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      Tick-borne encephalitis in pregnant women: A mini narrative review

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          Abstract

          Tick-borne encephalitis (TBE) incidence has been increasing in Europe the last decades, but very few cases in pregnant women have been described. We present two cases and describe the serology of both mother and infant at the time of diagnosis and delivery, as well as at months 3, 6, 9, and 12 of follow-up. In both cases, pregnancies and infants developed normally. The mothers had moderate-to severe symptoms of TBE and were positive for IgM and IgG at the time of diagnosis, and throughout the follow up period whilst both infants were PCR- and IgM-negative and positive for IgG during their first months in life. Declining IgG titres were seen in the infants during follow-up until they became negative at the age of nine months. TBE IgG was vertically transmitted in these two cases of infants born to TBE-infected mothers.

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          Tick-borne encephalitis.

          We review the epidemiological and clinical characteristics of tick-borne encephalitis, and summarise biological and virological aspects that are important for understanding the life-cycle and transmission of the virus. Tick-borne encephalitis virus is a flavivirus that is transmitted by Ixodes spp ticks in a vast area from western Europe to the eastern coast of Japan. Tick-borne encephalitis causes acute meningoencephalitis with or without myelitis. Morbidity is age dependent, and is highest in adults of whom half develop encephalitis. A third of patients have longlasting sequelae, frequently with cognitive dysfunction and substantial impairment in quality of life. The disease arises in patchy endemic foci in Europe, with climatic and ecological conditions suitable for circulation of the virus. Climate change and leisure habits expose more people to tick-bites and have contributed to the increase in number of cases despite availability of effective vaccines. The serological diagnosis is usually straightforward. No specific treatment for the disease exists, and immunisation is the main preventive measure.
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            Maternal Antibodies: Clinical Significance, Mechanism of Interference with Immune Responses, and Possible Vaccination Strategies

            Neonates have an immature immune system, which cannot adequately protect against infectious diseases. Early in life, immune protection is accomplished by maternal antibodies transferred from mother to offspring. However, decaying maternal antibodies inhibit vaccination as is exemplified by the inhibition of seroconversion after measles vaccination. This phenomenon has been described in both human and veterinary medicine and is independent of the type of vaccine being used. This review will discuss the use of animal models for vaccine research. I will review clinical solutions for inhibition of vaccination by maternal antibodies, and the testing and development of potentially effective vaccines. These are based on new mechanistic insight about the inhibitory mechanism of maternal antibodies. Maternal antibodies inhibit the generation of antibodies whereas the T cell response is usually unaffected. B cell inhibition is mediated through a cross-link between B cell receptor (BCR) with the Fcγ-receptor IIB by a vaccine–antibody complex. In animal experiments, this inhibition can be partially overcome by injection of a vaccine-specific monoclonal IgM antibody. IgM stimulates the B cell directly through cross-linking the BCR via complement protein C3d and antigen to the complement receptor 2 (CR2) signaling complex. In addition, it was shown that interferon alpha binds to the CD21 chain of CR2 as well as the interferon receptor and that this dual receptor usage drives B cell responses in the presence of maternal antibodies. In lieu of immunizing the infant, the concept of maternal immunization as a strategy to protect neonates has been proposed. This approach would still not solve the question of how to immunize in the presence of maternal antibodies but would defer the time of infection to an age where infection might not have such a detrimental outcome as in neonates. I will review successful examples and potential challenges of implementing this concept.
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              Teratogenic effects of the Zika virus and the role of the placenta.

              The mechanism by which the Zika virus can cause fetal microcephaly is not known. Reports indicate that Zika is able to evade the normal immunoprotective responses of the placenta. Microcephaly has genetic causes, some associated with maternal exposures including radiation, tobacco smoke, alcohol, and viruses. Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly conveys the Zika virus to the early embryo or fetus. Alternatively, the placenta itself might be mounting a response to the exposure; this response might be contributing to or causing the brain defect. This distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies to prevent Zika-induced teratogenesis.
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                Author and article information

                Contributors
                Journal
                New Microbes New Infect
                New Microbes New Infect
                New Microbes and New Infections
                Elsevier
                2052-2975
                29 August 2022
                July 2022
                29 August 2022
                : 48
                : 101017
                Affiliations
                [1) ]Department of Infectious Diseases, Mälarsjukhuset, Eskilstuna, Sweden
                [2) ]Public Health Agency, Sweden
                [3) ]Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden
                [4) ]Department of Women's Health, Karolinska University Hospital, Stockholm, Sweden
                [5) ]Department of Medicine, Division of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden
                Author notes
                [] Corresponding author: Helena Hervius Askling, Institutionen för medicin Solna (MedS), Karolinska Universitetssjukhuset Solna NB6:02, 17176 Stockholm, Sweden. Helena.hervius.askling@ 123456ki.se
                Article
                S2052-2975(22)00069-5 101017
                10.1016/j.nmni.2022.101017
                9513166
                36176540
                d554d621-963d-4e87-8f89-74c8fbe9edd3
                © 2022 The Author(s)

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 4 June 2022
                : 20 July 2022
                : 19 August 2022
                Categories
                Mini-Narrative Review

                case report,infant,neutralising antibodies,pregnancy,serology,tick-borne encephalitis,tick-borne encephalitis virus,vaccination,vertical transmission,virus,tbe, tick-borne encephalitis,tbev, tick-borne encephalitis virus,pcr, polymerase chain reaction

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