Metzitzah b' peh (MBP), the direct mouth-to-bleeding-penis-sucking done by haredi mohels after cutting off the baby's foreskin is a dangerous practice that can transmit disease, like Herpes Simplex 1. to the infants. Because neonates have very immature immune systems, herpes can – and has – killed some of them, and maimed and sickened others. Haredi rabbis refuse to stop this dangerous practice, however. But now there is more evidence of the extreme damage herpes can do to the mind – evidence that may support Rabbi Dr. Moshe Tendler's decade-old contention that herpes transmitted to infants through MBP may be causing learning disabilities.
Cold Sore Virus iIncreases The Risk Of Dementia
Infection with herpes simplex virus increases the risk of Alzheimer's disease. Researchers at Umeå University claim this in two studies in the journal Alzheimer’s & Dementia.
"Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer's disease. This also means that we have new opportunities to develop treatment forms to stop the disease," says Hugo Lövheim, associate professor at the Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, who is one of the researchers behind the study.
Alzheimer's disease is the most common among the dementia diseases. In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer's disease. A majority of the population carries this virus. After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause typical mouth ulcer. The hypothesis which links the herpes virus and Alzheimer's disease is based on that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain. There this can in turn start the process which results in Alzheimer's disease.
Hugo Lövheim and Fredrik Elgh, professor at the Department of Virology, have now confirmed this link in two large epidemiological studies. In one study, which is based on the Betula project, a study on ageing, memory and dementia, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer's disease. This study had 3,432 participants who were followed for 11.3 years on average. In another study, samples donated to the Medical Biobank at Umeå University from 360 people with Alzheimer's disease were examined and as many matched people who had not developed dementia. The samples were taken on average 9.6 years before diagnosis. This study showed an approximately doubled risk of developing Alzheimer's disease if the person was a carrier of the herpes virus.
"Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer's disease," says Hugo Lövheim.
Read the studies in Alzheimer’s & Dementia
Worse than this, the herpes virus remains active even when no visible signs, like cold sores, exist:
Herpes Remains Active Even When No Symptoms Appear
Australian National University
Scientists investigating the herpes virus have been surprised to find an ongoing conflict in the cells of sufferers, even when the virus is apparently dormant.
Herpes Simplex Type 1 is a virus that causes cold sores. It remains in the body’s nervous system indefinitely after infection. Around 80 per cent of Australians carry the virus, although it is usually in a dormant state.
“We thought when the disease was dormant, it was a truce,” said Associate Professor David Tscharke, from the Research School of Biology. “It turns out that the virus is waking up more often than we thought, but our cells are constantly pushing it down.”
The findings could lead to new treatments, and give researchers insights into why cold sores only flare up sporadically and why some infected people never suffer cold sores at all.
Associate Professor Tscharke’s team used both cells and viruses that were genetically modified so that infected cells changed colour to a bright yellow, even if the virus was dormant.
These individual cells were then identified using a microscope equipped with laser that can be used to cut them out, allowing their level of virus activity to be measured.
“We expected that we would see no activity in the dormant cells,” Associate Professor Tscharke said.
“The surprise came when we found the virus was doing something in many cells. Not all of these cells have the same level of virus activity either. For some it’s very low and in others more of the virus genes are turned on. The host cells were responding most strongly when there was lots of virus activity.
“When we thought there was nothing going on we had no targets to look at. Now we know there is an interaction we can look for ways to help the good guys to win.”
The research is published in PLOS Pathogens.