Bien Ag Nina Ian John “G” Rachel Mark Jocelle Edo Gienah Jho Kath Aynz Je Glad Nickie

Ricobear Teacher Dadang Niňa Arlene Vivs Paul fie Rico F. Ren Mai Revs Mavis Jepay Yana Mayi Serge Hung Tope

S3 L14: Herpesviruses by Dr. Bunyi November 14, 2010

HERPES VIRUSES

Herpes Simplex Virus (HSV) types 1 and 2 HERPES SIMPLEX VIRUSES

Varicella-Zoster Virus (VZV) PROPERTIES
Cytomegalovirus (CMV)
Belong to the -herpesvirus subfamily of herpesviruses
Epstein-Barr virus (EBV) Double stranded DNA enveloped virus with a genome of around 150
Herpesvirus 6 and 7 (HHV 6, HHV 7) kb
Herpesvirus 8 (Kaposi sarcoma-associated herpesvirus) 2 distinct types: HSV 1 and HSV 2
React serologically but some unique proteins exist for each type
STRUCTURE AND COMPOSITION Different mode of transmission:
Large viruses o Type 1: contact, saliva
o Type 2: sexual, maternal genital infection to newborn
Indistinguishable by Electron
The genome of HSV-1 and HSV-2
microscope o share 50 - 70% homology.
Core of dsDNA in the form of a o share several cross-reactive epitopes with each other.
toroid surrounded by a protein o also antigenic cross-reaction with Varicella Zoster Virus
coat with icosahedral symmetry (VSV).
Nucleocapsid surrounded by Man is the only natural host for HSV.
envelope
EPIDEMIOLOGY
Tegument: amorphous, asymmetric structure between capsid and
envelope HSV - spread by contact (shed in saliva, tears, genital and other
Striking feature: sequence arrangement secretions).
Most common form of infection results from a KISS given to a child
Genome possess terminal and internal repeated sequences
or adult from a person shedding the virus.
Some members undergo genome rearrangements giving rise to Primary infection
genome “isomers” o usually trivial or subclinical in most individuals.
o disease mainly of very young children ( < 5 yrs.)
PROPERTIES OF HERPES VIRUSES 2 peaks of incidence,
o 0 - 5 years
Enveloped double stranded DNA viruses. o late teens ( sexual activity commences).
Genome : long and short fragments orientated in either direction, 10% of the population acquires HSV infection through the genital
giving a total of 4 isomers. route and the risk is concentrated in young adulthood.
Set up latent or persistent infection following primary infection Generally : HSV-1 causes infection above the belt ; HSV-2
Reactivation - more likely during periods of immunosuppression belowthe belt.
Both 1º infection and reactivation are likely to be more serious in Clinical isolates :
immunocompromised patients. o 40% from genital sores are HSV-1
o 5% of strains isolated from the facial area are HSV-2.
THREE SUBFAMILIES: ( data is complicated by oral sexual practices)
Alphaherpesviruses - HSV-1, HSV-2, VZV Following 1º infection,
o rapid growth, latency in sensory ganglia 45% of orally infected individuals and
Betaherpesviruses - CMV, HHV-6, HHV-7 60% of patients with genital herpes will experience recurrences.
o slow growth ; restricted host range actual frequency of recurrences varies widely between individuals.
Gammaherpesviruses - EBV, HHV-8 mean number of episodes per year : 1.6
o growth in lymphoblastoid cells
PATHOGENESIS
1º infection, HSV spreads locally and a short-lived viremia occurs,
whereby the virus is disseminated in the body. Spread to the
craniospinal ganglia occurs.
virus then establishes latency in the craniospinal ganglia.
exact mechanism of latency - not known,
may be true latency where there is no viral replication or viral
persistence where there is a low level of viral replication.
Reactivation - triggers can provoke a recurrence.
Include:
 physical or psychological stress,
 infection ( pneumococcal and meningococcal),
 fever
 irradiation (including sunlight)
 menstruation

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 A mild meningitis may be present.
Recurrence of genital herpes: 60%
CLINICAL MANIFESTATIONS o Recurrent lesions in perianal area tend to be numerous
HSV is involved in a variety of clinical manifestations which includes and persists longer than their oral HSV-1 counterparts.
 Acute gingivostomatitis
 Herpes labialis (cold sore) HERPES SIMPLEX ENCEPHALITIS
 Ocular herpes One of the most serious complications of herpes simplex disease.
 Herpes genitalis There are two forms: neonatal and focal
 Other forms of cutaneous herpes Neonatal – global involvement brain is almost liquefied. (Mortality
 Meningitis
rate approaches 100%)
 Encephalitis
 Neonatal herpes Focal disease – temporal lobe most commonly affected ; appears
in children and adults. ; arise from reactivation of virus. The mortality
ACUTE GINGIVOSTOMATITIS and HERPES LABIALIS rate is high (70%) without treatment.
Utmost importance : make a diagnosis of HSE early.
• Acute Gingivostomatitis
IV acyclovir : given in all cases of suspected HSE before laboratory
o Most common manifestation of
results are available.
primary herpetic infection.
o Pain and bleeding of the gums.
NEONATAL HERPES SIMPLEX
 1 - 8 mm ulcers
Incidence varies from country to country
with necrotic bases
e.g. 1: 4,000 live births in the U.S.
 Neck glands enlarged, accompanied by fever.
1:10,000 live births in the UK
o Usually a self limiting disease which lasts around 13
days. Baby - usually infected perinatally during passage through the birth
canal.
• Herpes labialis (cold sore) PROM - well recognized risk factor.
o Following primary infection, Risk of perinatal transmission : greatest when there is a florid
45% of orally infected primary infection in the mother.
individuals will experience Smaller risk from recurrent lesions in the mother : lower viral load
reactivation. and the presence of specific antibody
o Herpes labialis (cold sore) is a Other sources : oral lesions from the mother or a herpetic whitlow in
recurrenc e of oral HSV. a nurse.
o Prodrome of tingling, warmth 75% of cases occurs as newborn comes in contact with
or itching at the site usually heralds the recurrence; 12 Herpetic lesions in the birth canal
hours later, redness appears followed by papules and The spectrum : mild disease , localized to the skin, fatal
then vesicles. disseminated infection.
Infection : dangerous in premature infants.
OCULAR HERPES Where dissemination occurs, the organs most commonly involved
HSV causes a broad spectrum of ocular disease, ranging from mild are the liver, adrenals and the brain.
superficial lesions involving the external eye, to severe sight- Brain : severe prognosis encephalitis is global and of such severity
threatening diseases of the inner eye. that the brain may be liquefied.
o Primary HSV keratitis – dendritic ulcers Survivors : residual disabilities.
o Recurrent HSV keratitis Acyclovir should be promptly given in all suspected cases of
o HSV conjunctivitis neonatal HSV infection.
o Iridocyclitis, chorioretinitis and cataract Only means of prevention : offer CS to mothers with florid genital
HSV lesions.
GENITAL HERPES
Genital lesions may be DISSEMINATED HERPES SIMPLEX
primary, recurrent or initial. more likely to occur in immunocompromised individuals.
Sites: penis, vagina, cervix, vesicular resembles that of chickenpox.
anus, vulva, bladder, sacral other organs involved
nerve routes, spinal nerves o e.g. liver, spleen, lungs, and CNS
and meninges
o Genital lesions OTHER CUTANEOUS MANIFESTATIONS
prone to 2º bacterial infection
Eczema herpeticum: potentially a serious disease that occurs in
o eg. S. aureus, Streptococcus, Trichomonas and
patients with eczema
C.albicans.
Herpetic whitlow : arise from implantation of the virus into the skin,
Dysuria: common complaint
typically affect fingers
o Urinary retention: in severe cases
“Zosteriform herpes simplex”: rare presentation where HSV
Local sensory nerves may be involved; leads to radiculitis.
lesions appear in a dermatomal distribution similar to herpes zoster

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 Herpes gladiatorum: lesions on the bodies of wrestlers
LABORATORY DIAGNOSIS
Direct Detection
o Electron microscopy of vesicle fluid - rapid result but
cannot distinguish between HSV and VZV
o IF skin scrapings - can distinguish between HSV and
VZV
o PCR - now used routinely for the diagnosis of herpes
simple encephalitis
Virus Isolation
o HSV-1 and HSV-2 - among the easiest viruses to
cultivate.( takes only 1 - 5 days for a result to be
available).
o Serology
o Not useful in the acute phase (it takes 1-2 weeks before
antibodies appear after infection).
o document recent infection.
1 varicella - endemic disease; classic diseases of childhood
highest prevalence : 4 - 10 years old
Varicella - highly communicable, attack rate of 90% in close
contacts.
Most people become infected before adulthood but 10% of young
adults remain susceptible.
Herpes zoster : occurs sporadically and evenly throughout the year.
PATHOGENESIS
Entry via the respiratory tract and spreads to the lymphoid system.
After an IP of 14 days, the virus arrives at its main target organ, the
skin.
Following 1º infection, the virus remains latent in the cerebral or
posterior root ganglia.
In 10 - 20% of individuals, a single recurrent infection occurs after
several decades.
The virus reactivates in the ganglion and tracks down the sensory
nerve to the area of the skin innervated by the nerve, producing a
varicella form rash in the distribution of a dermatome.

VARICELLA
1º infection results in varicella
(chickenpox)
IP : 14-21 days
fever, lymphadenopathy. a
widespread vesicular rash.
Features : characteristic;diagnosis
made on CLINICAL grounds alone.
Complications : rare ; more
frequent and severe in adults and immunocompromised patients.
Most common complication : 2º bacterial infection
Severe complications : life threatening –
MANAGEMENT
viral pneumonia, encephalitis, and hemorrhagic chickenpox.
Generally : antiviral chemotherapy indicated :
1. severe 1 infection HERPES ZOSTER (SHINGLES)
2. dissemination Herpes zoster mainly affect a single dermatome of t he skin.
3. sight is threatened May occur at any age; majority of
4. herpes simplex encephalitis.
patients are > 50 years of age.
The latent virus reactivates in a
Acyclovir
sensory ganglion and tracks down
DOC for most situations
the sensory nerve to the appropriate
I.V. (HSV infection in normal and immunocompromised patients) segment.
Oral (treatment and long term suppression of mucocutaneous Herpes zoster mainly affect a single
herpes and prophylaxis of HSV in immunocompromised patients) dermatome of the skin.
Cream (HSV infection of the skin and mucous membranes) Characteristic eruption of vesicles in
Ophthalmic ointment the dermatome
often accompanied by intensive pain
Famciclovir and Valacyclovir  may last for months (postherpetic
oral only, more expensive than acyclovir. neuralgia)
affecting the eye and face may pose great problems.
Other older agents – e.g. idoxuridine, trifluorothymidine, Vidarabine (ara-
far greater problem in immunocompromised patients in whom the
A). reactivation occurs earlier in life and multiple attacks occur as well
highly toxic and is suitable for topical use for ophthalmic infection as complications.
only Complications : rare, include encephalitis and
disseminated herpes zoster.
VARICELLA- ZOSTER VIRUS
Congenital VZV Infection
90% of pregnant women already immune, therefore 1º infection are
PROPERTIES
rare during pregnancy.
Belong to the -herpesvirus subfamily of herpesviruses
1º infection during pregnancy
Double stranded DNA enveloped virus o carries a greater risk of severe disease, in
Genome size 125 kbp, long and short fragments with a total of 4 particular pneumonia.
isometric forms.
One antigenic serotype only, although there is some cross reaction NEONATAL VARICELLA
with HSV. • VZV can cross placenta in late stages of pregnancy to infect the
fetus congenitally.
EPIDEMIOLOGY

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 • Neonatal varicella: vary from mild disease to a fatal disseminated
infection.
• If rash in mother occurs > 1 week before delivery, sufficient
immunity transferred to the fetus.
• Varicella Zoster Immunoglobulin (VZIg) should be given to
susceptible pregnant women who had contact with suspected cases
of varicella.
• VZIg should also be given to infants whose mothers develop
varicella during the last 7 days of pregnancy or the first 14 days
after delivery.
LABORATORY DIAGNOSIS
Clinical presentations : characteristic
Laboratory diagnosis :
only for atypical presentations, particularly in the immunocompromised.
Virus Isolation - requires 2-3 weeks for a results.
Direct detection - electron microscopy may be used for vesicle fluids
but cannot distinguish between HSV and VZV. IF on skin scrapings
can distinguish between the two.
Serology –
o (+) VZV IgG : past infection and immunity.
o (+) IgM : recent primary infection.
MANAGEMENT
Uncomplicated varicella : self limited ; no specific treatment.
o Acyclovir :
 accelerate the resolution of the disease
 should be given promptly :
 immunocompromised individuals with varicella
 normal individuals with serious complications
o (pneumonia and encephalitis).
Herpes zoster in a healthy individual :NOT a cause for concern.
o management of post herpetic neuralgia can be problematic
o International Herpes Management Forum recommends
antiviral therapy is offered routinely to all over age 50 years
presenting with herpes zoster.
o 3 drugs for herpes zoster: acyclovir, valacyclovir, and
famciclovir. There appears to be little difference in efficacy
between them.
o The International Herpes Management Forum : antiviral
therapy SHOULD be offered routinely to all patients > 50 yrs of
age with herpes zoster.
o acyclovir, valacyclovir, and famciclovir ( little difference in
efficacy between them).
PREVENTION
Preventive measures: considered at risk of contracting severe
varicella infection e.g. leukemic children, neonates, and pregnant
women
Where urgent protection is needed, passive immunization should be
given.
o Varicella Zoster immunoglobulin (VZIG) is the
preparation of choice but it is very expensive.
o A live attenuated vaccine is available.
 safe, even in children with leukemia provided
that they are in remission.
CYTOMEGALOVIRUS
PROPERTIES
Belong to the -herpesvirus subfamily of herpesviruses
double stranded DNA enveloped virus
Nucleocapsid 105nm in diameter, 162 capsomers
structure of the genome of CMV is similar to other herpesviruses,
consisting of long and short segments which may be orientated in
either direction, giving a total of 4 isomers.
A large no. of proteins are encoded for, the precise number is
unknown.
EPIDEMIOLOGY
CMV - one of the most successful human pathogens, can be
transmitted vertically or horizontally usually with little effect on the
host.
Transmission may occur in utero, perinatally or postnatally. Once
infected, the person carries the virus for life which may be activated
from time to time, during which infectious virions appear in the urine
and the saliva.
Reactivation can also lead to vertical transmission. It is also
possible for people who have experienced 1º infection to be
reinfected with another or the same strain of CMV, this reinfection
does not differ clinically from reactivation.
developed countries with a high standard of hygiene, 40% of
adolescents are infected and ultimately 70% of the population is
infected.
developing countries, > 90% of people are ultimately infected.
PATHOGENESIS
Once infected, the virus remains in the person for life
o May be reactivated from time to time, especially in
immunocompromised individuals.
Transmission: in utero, perinatally, or postnatally. Perinatal
transmission occurs.
Perinatal infection : acquired mainly through infected genital
secretions, or breast milk.
o Overall, 2 - 10% of infants are infected by the
o age of 6 months worldwide.
o 10x more common than congenital infection.
Postnatal infection mainly occurs through saliva.
o Others : sexual transmission
o blood and blood products
o transplanted organ
CLINICAL MANIFESTATIONS
Congenital infection - may result in cytomegalic inclusion disease
Perinatal infection - usually asymptomatic
Postnatal infection - usually asymptomatic. Minority of cases,
syndrome of IM may develop :
o fever, lymphadenopathy, and splenomegaly
o (-) heterophil antibody test
o (+) atypical lymphocytes in the blood
Immunocompromised patients : transplant recipients and AIDS
patients are prone to severe CMV disease such as pneumonitis,
retinitis, colitis, and encephalopathy.
Reactivation or reinfection with CMV is usually asymptomatic
EXCEPT in immunocompromised patients.
CONGENITAL INFECTION
Isolation of CMV from the saliva or urine within 3 wks of birth.
Commonest congenital viral infection affects 0.3 - 1% of all live
births.
2nd most common cause of mental handicap after Down's
syndrome
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 Responsible for more cases of congenital damage than rubella. Serology
Transmission - follow 1º or recurrent CMV infection. 40% chance of o (+) CMV
transmission to the fetus following a 1º infection. o IgG antibody : past infection.
May be transmitted to the fetus during all stages of pregnancy. o IgM : 1º infection
No evidence of teratogenicity, o found in immunocompromised patients
Damage to the fetus results from destruction of target cells once o with reactivation.
they are formed.
CYTOMEGALIC INCLUSION DISEASE
CNS abnormalities - microcephaly, mental retardation, spasticity, Cytopathic effect of CMV 
epilepsy, periventricular calcification.
Eye - choroidoretinitis and optic atrophy
Ear - sensorineural deafness
SPECIMEN FOR LABORATORY DIAGNOSIS
Liver - hepatosplenomegaly and jaundice due to
hepatitis.
Lung - pneumonitis
Heart - myocarditis
Thrombocytopenic purpura, hemolytic anemia
Late sequelae in individuals asymptomatic at birth - hearing defects
and reduced intelligence.

LABORATORY DIAGNOSIS
Direct detection
o biopsy - examined
histologically for CMV
inclusion antibodies or for the
presence of CMV antigens.
However, the sensitivity may
be low.
o The pp65 CMV antigenemia
test : routinely used for the
rapid diagnosis of CMV
infection
immunocompromised
patients.
o PCR for CMV-DNA : used in
some centers but there may be problems with
interpretation.
Virus Isolation
o conventional cell culture
: gold standard ; requires
up to 4 weeks for result.
o More useful : rapid
culture methods such as
the DEAFF test 
o provide a result in 24-48
hours.
TREATMENT
• Congenital infections:
– “Ganciclovir used to treat some congenitally infected
infants but is not recommended routinely” (Red Book 27th
Ed.)
• Potential toxicity of long term use
• Perinatal and postnatal infection: not necessary to treat such
patients
• Immunocompromised patients: early diagnosis of CMV infection and
give prompt antiviral therapy
– Anti-CMV agents in current use are ganciclovir,
foscarnet, and cidofovir.
PREVENTION
• No licensed vaccine available.
– Candidate live attenuated vaccine known as the Towne
strain
• Concern: administering a live vaccine which
in can become latent and reactivates.
• Prevention in transplant recipients: complicated and varies from
center to center. It may include the following measures.
– Screening and matching the CMV status of the donor
and recipient
– Use of CMV negative blood for transfusions
– Administration of CMV immunoglobulin to seronegative
recipients prior to transplant
– Give antiviral agents such as acyclovir and ganciclovir
prophylactically.
EPSTEIN-BARR VIRUS
Belong to the gammaherpesvirus subfamily of herpesviruses
Nucleocapsid 100 nm in diameter, with 162 capsomers
Membrane is derived by budding of immature particles through cell
membrane and is required for infectivity.
Genome is a linear double stranded DNA molecule with 172 kbp
The viral genome does not normally integrate into the cellular DNA
DEAFF TEST but forms circular epitomes which reside in the nucleus.
The genome is large enough to code for 100 - 200 proteins but only
a few have been identified.

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EPIDEMIOLOGY
Two epidemiological patterns seen with EBV.
Developed countries : 2 peaks of infection
o preschool children aged 1 - 6
o adolescents and young adults aged 14 - 20
o Eventually 80-90% of adults are infected.
Developing countries: much earlier age so that by the age of two,
90% of children are seropositive.
Transmitted by contact with saliva ( kissing)
Once infected, a lifelong carrier state develops whereby a low grade
infection is kept in check by the immune defenses.
PATHOGENESIS
• Lifelong carrier state develops once infected, whereby a low grade
infection is kept in check by the immune defenses.
• Low grade virus replication and shedding: demonstrated in epithelial
cells of the pharynx of all seropositive individuals.
• EBV: able to immortalize B-lymphocytes in vitro and in vivo
• Few EBV-immortalized B-cells can be demonstrated in the
circulation which is continually cleared by immune surveillance
mechanisms.
• EBV is associated with several very different diseases where it may
act directly or one of several co-factors.
Disease Association
1. Infectious Mononucleosis
2. Burkitt's lymphoma
3. Nasopharyngeal carcinoma
4. Lymphoproliferative disease and lymphoma in the
1. Immunosuppressed.
5. X-linked lymphoproliferative syndrome
6. Chronic infectious mononucleosis
7. Oral leukoplakia in AIDS patients
8. Chronic interstitial pneumonitis in AIDS patients.
INFECTIOUS MONONUCLEOSIS
• Primary EBV infection:
o usually subclinical in childhood
o Adolescents & adults: 50% chance this syndrome (of IM)
will develop.
• IM: self-limited disease: fever, lymphadenopathy & splenomegaly;
o In some: jaundice (due to hepatitis); (+) atypical
lymphocytes in the blood
• Complications: rare but may be serious
o e.g. splenic rupture, meningoencephalitis, pharyngeal
obstruction.
• Chronic IM may occur where eventually patient dies of
lymphoproliferative disease or lymphoma.
• Diagnosis of IM: heterophil antibody test and/or detection of EBV
IgM.
• NO specific treatment.
BURKITT’S LYMPHOMA
Burkitt's lymphoma (BL): occurs endemically in parts of Africa (most
common childhood tumor) & Papua New Guinea.
usually seen: children aged 3-14 yrs
Responds favorably to chemotherapy.
o Restricted to areas with holoendemic malaria. Therefore it
appears that malaria infection is a cofactor.
o Multiple copies of EBV genome and some EBV antigens can
be found in BL cells and patients with BL have high titers of
antibodies against various EBV antigens.
o BL cells show a reciprocal translocation between long arm of
chromosome 8 and chromosomes 14, 2 or 22.
This translocation result in the c-myc oncogene being transferred to
the Ig gene regions. This results in the deregulation of the c-myc
gene. It is thought that this translocation is probably already
present by the time of EBV infection and is not caused by EBV.
Sporadic cases of BL occur, especially in AIDS patients which may
or may not be associated with EBV.
In theory BL can be controlled by the eradication of malaria (as has
happened in Papua New Guinea) or vaccination against EBV.
NASOPHARYNGEAL CARCINOMA
Nasopharyngeal carcinoma (NPC) : malignant tumour of the
squamous epithelium of the nasopharynx ; prevalent in S. China ,
commonest tumour in men and the
2nd commonest in women.
Rare in most parts of the world,
though pockets occur in N. and C.
Africa, Malaysia, Alaska, and
Iceland.
Multiple copies of EBV genome and
EBV EBNA-1 antigen can be found
in cells of undifferentiated NPC.
Patients with NPC have high titres
of antibodies against various EBV antigens.
Environmental and genetic cofactors in NPC.
NPC usually presents late and thus the prognosis is poor.
In theory NPC can be prevented by vaccination.
IMMUNOCOMPROMISED PATIENTS
After primary infection, EBV maintains a steady low grade latent
infection in the body.
Should the person become immunocompromised, the virus will
reactivate.
In a few cases, lymphoproliferative lesions and lymphoma may
develop
lesions tend to be extranodal and in unusual sites such as the GI
tract or the CNS.
Transplant recipients e.g. renal - EBV is associated with the
development of lymphoproliferative disease and lymphoma.
AIDS patients - EBV is associated with oral leukoplakia and with
various Non-Hodgkin’s lymphoma.
Ducan X-linked lymphoproliferative syndrome - occurs exclusively in
males who had inherited a defective gene in the X-chromosome,
accounts for half of the fatal cases of IM.
DIAGNOSIS
Acute EBV infection : heterophil antibody test and/or
detection of anti-EBV VCA IgM.
Burkitt’s lymphoma : diagnosed by histology.
stained with antibodies to lambda light chains
 reveal a monoclonal tumour of B-cell origin.
>90% of cases, the cells express IgM at the cell
surface.
NPC : diagnosed by histology.
Anti-EBV VCA IgA : screen for early lesions of NPC and also for
monitoring treatment.
A patient with non-specific ENT symptoms who have elevated titres
of EBV IgA should be given a thorough examination.
VACCINATION
A vaccine against EBV which prevents primary EBV infection should
be able to control both BL and NPC.
Must be given early in life.; useful in seronegative organ transplant
recipients and those developing severe IM, such as the male
offspring of X-linked proliferative syndrome carriers.
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 Should NOT preferably be a subunit vaccine since there is a danger
that a live vaccine may still have tumorigenic properties.
The antigen chosen for vaccine development is the MA antigen gp
340/220 as antibodies against this antigen are virus neutralizing.
This vaccine is being tried in Africa.

OTHER HUMAN HERPES VIRUSES

PROPERTIES OF HHV-6 AND 7

Belong to the -herpesvirus subfamily of herpesviruses
Double stranded DNA genome of 170 kbp
Main target cell: T-lymphocyte, although B-lymphocytes may also be
infected.
HHV-6 and HHV-7 share limited nucleotide homology and antigenic
cross-reactivity.
It is thought that HHV-6 and HHV-7 are related to each other in a
similar manner to HSV-1 and HSV-2.

EPIDEMIOLOGY AND PATHOGENESIS

HHV-6 and HHV-7 : ubiquitous, found worldwide.
Transmitted mainly through contact with saliva and through breast
feeding.
HHV-6 and HHV-7 infection are acquired rapidly after the age of 4
months when the effect of maternal antibody wears off.
Adulthood, 90-99% of the population had been infected by both
viruses.
HHV-6 and HHV-7 remains latent in the body after primary infection
and reactivates from time to time.

CLINICAL MANIFESTATIONS
1º HHV-6 infection : associated with Roseola infantum
Infants : 4 months and 2 yrs.
A spiking fever develops over a period of 2 days followed by a mild Ang trans na ito ay inihahandog ng:
rash. The fever is high enough to cause febrile convulsions.
May be complicated by encephalitis. MICROBIOMAN (+ 1 )
If 1º infection is delayed until adulthood, there is a small chance that
an IM-like disease may develop in a similar manner to EBV and
CMV.
NO firm evidence linking HHV-6 to lymphomas or
lymphoproliferative diseases.
NO firm disease association with HHV-7 at present.
Although both viruses may be reactivated in immunocompromised
patients, it is yet uncertain whether they cause significant disease
since CMV is almost invariably present.

ROSEOLA INFANTUM

DIAGNOSIS AND MANAGEMENT

Roseola infantum : clinical
very few virology laboratories offer a diagnostic service for HHV-6 From 1st row (L to R): Paulfie, Edo, Teacher
or HHV-7 infection.
From 2nd row (L to R): Niña, Nickie, Turay
virus isolation : complicated
serology : mainstay of diagnosis ;
specific IgM and IgG are detected.
NO specific antiviral treatment

HUMAN HERPES VIRUS 8

Belong to the gammaherpesviruses subfamily of herpesviruses
Originally isolated from cells of Kaposi’s sarcoma (KS) -
associated with KS as well as some lesser known malignancies
such as Castleman’s disease and primary effusion lymphomas
HHV-8 DNA is found in almost 100% of cases of Kaposi’s sarcoma
Most patients with KS have antibodies against HHV-8
seroprevalence of HHV-8 : low among general population but is high
in groups of individuals susceptible to KS, such as homosexual
does not have a ubiquitous distribution

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