Following this consideration, we assume that the presence of HIV in the human population has the same genesis: we inherited this HIV genetic information from our ancestors since the beginning of humankind and subsequently it has been translated from generation to generation. But there is a very serious objection – if HIV information was in our bacteria from our beginning, why did it emerge just about 25 years ago? Was it hidden without any implication
all the time, for many thousands of years, in our bodies?
To answer this question, we should return to the ancient history of mankind. In the past, large epidemics often occurred when there were new patterns of communication and transport between populated areas and/or new patterns of settlement. According to historians, the first registered large epidemic occurred in Athens during the Peloponnesian War in 430 BCE. In the middle of the sixth century AD (542), there was a big outbreak of bubonic plague (Justinianus) in the Mediterranean countries, where 40 to 50% of the population died. The biggest cataclysm of bubonic plague epidemic started in 1346 in Europe and subsequently spread to Asia, with the population eventually decimated by 50 to 60%. At least 60 million people died in China alone. This plague continued up to the seventeenth and partially to the eighteenth century. In the sixteenth century, after Europeans reached America, new devastating
epidemics started among the native peoples resulting in a 90% population loss among American Indians within 120 years.
Who were particularly the victims of these plagues? Especially people who were weak, malnourished, sick, so people with depleted immune systems. As discussed above, bacteria carrying the rich extra chromosomal genetic information as plasmids, phages, transposons, retrotransposons, containing various genetic information, HIV including, are mostly pathogenic for the host and after penetration into the organism they continually attack the immune system
. This attack depends on the amount of these microbes which penetrate into the blood. The immune system of people with low amounts of these bacteria was stronger and their carriers had a chance to overwhelm any plague. One of the most important results of the set of plagues that occurred in the history of humankind, mainly in Europe, North Africa, North America and partially in Asia, was natural selection, resulting in “sanitation” of the human population. Hand in hand in this tremendous evolution process was the selection of people with low level of bacteria carrying pathogenic, mainly extra chromosomal genetic information, able to penetrate into the human body and attack the immune system. The result of this complex evolutional proceeding, which finished towards the end of the nineteenth century, was establishment of a balance between non-pathogenic and pathogenic (“good” and “bad”) microbes in the microflora of surviving individuals. In short, the result of this long process was the selection of individuals with a very limited number of bacteria carrying the HIV sequences and those carrying CCR-5 receptor deficiency on white blood cells.
This stability, acquired over many centuries, was interrupted in the middle of the twentieth century, in the time of the antibiotics era. It is generally accepted that due to ATB, practically all primary bacterial pathogens were liquidated over two-three decades. The success of antibiotics in elimination of many diseases induced by microbes was so expressive that in the mid-1950s the US Surgeon General Steward effusively proclaimed the era of bacterial diseases finished. This trend of ATB glorification was spread very quickly from the USA to Europe and microbiology found itself at the scientific periphery. In 1969, only a few people heard the voice of the English scientist J. A. Reaburn who said that antibiotics would bring us unforeseen vicious
tricks in the future. ATB treatment results in reduction of not only pathogens but also of symbiotic or otherwise beneficial microflora. For survival, bacteria need to acquire the ability to escape from ATB pressure by: a) induction of ATB resistance; b) penetration into mammalian cells, where they are able to survive for a rather long period of time; c) by changing their own face – pleomorphism - creation of a cell-wall-deficient (CWD) form.
Bacteria which obtained resistance to ATB are different from their ancestors. They achieved new properties in balancing the new condition, without respect of human hosts. Unlimited application of ATBs, drugs, pharmaceuticals on the one hand and anal sexual intercourse on the other, triggered
changes in the equilibrium of the human intestinal microflora, which was constituted during many centuries. A mass-scale usage of inhalants (e.g. popper) in the USA during the 1970s and drugs in the 1980s, especially in homosexual communities combined with unlimited intercourse (homo and anal sex), was the last heavy shot into the balance of intestinal microflora of many people. In addition, the situation in the USA became complicated because of African Americans who were not involved in the mentioned long-term selection “sanitary” process as were Americans who emigrated from Europe.
The wide range of HIV-positivity in Africa is explained by the long-term survival of Africans in isolated communities. There was no selection "sanitary" process (intensively occurring in Europe) causing limitation of potentially pathogenic bacteria carrying extrachromosomally localized viral sequences, genes for resistance, adhesion
and penetration into human cells. The presence of HIV sequences in bacteria of Africans is so widespread that it can not be used as "gold" standard. In light of our preliminary findings we suppose that the association of AIDS and TB in Africa is a result of transfer of HIV bacterial genetic information via plasmids, transposons, retrotransposons or other integrons into Mycobacterium tuberculosis.
The presence of HIV sequences in respiratory bacteria and yeast of Cambodian and Kenyan HIV-positive children shows that these microbes are present not only in the gastrointestinal tract but in the whole body. Because of their broad resistance to antibiotics and “resistance” to nucleoside analogue drugs (AZT), their elimination in GIT is practically impossible by various combinations of ART. According to our results, GIT bacteria may represent a very important HIV reservoir. The continual application of ART, including antibiotics, resulted in total reduction of sensitive bacteria and amplification of resistant ones. Toxicity of AZT plays a very important negative role in this process. The result of this spiral process is the presence of only resistant bacteria, many of them with HIV sequences. These microorganisms penetrate from the GIT into the body of patients, reduce the number of T-cells and ultimately induce immunodeficiency