Sunday, April 17, 2011

Herpes Simplex Virus Type 2

As one of the most common sexually transmitted diseases world wide, Herpes Simplex Virus-2 is without question a public health concern, (approximately 536 million are HSV-2 positive world wide.) Surprisingly though, recent findings reveal that, unlike what most of us think we know about STD's, one does not have to present with symptoms of the virus to be actively contagious in the community.   According to a study presented at a JAMA media research convention, Dr. Anna Wald, (University of Washington and Fred Hutchinson Cancer Research Center), discussed that "the risk of sexual transmission does not correlate with the recognition of clinical signs and symptoms of HSV-2 but most likely correlates with the activity of the virus on the genital skin or mucosa (viral shedding.)"

Data was collected from studies performed by Dr. Anna and her colleagues from 1992 to 2008, of 498 seropositive HSV-2 carriers. Polymerase Chain Reaction was performed on samples from these studies, (collected for 30 consecutive days), of the genital mucous of these individuals for testing of the viral DNA. Subclinical genital shedding rates along with the PCR testing revealed that "...the median [midpoint] amount of HSV detected ...was similar in persons with symptomatic and asymptomatic infection." The same studies also revealed that those individuals presenting lesions (symptoms) were indeed infectious while symptoms lasted (43% of the total amount of days they were tested for, carriers were shedding), but asymptomatic persons only presented 16.4% of the the time (in testing.)  These findings demonstrated that asymptomatic individuals were still at risk for "shedding" or passing on the infection, despite an absence of visible lesions.

Although it is not fully understood how the herpes virus invades cells, it is understood that "most viruses need cell-entry proteins called fusogens in order to invade cells," but herpes requires fusogens plus two other "entry" proteins to invade cells.  Efforts to combat the disease are ongoing, and research and experiments performed by many scientists including those of Dr. Ekaterina Hedwein have "led us to believe that this protein complex is not a fusogen itself but that it regulates the fusogen. We also found that certain antibodies interfere with the ability of this protein complex to bind to the fusogen, evidence that antiviral drugs that target this interaction could prevent viral infection."
As many already know, there is no cure for the herpes virus and it persists in the body for the infected person's lifetime, retreating or resurfacing at random and irregular intervals.  Known effects of the virus range from cold sores, encephalitis, blindness, cancer, and in cases of transmissions from mother to fetus, even death (of the fetus).  Hence, despite what we think we already know about risks of transmission and keys to avoiding infection, ongoing research is imperative to finding a cure for those who, for one reason or another, have contracted the virus


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