Vladimir Zajac
Cancer Research Institute BMC SAS, Slovakia
Scientific Tracks Abstracts: Arch Clin Microbiol
The idea that HIV itself is an etiological agent responsible for AIDS is generally accepted. According to this claim, the virus was transmitted to people from monkeys in Africa through random contacts 35-50 or even 100 years ago. This idea has not been sufficiently substantiated from an epidemiological or statistical point of view. From the historical point of view, the most important changes in human health have occurred during a series of epidemics, especially in Europe. The largest plague epidemic - Black Death - was caused by Yersinia pestis bacteria transmitted by rats and their blisters. It began in 1346 in Italy, from where it spread throughout Europe and Asia. It did not hit America and sub-Saharan Africa. After epidemics, the population decreased by 30-50%. The epidemic survived those who had mutation of delta 32 in the CCR5 co-receptor, which is predominantly expressed in T cells. The mutation protects not only the Yersenia pestis infection but also the pox virus and HIV. The "Black Dead" epidemic has increased the number of mutations in the Caucasian population to 10-20%. Although the role of Yersenia pestis in the "Black Dead" epidemic is indisputable, some accompanying symptoms of the epidemic raise some doubts. S. Scott, Ch. Duncan introduced the theory that "Black Death" may be caused by hemorrhagic viruses. This version corresponds to the speed, intensity of the epidemic, long incubation period allows the carrier to travel and infect more people. Our results suggest that HIV is very likely to be an integral part of human beings since the beginning of our existence and leads to the conclusion that HIV has participated in the Black Epidemic along with Yersenia pestis. The combination of these two agents has made the epidemic so devastating and leads to the removal of HIV carriers in the Caucasus population. In Sub-Saharan Africa, this epidemic did not occur, so HIV was not removed from the population. Therefore, there is no CCR5Δ32 mutation and the HIV level in the population is much higher than in other parts of the world.
Vladimir Zajac has completed his PhD in 1982 from the Cancer Research Institute of Slovak Academy of Sciences in Bratislava (Slovakia), where he worked as the Head of Department of Cancer Genetics from 1996 to 2010. He joined the Medical Faculty of the Comenius University as an Associate Professor of Genetics in 2007. He has published 74 papers mostly in reputed journals and he was editor of the book “Bacteria, viruses and parasites in AIDS process” (InTech, 2011).
E-mail: vladimir.zajac@savba.sk