vaccine reduces incidence of herpes by 70%

[Guest guest]

out of context i am guessing this was printed in 1998. it says vaccines

studies had been conducted for 60 yrs prior to this piece. i'd like to know how

they can conclude it successfully prevents contraction, i guess that is

ultimately my question for all these vaccines. do they have people locked away

who have

never been exposed to the enviroment or vaccines and then they expose them

and compare that with these idiots in these trials? Nevermind, i guess it's just

been a bad day!

http://www.utmb.edu/newsroom/02pr/nov02/herp_vacc.htm

 

University of Texas Medical Branch at Galveston

Public Affairs Office

301 University Boulevard, Suite 3.102

Galveston, Texas 77555-0144

(409) 772-2618 (800) 228-1841

www.utmb.edu

NEW VACCINE REDUCES INCIDENCE OF GENITAL HERPES DISEASE BY MORE THAN 70

PERCENT IN UNINFECTED WOMEN, STUDY FINDS

GALVESTON, Texas—Although it didn’t safeguard men, a new vaccine reduced by

more than 70 percent the incidence of genital herpes disease in women who were

previously uninfected with the oral and genital herpes viruses.

That is the conclusion of a report on two phase-three clinical trials testing

the vaccine in 2,714 people, 978 of them women, at centers across the globe

and published in the Thursday, Nov. 21, edition of the New England Journal of

Medicine.

“People have been trying to make a herpes vaccine without success for more

than 60 years,†said infectious disease specialist and vaccinologist Lawrence

R.

Stanberry, chairman of the Department of Pediatrics at the University of

Texas Medical Branch at Galveston (UTMB) and lead author of the paper. He added,

“

This is the first one to prove effective.â€

According to 1997 figures, the most recent statistics available from the

federal Centers for Disease Control and Prevention, about 45 million Americans

have contracted genital herpes. This means about one in five of all people over

age 12 outside jails, prisons, nursing homes and hospitals have the virus

technically known as herpes simplex virus type 2 (HSV-2). That virus is so named

to

distinguish it from herpes simplex virus type 1 (HSV-1), a closely related

virus that causes similar small, sometimes painful “fever blisters†around

the

lips and nostrils in about 80 percent of Americans.

“These are very exciting findings,†Stanberry said. “These new studies

suggest that a comprehensive campaign to vaccinate girls and women not infected

with either type of herpes simplex virus could significantly reduce the spread

of

the herpes epidemic in the general population.â€

As a result of these studies, the National Institutes of Health and the drug

company GlaxoKline are collaborating on new studies scheduled to begin

this month that will test the vaccine on 7,550 women between 18 and 30 years old

“who don’t have HSV-2 and don’t want to get it,†said a co-author of the

paper, K. Tyring, UTMB professor of dermatology and microbiology and

immunology and director of the UTMB Center for Clinical Studies. Tyring’s

center

enrolled more than 500 people in the two vaccine studies, the largest number

tested at any single center in the studies reported in the new paper.

The initial study analyzed the effects of the three-dose vaccine in a total

of 268 women and 579 men free from infection with both HSV-1 and HSV-2. The

type 2 virus may cause painful lesions in the genital region that can increase

susceptibility to other sexually transmitted diseases, including the AIDS virus.

In the United States alone, about 2,500 newborn babies are infected with the

virus, which is potentially fatal; they usually acquire it from their

HSV-2-infected mothers in the birth canal.

In the second study reported in the same paper, researchers focused on 710

women and 1,157 men who had not been infected with HSV-2. In both groups, the

study subjects’ regular sexual partners had a history of genital herpes. As in

the first study, the recipients were injected with the vaccine followed by a

second dose a month later and a third dose after six months.

In the first group of women tested, the vaccine proved 73 percent effective

in protecting against genital herpes disease for 19 months, the duration of the

study. In the second group, which was designed to focus on those not

previously infected with HSV-2 alone, analysis showed that the vaccine was 74

percent

effective in preventing genital herpes in women who had not been infected with

either HSV-1 or HSV-2. Vaccines generally protect against disease, not

infection, Stanberry noted, and it is unclear whether latent infection in those

vaccinated might lead to transmission.

In addition to not working in men, the vaccine was not effective in women who

had been exposed to HSV-1. Stanberry said the current studies suggested that,

in women specifically, prior infection with oral herpes seems to confer some

protection against acquiring genital herpes. But he said that conclusion is

likely to be controversial because previous studies have reported contrary

findings.

The paper’s authors said it wasn’t clear why the vaccine was effective in

women and not in men but said it might have something to do with how the virus

enters the body, which is thought to be different in men and women. In men,

breaks or tears in skin of male sex organs are thought to be the main way HSV

gains entry. Intact skin is “a highly effective barrier against penetration by

HSV,†the authors write.

Given the same number of sexual partners, women are twice as likely to

contract herpes as men, Stanberry noted. Possibly this is so because in women,

“

acquisition of HSV is likely to occur though the vaginal-cervical mucous

membrane,â€

which lacks a typical skin barrier, the studies’ authors note. That same

female biological structure may help explain why the vaccine works in women, the

paper speculates: “Secretions containing antibodies and migratory white cells

constantly bathe this membrane. HSV-specific responses induced by vaccination

could act locally to provide an immunologic barrier to acquisition at this

mucosal site that is not applicable to men.â€

Stanberry said the researchers suspect that a new adjuvant—a novel

combination of substances called alum and 3-O-deacylated-monophosphoryl lipid A,

designed to make the vaccine more potent in generating an immune system

response—may

make the vaccine work differently in women than in men by inducing a cascade

of useful immune responses in the vaginal-cervical mucous membranes. The

so-called adjuvant vaccine consists of a genetically altered snippet of the

HSV-2

virus called HSV-2 glycoprotein-D-subunit plus the adjuvant.

Stanberry said animal studies suggest that the vaccine also may have a

protective effect in women against acquiring HSV-1 as well as against HSV-2.

HSV-1—

oral herpes—can cause herpes keratitis, an eye inflammation that can lead to

blindness, herpes encephalitis, a potentially fatal inflammation of the brain,

and gingivostomatis, an extremely painful inflammation of the mouth, mostly in

children.

“If further testing confirms that this vaccine is effective against HSV-1 as

well as against HSV-2,†Stanberry said, “I can envision a day when younger

girls are vaccinated once to protect them against HSV-1 and then get a booster

shot again before puberty to protect them down the road†against the sexually

transmitted type 2 virus.

The HSV-2 glycoprotein-D-adjuvant vaccine is currently available only to

those participating in clinical trials. If those tests continue to prove

successfu

l and the Food and Drug Administration gives the new vaccine a green light,

the new vaccine could be on the market in about five years.

GlaxoKline Biologicals of Rixensart, Belgium, and GlaxoKline

Pharmaceuticals of Collegeville, Pa., funded the newly reported studies.

Note: Women wishing to enroll in expanded clinical trials of the new

anti-herpes vaccine may contact the UTMB Center for Clinical Studies at (281)

333-2288.

-UTMB-