Epstein-Barr virus (EBV) efficiently infects and immortalizes human B lymphocytes through expression of at least 12 viral genes, which include the EBNA-LP protein. Recent work discusses the current state of knowledge about how EBNA-LP contributes to EBV biology.

EBNA-LP is an enigmatic protein comprised largely of 22 and 44 amino acid repeated sequences. Elucidation of EBNA-LP functions has been guided by identification of interacting cellular and viral proteins. The functions of these cofactors implicate EBNA-LP as a potential modulator of apoptosis, cell cycle processes, and transcriptional pathways. Recent studies have linked EBNA-LP with Sp100, a protein associated with promyelocytic nuclear body proteins (PML NBs), which mediate intrinsic cellular defenses against viral infections.

Alpha and beta herpesviruses encode proteins, which interact with and modulate PML NBs or PML NB-associated proteins to counteract this intrinsic cellular defense. These results link EBNA-LP with pathways that counteract or modulate the intrinsic host defense mechanisms.

from Epstein-Barr Virus: Latency and Transformation

Further reading:

• Epstein-Barr Virus
• RNA Interference and Viruses
• Virology publications

Labels: Apoptosis, EBNA-LP, EBNA-LP protein, EBV Leader Protein, Herpesviruses, Sp100

A number of pathogens, including viruses, bacteria, and parasites, have evolved mechanisms to subvert apoptosis by either positively or negatively modulating host defenses. In particular, the inhibition of the apoptotic process by microbial pathogens has previously demonstrated importance in securing intracellular niches, which may be an important mechanism for microbial survival, replication or immune evasion.

Similarly, the induction of apoptosis may be beneficial to pathogens by promoting escape from host cells or diminishing their effector functions, again promoting immune evasion.

Conflicting studies have reported that infection with the facultative intracellular pathogens Neisseria gonorrhoeae and Neisseria meningitidis can either inhibit or induce apoptosis. Reports on Neisserial influence on the apoptotic response of host cells have been published consistently for almost ten years and will be the focus of this chapter.

Overall, it seems that Neisseria species more often inhibit apoptosis, and this inhibition may allow time for adaptation to a new environment, intracellular replication, or immune evasion presumably leading to the spread of infection read more ...

from Sarah A. Follows and Paola Massari in Neisseria: Molecular Mechanisms of Pathogenesis

Labels: Apoptosis, Neisseria, Neisseria gonorrhoeae, Neisseria meningitidis