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    • br Discussion Immune response to CMV is a

    2021-06-21


    Discussion Immune response to CMV is a series cell-mediated immune response initiated by innate innate NK cells, followed by adaptive CD8+ and CD4+ T cells and humoral immunity by B cell [3]. Prior to transplant, measurement of humoral immune responses (CMV serology) of donor and recipient is commonly used to stratify the risk of CMV replication and post-transplant disease. CMV-seronegative recipients of seropositive grafts are at the highest risk of CMV disease. Although pre-transplant serology is routinely used to inform decisions regarding optimal post-transplant prevention strategies, post-transplant seroconversion is not a reliable predictor of CMV disease [2]. The seroprevalence of CMV IgG and IgM is estimated to be 98.1% and 1.7%, respectively, in Korea [4]. In this study, seroprevalence of CMV IgG and IgM was 100% and 3.1%, respectively, and these serology results did not predict CMV reactivation. Humoral immunity is not sufficient to predict CMV reactivation, and therefore several studies have been conducted to predict reactivation by measuring cellular immunity in solid organ transplantation. However, a single study of CMV reactivation in liver transplant recipients has been reported [5], and this study was based on quantiferon assays. To the best of our knowledge, this is the first study for prediction of CMV viremia using ELIspot for measuring CMV-specific Wortmannin in liver transplant recipients. Previous reports showed conflicting results for correlation between virus-specific immune responses and CMV viremia in solid organ transplantation recipients. In 27 heart and lung transplant patients, a frequency of IE-1–specific CD8+ T-cells >0.4% any time after transplantation was protective against CMV disease [6]. In other studies, heart and kidney transplant recipients who develop CMV viremia have significantly lower IFN-γ expression (ELISpot assay) prior to viremia than those without viremia [7,8]. In a cohort of kidney transplant patients and a cohort of R+ transplant patients at high risk of CMV disease, Quantiferon-CMV assay results were able to predict subsequent CMV disease [9,10]. Quantiferon-CMV assays, when performed at the onset of viremia, can differentiate whether patients spontaneously resolve viremia or require antiviral treatment [11]. However, a single measurement with Quantiferon-CMV is not predictive of CMV reactivation as measured by viral loads in bronchoalveolar lavage fluid in a lung transplant cohort [12] In addition, a liver transplant recipient's pre-transplant Quantiferon-CMV results were not associated with development of CMV DNAemia, although Quantiferon-CMV measured 1 or 2 weeks after transplant was significantly associated with development of CMV DNAemia [5]. In this study, no reactive T cell in preoperative CMVspot results predicted CMV viremia, and the patient with reactive or borderline IE-1 results did not develop viremia that started late (after 2 months) after transplantations. CD4+ and CD8+ T cells may target a wide range of immunogenic CMV proteins. In particular, Wortmannin dominant T cell responses against IE-1 and pp65 seem to be essential for CMV control [13,14]. In previous reports, the IE-specific T cell response is associated with CMV development and pp65-specific T cell response is associated with viremia [15,16]. In this study, the patient with positive or borderline IE-1 results did not develop viremia that started late (after 2 months) after transplantation. In addition, the pp65-specific results showed high specificity for prediction of CMV viremia.
    Conclusion
    Authors' contribution
    Conflicts of interest This research was supported by National Research Foundation of Korea (NRFK) grant funded by the Korean Government (Grant No. NRF-2016R1C1B1012661).
    Introduction Congenital human cytomegalovirus (cCMV) is a Herpes virus associated with intellectual impairment, sensorineural hearing loss (SNHL) and multisystem organ failure in children. However, a majority of children with cCMV infection have no significant clinical findings at birth or long-term disabilities related to the infection. It is a global health problem affecting approximately 0.3–1.7% of all newborns [1,2]. The infection can be asymptomatic or cause severe symptomatic disease, which in part is attributed to when the infection occurred during pregnancy [3]. Among children with severe disease associated with cCMV infection, approximately 30–50% of those children will have sensorineural hearing loss, which has been found to be progressive and fluctuating in nature [4,5]. In fact, cCMV is a leading non-genetic cause of SNHL worldwide [1].