About this Research Topic
Since its discovery in 1964 by Anthony Epstein and his co-workers Yvonne Barr and Bert Achong, the Epstein Barr virus has drawn the attention of tumour virologists, due to its particular behaviour. 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 the immune response of healthy carriers. However, given that EBV encodes numerous latent and lytic antigens with oncogenic capacities, it has been associated with tumours in specific individuals. There is a complex interplay between malignant transformation and immune response, given that it could be a result of an imbalance. In fact, EBV develops several strategies employed to manipulate the tumours microenvironment in favour of tumour cell immune escape and proliferation.
The early phase of viral infection is crucial for EBV to establish latency, but different viral components are sensed by cellular sensors called pattern recognition receptors (PRRs) as the first line of host defense. The efficacy of innate immunity, in particular the interferon-mediated response, is critical to control viral infection initially and to trigger a broad spectrum of specific adaptive immune responses against EBV later. EBV is an antigenically rich infectious agent that stimulate strong CD8+/CD4+ T cell responses in its primary infection and these T cell responses persist for life and are challenged by recurrent EBV lytic replication.
Despite these restrictions, the virus has developed various strategies to evade the immune reaction of its host and to establish its lifelong latency. In its different phases of infection, EBV expresses up to 44 different viral miRNAs. Some act as viral immunoevasins because they have been shown to counteract innate as well as adaptive immune responses. Similarly, certain virally encoded proteins also control antiviral immunity.
Studies concerning the long way from the first steps of EBV infection through the development of EBV-associated cancers that disrupts the balance between the virus and the host immune response will lead to a better understanding of EBV-related diseases, and the development of specific treatments to prevent malignant transformation, in particular in specific susceptible populations. Even though huge progress has been made in understanding this process, there is still a need to prevent transformation or to improve treatment once the latter has been established.
This Research Topic accepts Original Research papers, Reviews, Mini-Reviews, Perspectives, Case Reports, and Brief Research Reports. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
- Microenvironment composition in EBV-associated lymphomas
- Immune response in EBV-primary and persistent infection
- Primary immunodeficiencies associated with deficits in specific EBV immune response.
The early phase of viral infection is crucial for EBV to establish latency, but different viral components are sensed by cellular sensors called pattern recognition receptors (PRRs) as the first line of host defense. The efficacy of innate immunity, in particular the interferon-mediated response, is critical to control viral infection initially and to trigger a broad spectrum of specific adaptive immune responses against EBV later. EBV is an antigenically rich infectious agent that stimulate strong CD8+/CD4+ T cell responses in its primary infection and these T cell responses persist for life and are challenged by recurrent EBV lytic replication.
Despite these restrictions, the virus has developed various strategies to evade the immune reaction of its host and to establish its lifelong latency. In its different phases of infection, EBV expresses up to 44 different viral miRNAs. Some act as viral immunoevasins because they have been shown to counteract innate as well as adaptive immune responses. Similarly, certain virally encoded proteins also control antiviral immunity.
Studies concerning the long way from the first steps of EBV infection through the development of EBV-associated cancers that disrupts the balance between the virus and the host immune response will lead to a better understanding of EBV-related diseases, and the development of specific treatments to prevent malignant transformation, in particular in specific susceptible populations. Even though huge progress has been made in understanding this process, there is still a need to prevent transformation or to improve treatment once the latter has been established.
This Research Topic accepts Original Research papers, Reviews, Mini-Reviews, Perspectives, Case Reports, and Brief Research Reports. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
- Microenvironment composition in EBV-associated lymphomas
- Immune response in EBV-primary and persistent infection
- Primary immunodeficiencies associated with deficits in specific EBV immune response.
Keywords: EBV, innate immunity, adaptative immunity, immunodeficiencies, tumor microenvironment
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
