Collective findings showed that immunotherapy or vaccine development against EBV proteins (particularly LMP1, LMP2A, and EBNA1) for cancer therapy is promising.
Cumulative findings suggest that latent proteins, that is, LMP2A and EBNA1, are promising EBV targets for therapeutic vaccine development against NPC.
First, current therapeutic and preventive strategies are only limited to LMP2A, LMP1, and EBNA1 due to the lack of suitable animal model, poor immunogenicity, and adjuvant .
LMP2A and EBNA1 are by far the most promising proteins that are used for therapeutic vaccine development; others remain underexplored.
Cao et al., "Epstein-barr virus-encoded LMP2A induces an epithelial--mesenchymal transition and increases the number of side population stem-like cancer cells in nasopharyngeal carcinoma," PLoS Pathogens, vol.
In addition to EBNA1, half of all EBVaGCs also express LMP2A, and therefore EBV latency configurations should be classified into Ia or Ib based on the presence or absence of LMP2A [38, 44].
 also demonstrated that LMP2A induced the expression of phosphorylated signal transducer and activator of transcription 3 (pSTAT3), which stimulated the upregulation of DNA methyltransferases (DNMT) DNMT1 and DNMT2 in EBV-infected GC cells .
Specifically, these authors indicate that all the latency type I genes such as Bam HI-A rightward reading frame (BARF0), EBERs, EBNA1, and LMP2A have a synergetic effect on these processes and contribute to the downregulation of the mature miR-200 family and the subsequent upregulation of the E-cadherin transcription repressors, zinc finger E-box binding factor 1 (ZEB1) and ZEB2, resulting in the inhibition of E-cadherin expression and induction of the epithelial-to-mesenchymal transition (EMT) .
It is classified as latency type I because the expressed latent genes are restricted to BARF0, EBERs, EBNA1, and LMP2A, excluding EBNA2 or LMP1 which are essential for its transforming ability [107-109].
Raab-Traub, "Epstein-Barr virus LMP2A transforms epithelial cells, inhibits cell differentiation, and activates Akt," Journal of Virology, vol.