Solving the Riddle of EBV: A Review of Cancer Virus

In Cancer Virus: The discovery of the Epstein-Barr Virus, the book I recently finished, one of the most intriguing anecdotes recounted is how Michael Anthony Epstein attended a lecture by Denis Burkitt. For those who know anything about Epstein-Barr Virus (EBV), the cause of infectious mononucleosis, the importance of these two individuals meeting is obvious as it launched a revolution in virology that lead to EBV being established as the first human tumor virus. 

To recount the major points of the story: Burkitt was a surgeon working in Africa who noticed a peculiar jaw tumor that had specific pathologic findings and a specific geography; Epstein was a researcher working on animal tumor viruses along with Yvonne Barr (see this Youtube clip of her in 2014). The ending of the story is no surprise: EBV was established as a causative factor--when coupled with malaria--in the development of Burkitt's lymphoma. 

Similar stories established EBV's role in nasopharyngeal carcinoma, certain types of Hodgkin's Disease, post-transplant lymphoproliferative disease (PTLD), and HIV-associated CNS lymphomas.

This book, written by EBV researchers Dorothy Crawford, Ingolfur Johannessen, and Alan Rickinson, provides a comprehensive picture of how the science, medicine, and epidemiology were integrated together. The result was a fundamental reshaping of the thinking in virology and oncology. It is obvious that the authors' expertise in the field greatly benefited the historical narrative account they provided. 

Control of tumor viruses through vaccination, as is done with the human papillomavirus (HPV) and hepatitis B virus (HBV), can be viewed as derivative applications stemming from understanding EBV.  For making that giant inductive leap and for their pathbreaking integrations Burkitt, Epstein, Barr, and their many collaborators (who included Nobel laureate Harald zur Hausen as well as Werner and Gertrude Henle) deserve adulation.

Strep and Mono: Bonnie & Clyde or Crips & Bloods?

A recent study published in the Journal of Infectious Diseases provides a great illustration of the intricate interplay between humans and 2 microbes, highlighting how pathogens interact with each other in order to facilitate their spread. 

The study is focused on the interaction between Group A streptococcus (GAS)--the cause of "strep throat"--and Epstein-Barr Virus (EBV), the cause of infectious mononucleosis.

As 20% of children are colonized with Group A streptococcus and EBV persistently infects 90% of the population, the two pathogens may have important influences on each other given that both of their habitats are the oropharynx.

EBV infects cells in two manners, lytically and latentenly. The lytic type of infection results in active viral replication, viral shedding and cell death facilitating spread. The latent type of infection, on the other hand, is relatively quiescent. Understanding what causes the switch from latency to a lytic infection is of great interest.

In this study, it was determined that GAS colonization can prompt EBV to emerge from latency and become lytic and enhance its presence in saliva thereby increasing the likelihood that it will spread to other humans. 

I think that this paper is fascinating because it highlights the fact that pathogens interact, not only with the host, but, with each other in an elaborate manner that impacts transmission. 

EBV's exploitation of GAS colonization is akin to one criminal exploiting the distraction that the presence of a rival criminal creates to go on a crime spree of contagion. Or maybe they're more like Bonnie and Clyde?