —7. Epidemiol Infect. PubMed CrossRef. Women were excluded from the study if, they were less than 18 years old, menstruating or pregnant. At enrolment, participants were asked to answer a questionnaire about demographic information, sexual behavior, duration of sex work, number of sex partners, condom use, vaginal douching practices, and reproductive history.
Each participant underwent a genital examination by a physician.
Vaginal specimens were obtained for diagnosis of candidiasis, trichomoniasis and bacterial vaginosis by microscopic examination and herpes simplex virus HSV infection by PCR. None of these women were injecting drug users. The three study groups were all in the follicular phase of their menstrual cycle, as determined by blood progesterone levels, not taking oral contraception or injectable contraception such as DMPA or implanted ring, had no HSV, N gonorrhoeae , C trachomatis infection, bacterial vaginosis, trichomoniasis or candidiasis.
Written informed consent was obtained from all subjects who participated in the study. Mucus was removed initially prior to performing the Cervico-vaginal lavage CVL. CVL samples were obtained from all study participants by a physician, using a ml syringe filled with sterile 1x phosphate-buffered solution PBS and aimed directly into the cervical os. CVL fluids were then collected, transferred immediately into 20 ml of RPMI, kept on ice, and processed within 1 hour.
The CVL cellular fractions were cryopreserved in liquid nitrogen. CVL cells were fixed with 1. Flow-cytometry data analysis quadrants were set based on the expression values obtained with fluorescence minus one FMO and isotype controls. Cell processing, staining and analysis were performed as mentioned above. HIV-gp and -gp41 Ig reactivity was detected based on the method previously described [ 14 , 15 ]. The remaining supernatants following IgA recovery were used to detect IgM reactivity.
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Analyses were performed using GraphPad Prism 5. There were no statistical differences for age between HESNs and the two other groups. All women were practicing vaginal douching. Gating strategies are found in S1 Fig. SD, standard deviation. Gating strategies are found in S3 Fig. Cells were pre-incubated with fully glycosylated gp IIIB and processed for flow-cytometry.
There were no significant differences in total IgM and IgA levels between the groups. Values below the dotted line were considered as negative. We hypothesized that maintenance of low-inflammatory conditions in the female genital tract of HESN individuals may help to prevent excessive immune activation and lower HIV target availability, likely maintaining the integrity of the mucosal barrier to protect from HIV infection [ 4 , 20 ]. As to whether these are related to advantageous genetic polymorphisms remain to be established.
Growing importance is given to innate MZ B-cells in health and disease [ 11 ], as they constitute early first-line defense against invading pathogens and participate in the development of adaptive antibody Ab responses by trafficking to follicular B-cell areas of lymphoid structures and promoting germinal center reactions [ 25 ]. Although this suggests that these cells have the capacity to transfer HIV to target cells, it is unlikely that they get infected by the virus since it has not yet been convincingly shown to infect or replicate in B-cells in vivo [ 29 ].
It is possible that the relative binding capacity was lower in the HIV-infected CSWs because gp receptors were saturated in these individuals. In contrast to that observed by He et al [ 17 ], pre-incubation of total B-cells with mannose did not significantly diminish gp binding S2B Fig , suggesting receptors of various types might be involved. Identifying these receptors and B-cell sub-population s binding gp that are increased in HESNs will require further experimentation. In humans, MZ B-cells recirculate and have been found in front-line areas such as the sub epithelial lamina propria of mucosal associated lymphoid tissues MALT [ 11 ].
To our knowledge, we show for the first time that MZ-like B-cells can be found in the female genital tract, which is part of the MALT and is populated by a commensal microflora [ 4 , 30 ]. Moreover, it has been shown that the gut lamina propria can be a T-independent inductive site in humans [ 31 ] and likely similar mechanisms operate at the genital lamina propria. The fact that HESNs who undergo sex-break eventually seroconvert [ 33 ], suggests natural immunity involves populations of which pool maintenance in the genital mucosal niche requires frequent antigen exposure, and this is consistent with first-line responses.
Most genital immunoglobulins Ig are found in the mucus [ 35 ], unfortunately the latter was removed prior to CVL sample collection in our study. It is possible that lower levels of Ig are present in the samples of HESNs but mucus removal has precluded their detection. Interestingly, we could detect IgG1 reactivity to gp41 in some HESNs, which could be derived from a microbiota reactive, possibly first-line B-cell pool [ 37 ], as most gp41 reactive Abs cross-react with microbiota [ 38 ].
There is increasing evidence for non-neutralizing functions of antibodies in decreasing the viral load, and in conferring some level of protection [ 39 ]. In this view, anti-gp41 IgG antibodies are found in the plasma of HIV-infected individuals shortly after transmission, and form antibody-virion complexes, which although ineffective at controlling disease progression [ 40 ], have been associated with infectivity decay [ 41 ]. Comparison between HESN and women involved in sex work but not yet HESN should also be done to control the effects of sex work itself on genital immunology.
The fact that human genital innate MZ-like B-cells naturally bind to fully glycosylated gp renders these cells of particular interest because MZ B-cells can acquire Ig somatic mutations and could be harnessed to increase HIV-ENV affinity.
Statistical significance of differences were evaluated with Mann Withney U test when statistical no-parametric and with Unpaired T test when statistical parametric between HESNs and the two other groups. We are grateful to the Beninese study participants. We are indebted to N. Geraldo, A. Gabin, C. Assogba and C. Agossa-Gbenafa for their clinical expertise, to M. Massinga-Loembe, G. Ahotin, L. Djossou, and E. Goma for their technical assistance and to G. Batona and other field workers who helped with recruitment of commercial sex workers.
We also thank K. Beauchemin and V. Thibodeau for their help in managing the cohort. We are grateful to D. We are grateful to Christian Charbonneau for help with imaging. Author summary Worldwide, most human immunodeficiency virus HIV infections affect women through heterosexual intercourse. Ethics statement Written informed consent was obtained from all subjects who participated in the study.
Flow-cytometry characterization of total B-cells, plasmablasts and plasma cells in the CVL cellular fraction Cell processing, staining and analysis were performed as mentioned above. Download: PPT.
Table 1. Fig 1. Fig 2. Fig 3.