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Latent herpes can boost
Herpes Virus Latent Infections May Boost Human Immune System

Researchers reported in Nature, in May 2007 that mice with chronic herpes virus infections could better withstand diseases caused by plague and certain food poisoning bacteria.  

Scientists at Washington University School of Medicine in St. Louis, U.S.A., presented the surprising finding that good changes in the immune system were triggered by the long-term presence of a latent herpes virus infection in mice. In latent viral infections, the virus is present for the lifetime of the host and may or may not manifest regularly as a disease problem.  

Researchers stressed that they did not want to minimize the human suffering and health risks caused by disease-causing herpes infections. However, they noted that several strains of herpes viruses found in much of the human population remain symptom-free for most of their lives.  

 

 



Their results suggested that they could look at whether humans receive similar advantages from herpes virus and other chronic infections that do not cause active disease. If so, that would have public health implications because they would have to carefully weigh the risks and benefits of eliminating a virus that our bodies have to live with and have learned to live with. 

Scientists used vaccination to eliminate the deadly and highly contagious smallpox virus.  

Vaccines are currently in use or in clinical trials for several disease-causing strains of herpes.  

Human herpes viruses include oral (head region cold sores) and genital herpes, the chickenpox virus, cytomegalovirus, Epstein-Barr virus and Kaposi's sarcoma-associated herpes virus. During the initial, acute infection, many of these viruses cause symptoms, such as fever, cold sores or blisters. Then they enter periods of latency. Sometimes symptoms never recur during the infected person’s life time. Sometimes they flare up periodically before becoming quiescent again. Also, less infamous herpes viruses like HHV6 and HHV7 permanently infect most humans without ever producing any significant symptoms.  

The above study’s results have potentially wide-reaching implications for immune research. The new results imply that infections over a long period of time may have altered man’s immune systems at a fundamental level. It could also mean the virus-free animal models scientists use to study vaccines, autoimmune diseases, and other immune system issues have the potential to produce misleading results. 

It’s been known for years that many types of bacteria live in the human gut to the advantage of both the microbes and their human hosts. The results from this study are among the first to suggest the potential for symbiotic benefits from viral infections that live in areas beyond epithelial surfaces like the skin, throat or intestines.  

For this study, the strains of mouse herpes virus were closely related to human Epstein-Barr virus, Kaposi's sarcoma-associated herpes virus and cytomegalovirus.  

During studies of how mouse herpes viruses transition from acute to latent infections, it was discovered that latent infections might confer unrecognized benefits.  

They found evidence that the mouse immune system controls latent herpes infections in part by increasing production of a protein hormone called interferon gamma, which is a signaling hormone that in effect puts some immune system soldiers on yellow alert, causing them to patrol for invaders with their eyes wide open and defense weapons ready.  

Other researchers previously had shown that interferon gamma helps the immune system fight off some strains of bacteria. They tested herpes-infected mice with exposure to two bacteria: Yersinia pestis, which causes plague, and Listeria monocytogenes, which is a minor cause of food poisoning and can infect the central nervous system. Many aspects of Listeria infection in mice parallel those that occur in humans infected with tuberculosis. They found that when mice had a latent herpes infection, the bacteria replicated more slowly and were less likely to kill the mice.  

Generally, when herpes is still in the acute phase of infection, no protective effect was present. When they exposed the mice to a mutant herpes virus that can infect but cannot establish latency, the herpes infection did not confer resistance.  

They think that the virus may be prompting the immune system to produce more interferon gamma to keep itself from emerging from latency. If the virus stays latent, it prevents itself from seriously endangering the host and losing its home if the host dies.  

These researchers noted that human herpes viruses and mouse herpes viruses are genetically very closely related.  

So, since it is known that the human herpes viruses, whether cold sore or genital herpes varieties have developed complex defense mechanisms to AVOID immune system surveillance and hence their destruction by the same, in another way, they have also paid some tribute to the same biological government by enhancing its functioning against other body microbe invaders


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