Infection: a hypothesis on active susceptibility and species immunity with implications for AIDS prevention.
There is no fundamental difference in contagiousness or pathogenicity between the normal and pathogenic microfloras: both are contagious, and both may either cause illness or persist in the body of a healthy carrier. The contagiousness of the normal microflora is determined by its positive function in the host. In addition to the normal microflora, endogenous retrovirus genes are also useful for a macroorganism: they have been found to be integral elements of many animal and plant genomes and participate in vital functions, such as genome activity control, antiviral defense, and formation of the placenta; dysfunction of some endogenous retrovirus genes causes pathology. Components of bacterial cells cause protective effects with respect to noninfectious somatic diseases. Therefore, it is reasonable to assume that natural susceptibility to both "normal" and "pathogenic" microfloras results from vital necessity for a macroorganism to interact with them. The necessity to interact with specific microorganisms and, hence, susceptibility to them is the cause of their infectivity. In this connection, studies on the positive functions of specific "pathogenic" microflora in a macroorganism with the use of SPF animals would be of interest. Even more interesting would be experiments with transfer of specific microbial genes into the genomes of susceptible species, which may help to understand the causes and mechanisms of susceptibility/insusceptibility as a basis of species immunity and develop fundamentally new and more natural methods for preventing and treating infectious diseases.
Malyshkin
A P
AP
Orenburg State Medical Academy, Orenburg 460014, Russia. Malishkin_54@mail.ru
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology* / Q000517:prevention & control*; D000818:Animals; D002353:Carrier State; D003141:Communicable Diseases / Q000276:immunology* / Q000382:microbiology*; D020077:Endogenous Retroviruses / Q000502:physiology*; D015658:HIV Infections / Q000821:virology; D054884:Host-Pathogen Interactions; D006801:Humans