Busybody. A new study suggests that HSV-2, seen here as orange particles, is always active, even when patients do not show symptoms.
Dennis Kunkel Microscopy Inc./Visuals Unlimited, Inc.
Genital herpes comes and goes - at least that what it looks like to patients. But a mathematical model published in the November issue 18 Science Translational Medicine suggests that herpes never slumbers. Instead, nerve cells pump continuously tiny amounts of virus in the life of a victim. If the conclusions are, it can be much harder to stop the patient transmitting infection than researchers thought.
As many as one in five people is infected permanently with herpes simplex virus 2 (HSV-2), the most common cause of genital ulcers of the skin. The virus is transmitted through sexual intercourse; After infection, it takes refuge in the nerve cells that have their endings in the genital skin. HSV-2 is not a problem in 80% of those infected, but a minority suffering from blisters and sores once or twice a month. For decades, most scientists thought the virus was just "off" in the intervals between epidemics, said William Halford, who studies herpes at Southern Illinois University School of Medicine in Springfield.
But this view is under fire the past decade, researchers have shown that the virus is sometimes present in genital skin, even if no lesions are apparent. The new work, by infectious diseases researcher Lawrence Corey and his colleagues from the University of Washington and the Center for Research on Cancer Fred Hutchison, both in Seattle, goes even further.
Joshua Schiffer, a clinician and mathematical modeler Corey group built mathematical models from a large number of patients and virological data - including the amount of virus in the skin of patients who took four samples per day for 60 days. This is what seems to happen: the nerve cells lose tiny amounts of virus almost constantly in the genital skin. Frequently, a virus infects an epithelial cell, which in relation to a nerve cells are "real virus factories" said Schiffer They produce massive amounts of virus that can infect other epithelial cells nearby and can likely also infect . sexual partners in most cases the infected epithelial cells are rapidly killed by CD8 + cells, another type of white blood cells only occasionally does infection overwhelm the immune system, resulting in a lesion [
"It is impressive that they were able to build a model that makes sense of a large amount of clinical data," said Philip Krause, a researcher herpes to the Food and Drug administration of the United States. "It is a very thoughtful way of looking at the data." Halford said the document should help dispel the notion, still supported by many scientists of herpes, the virus "does nothing" between clinical episodes.
The results may also explain certain properties of Antiherpes drugs like acyclovir, says Schiffer. For example, in a case where the herpes patients acyclovir to prevent their infection from partners, the drug was only 50% effective. If virus shedding never ceases, these drugs have a much harder job, said Schiffer, in particular compounds, such as acyclovir that quickly disappear from the body of a patient. To really prevent transmission, the drugs should last longer or stop the shedding by nerve cells, he adds -. But it's a challenge
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