Epstein-Barr Virus
Latency III-II
During primary infection, EBV infects B cells and expresses all its latency gene complexes, including 10 proteins and 2 small RNAs. Most of these immunogenic cells are eliminated by EBV specific T cells. The survivors then downregulate the viral proteins to latency II where only three viral proteins are expressed,
Latency 0-I
Exisiting the lympho node, EBV down-regulate all the viral proteins, being invisible to the immune system. Latency I occurs when the virus expresses a single viral protein EBNA1 to ensures viral genome deviding along with the cell genome during B cell division.
EBV reactivation
Under certain circumstances, EBV exit latency and reactivate into lytic cycle, during which more infectious virions are produced. The virions may lyse the host cell and infect into cells nearby. The process, however, is usually benign and unnoticeable.
Epstein–Barr virus (EBV), a gamma herpesvirus in the herpes family first discovered from cell cultures of Burkitt’s Lymphoma, proves one of the most common viruses in human. Nearly 90-95% of all human population are EBV carriers in a lifetime asymptomatically.
EBV life cycle involves various latency patterns followed by entry into the host as well as virus reactivation into lytic cycle. During primary infection, EBV infects naive B cells and expresses its entire latency gene complex, including 10 proteins and two small RNAs (type III latency). Type III latency drives B-cell transformation and proliferation, but because the cells are highly immunogenic they are rapidly eliminated by EBV-specific T cells. The virus survives in B cells by downregulating its immunogenic proteins in two phases. Initially B cells enter lymphoid follicles where they proliferate and express only three viral proteins (type II latency). Finally, they exit the lymph node and downregulate all viral proteins (type 0 latency), and thus are invisible to the immune response. If circulating infected B cells divide homeostatically they express a single viral protein (EBNA1, type I latency) that ensures that the virus genome divides with the cell genome. Under certain circumstances, EBV exit latency and get reactivated into lytic cycle, so called EBV-reactivation, during which more infectious virions are produced. The virions may lyse the host cell and infect into cells nearby. The process, however, is usually benign and unnoticeable.
The Epstein-Barr-virus, though appears non-symptomatic for most of the time, can lead to a spectrum of diseases during different latency patterns, namely Infectious Mononucleosis (IM), Post-transplant lymphoproliferative disorder (PTLD), nasopharyngeal carcinoma (NPC) and hemophagocytic lymphohistiocytosis (HLH), etc.
The Chiang lab focuses on the understanding of host-virus interactions in primary and persistent EBV infection and on the elucidation of pathogenic mechanisms of EBV in lymphoid and epithelial cancers. Our research programs enbrace three directions, focusing on immune reponses, sequencing analysis and novel drug therapy accordingly. [More details]