Sunday, March 18, 2007

A possible mechanism for the evolution of the killer virus?

Virology studies have come a long way and a wealth of scientific literature has been written about the subject. Yet, some viruses remain one of the most elusive stealth fighters ever known to mankind.

Take the cytomegalovirus or herpes virus for example. Both are known to go into stealth mode by entering a latent or lysogenic phase. During this phase, the virus lies dormant within the genome of the infected cell. Even the common cold virus is capable of hiding and remaining dormant within the genome (ScienceDaily). It has been thought that influenza lies dormant in humans (Knowledge of health).

Under certain stimulus, the dormant virus can become active, resulting in the production of new virus particles. This is known as the lytic phase. There lies a possibility of a cacophony of viruses residing within the cell all in the dormant phase. However, they could be chugged into life by a stimulus, which results in the production of viral particles. If that happens, there lies the possibility of antigen shift, resulting in the reassortment of viral genes from more than one species of viruses.

The thought of more than one virus infecting the cell, lying dormant until a stimulus resulting in production of viral particles with the possibility of antigen shift is attractive if we studied the pattern of killer virus outbreaks. There lies a period of dormancy for a number of years followed by an outbreak of a new strain of deadly virus. Indeed, we are facing an evolving stealth fighter of destruction.......

Citations
1) Anders DG, Punturieri SM. Multicomponent origin of cytomegalovirus lytic-phase DNA replication. J Virol. 1991 Feb;65(2):931-7.

2) Researchers discover cold virus can "hit and hide". http://www.sciencedaily.com/releases/2004/04/040426055429.htm

3) http://www.knowledgeofhealth.com/report.asp?story=Why%20Flu%20Epidemics%20Occur%20in%20Winter&catagory=Infectious%20Disease,%20Vaccines,%20Flu,%20Vitamin%20D

3) Introduction to the viruses. http://www.ucmp.berkeley.edu/alllife/virus.html

3 comments:

Anonymous said...

Hi, I'm not an expert on virology (far from it, my highest qualification is O' Level biology) but if this model is correct, wouldn't we be expecting that the killer viruses be of the same strain as previous ones? I see no mechanism for the development of new strains.

I still like the old random mutation theory better, because it needs less assumptions and the regularity of outbreaks is not entirely incompatible with mathematical probability (I think can be modelled using exponential distribution).

Cheers,
RSE

Anonymous said...

Sorry, I meant that I don't see how antigenic shift is sufficient for the development of new strains.

As I see it, antigenic shift within the same host does not make a drastic difference to the virulence.

Socrates_Reincarnate said...

Dear RSE:

Antigen shift will result in the production of a new virus strain with reassorted genome, because genetic materials from another virus might be introduced. I wouldn't say that killer virus is completely similar to their predecessors. Take the case of Avian flu for example. It happens that the human strain and the avian strain of the virus infects the same host. During the production of the viral particles, there is potential for genetic assortment (antigen shift). The new strains would have combination of both avain strains and human strains. The issue of virulence might be a little complicated, but I would try to get back to you on that later. If I did not, just remind me by posting a comment.