Document 3128
 DOCN  M94A3128
 TI    Pathogeny recapitulates epidemogeny.
 DT    9412
 AU    Pieczenik G; Cook College, Rutgers University, New Brunswick, N.J.
       08903.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):147 (abstract no. PB0014). Unique
       Identifier : AIDSLINE ICA10/94369447
 AB    I wish to propose that the course of the pathology of a disease in an
       individual, pathogeny, can recapitulate the fluctuations in virulence in
       a population during the course of an epidemic, epidemogeny. One model
       for the fluctuation in virulence in a population during the course of an
       epidemic is that of a non or less pathogenic strain competing out a more
       pathogenic strain. This may be the evolution of the AIDS epidemic. This
       model predicts a high degree of infectious virulence, followed by
       clusters of infectious hypovirulence, followed by an attenuation of the
       symptoms of the disease, followed by a termination of the epidemic.
       Pathogeny recapitulating epidemogeny suggests that in an individual
       infected with a pathogenic strain of HIV-1 can become infected, post
       exposure, to a competitive non-pathogenic strain of HIV-1. This would
       lead to a concomitant attenuation of clinical symptoms; followed by an
       HIV-1 positive asymptomatic status; followed by a seroconversion to an
       asymptomatic HIV-1 negative status. One can, therefore, expect that the
       AIDS epidemic will follow the natural course of epidemics and evolve a
       less pathogenic, avirulent, but more competitive strains of HIV-1. This
       non-pathogenic competitive strain should limit the severity and spread
       of the AIDS epidemic in time. I have recently identified a recombinant
       HIV-1 strain isolated from a healthy long term asymptomatic American,
       who showed infectious hypovirulence, (1) and which contains sections of
       an avirulent African strain. This suggests that such a virus has
       recently evolved and is entering the population at large. Because of the
       Africans strain's nucleotide homology to Western strains, it was able to
       recombine with the more pathogenic Western strain. However, this
       recombinant retained the avirulence phenotype of the African strain. The
       region of recombination between these two strains, therefore, identifies
       more precisely, the nucleotide sequence responsible for the clinical
       phenotype of pathogenicity; or, in this case, the clinical phenotype of
       being a long term asymptomatic. In summary, a pathogenic African strain
       is competed out by a less pathogenic African strain which enters the
       American population as an avirulent competitive recombinant, which in
       turn should compete out the more pathogenic strains in America, limiting
       the course of the epidemic. Individuals infected with this
       non-pathogenic strain, post-exposure to a pathogenic strain, show an
       amelioration of symptoms and viral conversion to the non-pathogenic
       strain. This recapitulates the course of the epidemic which, also, shows
       a conversion from more virulence to less virulence.
 DE    Acquired Immunodeficiency Syndrome/*EPIDEMIOLOGY/*PHYSIOPATHOLOGY
       Africa  Human  HIV-1/GENETICS/ISOLATION & PURIF/*PATHOGENICITY  Models,
       Theoretical  Recombination, Genetic  Species Specificity  United
       States/EPIDEMIOLOGY  Virulence  MEETING ABSTRACT

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