HERPES SIMPLEX

OPPORTUNISTIC INFECTION HIV/AIDS

VIRUS (HSV)
Liza Qurrah Ayuniyyah
St. Wahida Adawiah Ansar
Tya Putri Permata
Opportunistic Infections
OPPORTUNISTIC INFECTIONS (OIS) ARE INFECTIONS THAT
OCCUR MORE OFTEN OR ARE MORE SEVERE IN PEOPLE WITH
WEAKENED IMMUNE SYSTEMS THAN IN PEOPLE WITH
HEALTHY IMMUNE SYSTEMS. PEOPLE WITH WEAKENED
IMMUNE SYSTEMS INCLUDE PEOPLE LIVING WITH HIV
 opportunistic infections (OIs), including a variety of viral, fungal,
bacterial, and protozoal diseases. Herpes simplex virus (HSV)
infections in persons infected with HIV usually occur as a result of
the reactivation of virus that has been present in the body long
before infection with HIV. HSV causes skin and mucous
membrane infections in persons with HIV infection, just as it does
in individuals with normal immune systems. In persons with HIV,
however, these reactivated infections may be severe and
protracted. Longstanding severe HSV lesions, in fact, can be one
of the first symptoms of AIDS. Nonetheless, even in AIDS patients,
HSV lesions typically remain localized and do not spread
throughout the body
 HERPES SIMPLEX
VIRUS
Herpes simplex viruses (HSV) commonly
known as herpes. herpes simplex is an
infection of the skin with the hsv. HSV
remains latent in nerve root ganglia of
infected persons and is trought to reactive
several time yearly. hsv is transmitted by
closed personal contact and infection occur via
inoculation of virus into susceptible mucosal
surfaces (eg. oropharyx, cervix, conjunctiva)
or through small cracks in the skin.
There are 2 types of herpes
virus :
HERPES TYPE 1 (HSV-1) WHICH IS TRANSMITTED
THROUGH ORALSECRETION OR SORES ON THE
SKIN.
HERPES TYPE 2 (HSV-2) TRANSMITTED DURING
SEXUAL CONTACT WITH SOMEONE WHO HAS A
GENITAL HSV-2 INFECTION.
 Epidemiology
Worldwide rates of either HSV-1 or HSV-2 are
between 60 and 95% in adults.
Prevalence of HSV-2 in those between the ages of
15 and 50 is about 535 million as of 2003 or 16% of
the population, with highest rates in in sub-Sahara
Africa and lowest in western Europe, and with
greater rates among women and those in the
developing world
In 2012, an estimated 3.7 billion people under the age of 50,
or 67% of the population, had HSV-1 infection. Estimated
prevalence of the infection was highest in Africa (87%) and
lowest in the Americas (40-50%). With respect to genital
HSV-1 infection, 140 million people aged 15-49-years were
estimated to have genital HSV-1 infection worldwide in 2012,
but prevalence varied substantially by region. Most genital
HSV-1 infections are estimated to occur in the Americas,
Europe and Western Pacific, where HSV-1 continues to be
acquired well into adulthood.
 CLINICAL MANIFESTATION
MANY PEOPLE INFECTED WITH
HSV-2 DISPLAY NO PHYSICAL
SYMPTOMS-INDIVIDUALS WITH
NO SYMPTOMS ARE DESCRIBED
AS ASYMPTOMATIC OR AS
FOLLOWING A PRIMARY INFECTION, SUBCLINICAL HERPES. PEOPLE
THE VIRUS ENTERS AT THE SITE OF WITH IMMATURE OR
PRIMARY INFECTION, MIGRATES TO
SUPPRESSED IMMUNE SYSTEMS,
CELL BODY OF THE NEURON, AND
SUCH AS NEWBORNS,
BECOMES LATENT IN THE GANGLION.
TRANSPLANT RECIPIENTS, OR
AS A RESULT OF PRIMARY
PEOPLE WITH AIDS, ARE PRONE
INFECTION; THE BODY PRODUCES
TO SEVERE COMPLICATIONS
ANTIBODIES TO PARTICULAR TYPE OF
FROM HSV INFECTIONS
HSV INVOLVED, PREVENTING A
SUBSEQUENT INFECTION OF THAT
TYPE AT A DIFFERENT SITE
NEONATAL HERPES SIMPLEX IS
A HSV INFECTION IN AN GINGIVOSTOMATITIS AND
INFANT. IT IS A RARE BUT OROLABIAL HSV INFECTION.
SERIOUS CONDITION, USUALLY GINGIVOSTOMATITIS IS A
CAUSED BY VERTICAL SYMPTOMATIC PRIMARY HSV-1
TRANSMISSION OF ( HSV-1 OR 2) INFECTION, USUALLY
FROM MOTHER TO NEWBORN. OCCURRING IN CHILDREN, AND
DURING IMMUNODEFICIENCY CHARACTERIZED BY LESIONS IN
,HERPES SIMPLEX CAN CAUSE AND AROUND THE ORAL CAVITY.
UNUSUAL LESIONS IN THE SKIN CHILDREN ARE OFTEN UNABLE
.ONE OF THE MOST STRIKING IS TO SWALLOW BECAUSE OF THE
THE APPEARANCE OF CLEAN ASSOCIATED PAIN AND MAY
LINEAR EROSIONS IN SKIN BECOME DEHYDRATED.
CREASES

FIRST CLINICAL EPISODE OF
GENITAL HSV INFECTION
WHO STI guideline suggests a
standard dose :
a. Aciclovir 400 mg orally thrice
daily for 10 days (standard dose)
b. Aciclovir 200 mg orally five
times daily for 10 days
c. Valaciclovir 500 mg orally twice
daily for 10 days
d. Famciclovir 250 mg orally thrice
daily for 10 days
TREATMENT
RECURRENT CLINICAL EPISODES OF GENITAL HSV
INFECTION THAT ARE FREQUENT, SEVERE OR CAUSE
DISTRESS (SUPPRESSIVE THERAPY)
WHO STI guideline suggests
RECURRENT CLINICAL EPISODE OF Dosages for adults, adolescents and pregnant
GENITAL HSV INFECTION (EPISODIC
THERAPY)
women:
WHO STI guideline suggests a. Aciclovir 400 mg orally twice daily
Dosages for adults, adolescents and pregnant b. Valaciclovir 500 mg orally once daily
women: c. Famciclovir 250 mg orally twice daily
a. Aciclovir 400 mg orally thrice daily for 5 days, Dosages for people living with HIV and people
800 mg twice daily for 5 days, or 800 mg thrice
who are immunocompromised:
daily for 2 days
a. Aciclovir 400 mg orally twice daily
b. Valaciclovir 500 mg orally twice daily for 3 days
c. Famciclovir 250 mg orally twice daily for 5 days
b. Valaciclovir 500 mg orally twice daily
Dosages for people living with HIV and people who c. Famciclovir 500 mg orally twice daily
are immunocompromised:
a. Aciclovir 400 mg orally thrice daily for 5 days
b. Valaciclovir 500 mg orally twice daily for 5 days
c. Famciclovir 500 mg orally twice daily for 5 days
DIAGNOSIS
GENITAL HSV INFECTION IS OFTEN DIAGNOSED CLINICALLY.
HOWEVER, LABORATORY TESTING IS REQUIRED TO DIFFERENTIATE
BETWEEN HSV-1 AND HSV-2. WHEN VESICLES ARE NOT PRESENT,
LABORATORY CONFIRMATION MAY BE NEEDED TO RULE OUT OTHER
CAUSES OF GENITAL ULCERS. LABORATORY METHODS FOR THE
DIAGNOSIS OF HSV-2 INCLUDE DIRECT DETECTION FROM LESIONS
AND INDIRECT SEROLOGICAL METHODS. AVAILABLE TESTS FOR HSV-2
INCLUDE ANTIGEN DETECTION, ISOLATION OF VIRUS BY CULTURE AND
NUCLEIC ACID AMPLIFICATION TESTS (NAATS) FOR VIRAL DNA.
SEROLOGICAL ASSAYS ARE ALSO AVAILABLE TO SCREEN FOR HSV-2
INFECTION BY DETECTION OF TYPE-SPECIFIC ANTIBODIES, WHICH
DEVELOP IN THE FIRST SEVERAL WEEKS AFTER INITIAL INFECTION
AND PERSIST INDEFINITELY. ALTHOUGH VIRAL CULTURE HAS
PREVIOUSLY BEEN CONSIDERED THE GOLD STANDARD FOR HSV-2
DIAGNOSIS, NAATS ARE INCREASINGLY PREFERRED DUE TO HIGHER
SENSITIVITY, EASE OF SPECIMEN COLLECTION AND
TRANSPORTATION, AND FASTER RESULTS.
PREVENTION
ON AN ANNUAL BASIS, WITHOUT THE USE OF ANTIVIRAL OR CONDOMS, THE
TRANSMISSION RISK OF HSV-2 FROM INFECTED MALE TO FEMALE IS ABOUT
8-11 %. THE TRANSMISSION RISK FROM INFECTED FEMALE TO MALE AROUND
4-5 % ANNUALLY.

SUPPRESSIVE ANTIVIRAL THERAPY REDUCES THESE RISKS BY 50%. ANTIVIRAL

ALSO HELP PREVENT THE DEVELOPMENT OF SYMPTOMATIC HSV IN
INFECTION SCENARIOS, MEANING THE INFECTED PARTNER WILL BE
SEROPOSITIVE BUT SYMPTOM-FREE BY AROUND 50%.

CONDOM USE IS MUCH MORE EFFECTIVE AT PREVENTING MALE-TO-FEMALE

TRANSMISSION THAN VICE VERSA. THE EFFECTS OF COMBINING ANTIVIRAL
AND CONDOM USE IS ROUGHLY ADDITIVE, THUS RESULTING IN A 75%
COMBINED REDUCTION IN ANNUAL TRANSMISSION RISK.
PREVENTION OF VERTICAL
HSV TRANSMISSION
The most common strategies for preventing transmission seek to
reduce neonatal exposure to active genital lesions. In women with
active recurrent genital HSV lesions, antiviral suppressive therapy
with oral acyclovir or valacyclovir can be started at 36 weeks of
gestation, a practice that has been associated with decreased
genital lesions at the time of delivery, decreased viral detection by
viral culture or PCR, and subsequently a reduced need for
cesarean delivery for the indication of genital HSV.