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Surprise: Viruses Can Cause Disease during Latent Phase; New Evidence Supports Microcompetition Theory
Date:11/15/2013

Rochester, NY (PRWEB) November 15, 2013

The CDC says that over 776,000 people are newly infected with HSV-2 every year in the United States (1), according to a page last updated on February 11, 2013. The number of cases of HSV-1 is even higher. Doctors and scientists know that herpes viruses 1 and 2 establish a latent infection in the host that lasts for the life. However, these health professionals believe that latent herpes viruses cause disease only when they reactivate. That is, when they cause fever blisters, cold sores, etc.

This is a misconception.

Health professionals may then ask “How is this a misconception?” Or, more specifically, “How can a virus cause disease during latency?”

The CBCD reviews a study that summarizes the most recent discoveries regarding latent herpes viruses.

It should be noted that latency is an essential mechanism of survival for the virus. Without latency, the virus would disappear. Therefore, latency is a widespread mechanism used by many viruses. Authors of this study wrote that “The mission of HSV-1 and HSV-2 is to replicate and spread. To spread, the virus replicates vigorously at the portal of entry and is transmitted by physical contact between infected and uninfected individuals. In effect, the portal of entry into the body is also the portal of transmission. The natural history of HSV in humans strongly suggests that the virus would disappear or at least would be significantly less prevalent if it were not able to establish a latent, silent infection (1).”

However, during the latent phase, the virus is not dormant, it is still active. During the latent phase, it does not produce proteins or replicate in large numbers. It continues to make viral proteins and replicate.

Research shows that latent viruses (including latent herpes viruses) are not dormant. They show viral replication and transcription of viral proteins. For instance, researchers wrote that human ganglia, which were infected with the latent Varicella Zoster Virus, showed multiple VZV transcripts. This is according to a study published on September 4, 2013 in the medical journal Viruses (2).

“RT-PCR and in situ hybridization studies have identified multiple VZV transcripts in latently infected human ganglia. State-of-the-art multiplex PCR technology, capable of detecting all 68 annotated VZV gene transcripts, revealed transcription of at least 12 VZV genes during latency… (2)” In short, the VZV produces its proteins while latent.

How can the production of viral proteins during latency cause disease?

The following is a simplified explanation of the Theory of Microcompetition with Foreign DNA as described by Dr. Hanan Polansky.

Dr. Polansky discovered that foreign DNA fragments, called N-boxes, cause most major diseases. When the foreign N-boxes belong to a virus, microcompetition between the viral DNA and the human DNA can lead to disease even when the virus is latent or the viral DNA is broken into pieces and cannot express proteins.

The Center recommends that health professionals turn to Dr. Polansky’s book, “Microcompetition with Foreign DNA and the Origin of Chronic Disease” for a better understanding of the risks posed by latent viruses.

To learn more about Dr. Hanan Polansky’s research and the Theory of Microcompetition with Foreign DNA, visit: http://www.cbcd.net.

References:

(1)    http://www.ncbi.nlm.nih.gov/pubmed/24024635
(2)    http://www.ncbi.nlm.nih.gov/pubmed/24008377

The CBCD is a research center recognized by the IRS as a 501(c)(3) non-for-profit organization. The mission of the CBCD is to advance the research on the biology of chronic diseases, and to accelerate the discovery of treatments.

The CBCD published the “Purple” book by Dr. Hanan Polansky. The book presents Dr. Polansky’s highly acclaimed scientific theory on the relationship between foreign DNA and the onset of chronic diseases. Dr. Polansky’s book is available as a free download from the CBCD website.

Read the full story at http://www.prweb.com/releases/2013/11/prweb11333722.htm.


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