Since its discovery in 1964 by Anthony Epstein and his co-workers, Yvonne Barr and Bert Achong, Epstein Barr virus has drawn the attention of tumor virologists due to its particular behavior. In most people, the virus infects its host and establishes a latent infection for life as a harmless passenger, in a delicate and fascinating balance with healthy carriers. However, given that EBV encodes numerous latent and lytic antigens with oncogenic capacities, it has been associated with tumors in specific individuals. There is a complex interplay between age of acquisition, symptomatic versus asymptomatic infection, and the subsequent risk of EBV-associated cancers. When primary infection occurs in adolescents and young adults, they are more likely to experience infectious mononucleosis during primary infection than children, who almost always experience asymptomatic infection.
Therefore, the way young children contract EBV is unknown. They might be infected by their parents or siblings who are “carriers” of the virus and who intermittently shed it in their oral secretions, or by unclean toys, in particular in the context of crowded family conditions observed in low socioeconomic status. In developed populations, infectious mononucleosis in young adults increases the risk of Hodgkin’s lymphoma. However, several studies proved an increased incidence of EBV-associated lymphomas in children younger than 10 years old. Thus, since the age of primary EBV infection is an important factor in infectious mononucleosis, it is an important consideration for EBV-related diseases.
In this Research Topic, we welcome Original Research and Reviews discussing the pathogenesis of different EBV-associated pediatric tumors. Submissions should also address, but not be limited to, the following sub-themes:
1. The immune response and tumor microenvironment composition
2. The link between age or primary infection and the development of EBV-related malignancies
3. The molecular epidemiology of EBV variants associated with specific pediatric neoplasia
4. The cellular pathways triggered by EBV in children.
Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in Frontiers in Oncology.
Since its discovery in 1964 by Anthony Epstein and his co-workers, Yvonne Barr and Bert Achong, Epstein Barr virus has drawn the attention of tumor virologists due to its particular behavior. In most people, the virus infects its host and establishes a latent infection for life as a harmless passenger, in a delicate and fascinating balance with healthy carriers. However, given that EBV encodes numerous latent and lytic antigens with oncogenic capacities, it has been associated with tumors in specific individuals. There is a complex interplay between age of acquisition, symptomatic versus asymptomatic infection, and the subsequent risk of EBV-associated cancers. When primary infection occurs in adolescents and young adults, they are more likely to experience infectious mononucleosis during primary infection than children, who almost always experience asymptomatic infection.
Therefore, the way young children contract EBV is unknown. They might be infected by their parents or siblings who are “carriers” of the virus and who intermittently shed it in their oral secretions, or by unclean toys, in particular in the context of crowded family conditions observed in low socioeconomic status. In developed populations, infectious mononucleosis in young adults increases the risk of Hodgkin’s lymphoma. However, several studies proved an increased incidence of EBV-associated lymphomas in children younger than 10 years old. Thus, since the age of primary EBV infection is an important factor in infectious mononucleosis, it is an important consideration for EBV-related diseases.
In this Research Topic, we welcome Original Research and Reviews discussing the pathogenesis of different EBV-associated pediatric tumors. Submissions should also address, but not be limited to, the following sub-themes:
1. The immune response and tumor microenvironment composition
2. The link between age or primary infection and the development of EBV-related malignancies
3. The molecular epidemiology of EBV variants associated with specific pediatric neoplasia
4. The cellular pathways triggered by EBV in children.
Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in Frontiers in Oncology.
