Why Some Hemorrhagic Fever Viruses, including Ebola, Deplete the Body of Selenium, Which Leads to Deadly Hemorrhaging.

In 1994, Dr. Will Taylor, then of the University of Georgia, discovered that HIV genes encode for selenium. (http://www.drpasswater.com/selemiumtaylor.htm). In 1996, Dr. Taylor discovered that the Ebola Hemorrhagic Virus genes also encode for selenium and postulated that the hemorrhaging was linked to selenium depletion in the host. (http://www.drpasswater.com/nutrition_library/selenium1.html). In 1997, Dr. Taylor and his colleague, Dr. C. S. Ramanathan published their theory in the journal, “Biological Trace Elements Research.” The abstract of that article is given below.


Biol Trace Elem Res.  1997 Jan;56(1):93-106.

Computational genomic analysis of hemorrhagic fever viruses. Viral selenoproteins as a potential factor in pathogenesis.

Ramanathan CS 1, Taylor EW .

Pub Med Abstract (http://www.ncbi.nlm.nih.gov/pubmed/9152513)

A number of distinct viruses are known as hemorrhagic fever viruses based on a shared ability to induce hemorrhage by poorly understood mechanisms, typically involving the formation of blood clots ("disseminated intravascular coagulation"). It is well documented that selenium plays a significant role in the regulation of blood clotting via its effects on the thromboxane/prostacyclin ratio, and effects on the complement system. Selenium has an anticlotting effect, whereas selenium deficiency has a proclotting or thrombotic effect. It is also well documented that extreme dietary selenium deficiency, which is almost never seen in humans, has been associated with hemorrhagic effects in animals. Thus, the possibility that viral selenoprotein synthesis might contribute to hemorrhagic symptoms merits further consideration. Computational genomic analysis of certain hemorrhagic fever viruses reveals the presence of potential protein coding regions (PPCRs) containing large numbers of in-frame UGA codons, particularly in the -1 reading frame. In some cases, these clusterings of UGA codons are very unlikely to have arisen by chance, suggesting that these UGAs may have some function other than being a stop codon, such as encoding selenocysteine. For this to be possible, a downstream selenocysteine insertion element (SECIS) is required. Ebola Zaire, the most notorious hemorrhagic fever virus, has a PCR with 17 UGA codons, and several potential SECIS elements can be identified in the viral genome. One potential viral selenoprotein may contain up to 16 selenium atoms per molecule. Biosynthesis of this protein could impose an unprecedented selenium demand on the host, potentially, leading to severe lipid peroxidation and cell membrane destruction, and contributing to hemorrhagic symptoms. Alternatively, even in the absence of programmed selenoprotein synthesis, it is possible that random slippage errors would lead to increased encounters with UGA codons in overlapping reading frames, and thus potentially to nonspecific depletion of SeC in the host.



[PubMed - indexed for MEDLINE]